[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 461
1. Jones EL, Samulski TV, Dewhirst MW, Alvarez-Secord A, Berchuck A, Clarke-Pearson D, Havrilesky LJ, Soper J, Prosnitz LR: A pilot Phase II trial of concurrent radiotherapy, chemotherapy, and hyperthermia for locally advanced cervical carcinoma. Cancer; 2003 Jul 15;98(2):277-82
Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A pilot Phase II trial of concurrent radiotherapy, chemotherapy, and hyperthermia for locally advanced cervical carcinoma.
  • BACKGROUND: Five randomized studies have demonstrated a benefit derived from adding cisplatin (CDDP)-based chemotherapy to radiotherapy (RT) for treatment of cervical carcinoma.
  • The authors evaluated response and toxicity in patients with locally advanced cervical carcinoma (LACC) who were treated with concurrent weekly CDDP, HT, and RT (whole pelvis [n=7] and whole pelvis and paraaortic nodes [n=5]).
  • METHODS: From August 1998 through December 2000, 12 patients with LACC or locally recurrent cervical carcinoma (LRCC) following hysterectomy were enrolled on a pilot study combining weekly CDDP, HT, and RT.
  • Two of the 10 experienced recurrence outside the pelvis; 1 of these patients had pulmonary metastasis, and the other had isolated paraaortic nodal involvement.
  • Two patients treated for LRCC experienced local and systemic progression and died of disease within 6 months.
  • CONCLUSIONS: In this small series, trimodality therapy resulted in an excellent clinical response and was well tolerated.
  • [MeSH-major] Adenocarcinoma / therapy. Antineoplastic Agents / therapeutic use. Carcinoma, Squamous Cell / therapy. Cisplatin / therapeutic use. Hyperthermia, Induced. Uterine Cervical Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Female. Humans. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / radiotherapy. Neoplasm Recurrence, Local / therapy. Pilot Projects. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Cervical Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2003 American Cancer Society.
  • [CommentIn] Cancer. 2003 Jul 15;98(2):219-21 [12872338.001]
  • (PMID = 12872345.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA42745-16
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


2. Shanbhag S, Smith MR, Emmons RV: Tackling mantle cell lymphoma (MCL): Potential benefit of allogeneic stem cell transplantation. Stem Cells Cloning; 2010;3:93-102
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tackling mantle cell lymphoma (MCL): Potential benefit of allogeneic stem cell transplantation.
  • Mantle cell lymphoma (MCL) is a type of non-Hodgkins lymphoma (NHL) associated with poor progression-free and overall survival.
  • There is a high relapse rate with conventional cytotoxic chemotherapy.
  • Intensive combination chemotherapy including rituximab, dose intense CHOP- (cyclophosphamide-doxorubicin-vincristine-prednisone) like regimens, high dose cytarabine, and/or consolidation with autologous stem cell transplant (autoSCT) have shown promise in significantly prolonging remissions.
  • Data from phase II studies show that even in patients with chemotherapy refractory MCL, allogeneic stem cell transplant (alloSCT) can lead to long term disease control.
  • Most patients with MCL are not candidates for myeloablative alloSCT due to their age, comorbidities, and performance status.
  • Treatment decisions are complicated by introduction of novel agents which are attractive options for older, frail patients.
  • Further studies are needed to determine the role and timing of alloSCT in MCL.
  • Currently, for selected fit patients with chemotherapy resistant MCL or those who progress after autoSCT, alloSCT may provide long term survival.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 24198514.001).
  • [ISSN] 1178-6957
  • [Journal-full-title] Stem cells and cloning : advances and applications
  • [ISO-abbreviation] Stem Cells Cloning
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC3781733
  • [Keywords] NOTNLM ; GVL / allogeneic SCT / mantle cell lymphoma / nonmyeloablative
  •  go-up   go-down


3. Tunggal JK, Melo T, Ballinger JR, Tannock IF: The influence of expression of P-glycoprotein on the penetration of anticancer drugs through multicellular layers. Int J Cancer; 2000 Apr 1;86(1):101-7
Hazardous Substances Data Bank. SUCROSE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The influence of expression of P-glycoprotein on the penetration of anticancer drugs through multicellular layers.
  • The success of chemotherapy in the treatment of solid tumours may be limited by cellular mechanisms leading to drug resistance and/or by the slow penetration of drugs through tissue, resulting in a steep concentration gradient from tumour blood vessels.
  • The relationship between expression of P-gp by constituent cells and the penetration of P-gp substrates through tissue was studied by comparing the penetration of P-gp substrates through multicellular layers derived from either wild-type or P-gp overexpressing cell lines.
  • 1) penetration of the P-gp substrates, 99mTc-sestaMIBI and 14C-doxorubicin, is greater through multicellular layers formed from P-gp overexpressing cell lines as compared with wild-type cells;.
  • 2) the addition of agents that inhibit the function of P-gp results in decreased penetration of these substrates through multicellular layers with P-gp expression.
  • Our data suggest that the administration of agents that inhibit the function of P-gp might have opposing effects on therapeutic index in solid tumours: increased sensitivity of perivascular tumour cells but decreased penetration of P-gp substrates to more distal cells.
  • These effects may explain, in part, the limited therapeutic benefit for solid tumours that has accrued from use of agents that reverse the effects of P-gp.
  • [MeSH-minor] Animals. Carbon Radioisotopes. Doxorubicin / pharmacokinetics. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Fluorouracil / pharmacokinetics. Humans. Mice. Models, Biological. Radiopharmaceuticals / pharmacokinetics. Sarcoma, Experimental / drug therapy. Sarcoma, Experimental / metabolism. Sucrose / pharmacokinetics. Technetium Tc 99m Sestamibi / pharmacokinetics. Tumor Cells, Cultured. Verapamil / pharmacokinetics

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. VERAPAMIL HYDROCHLORIDE .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10728602.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbon Radioisotopes; 0 / P-Glycoprotein; 0 / Radiopharmaceuticals; 57-50-1 / Sucrose; 80168379AG / Doxorubicin; 971Z4W1S09 / Technetium Tc 99m Sestamibi; CJ0O37KU29 / Verapamil; U3P01618RT / Fluorouracil
  •  go-up   go-down


Advertisement
4. Spindler KP, Dawson JM, Stahlman GC, Davidson JM, Nanney LB: Collagen expression and biomechanical response to human recombinant transforming growth factor beta (rhTGF-beta2) in the healing rabbit MCL. J Orthop Res; 2002 Mar;20(2):318-24
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Collagen expression and biomechanical response to human recombinant transforming growth factor beta (rhTGF-beta2) in the healing rabbit MCL.
  • We investigated biomechanical and collagen expression in a healing bilateral rabbit medial collateral ligament (MCL) model to human recombinant transforming growth factor beta (rhTGF-beta2) at three and six weeks.
  • All MCL healed with rhTGF-beta2 producing a profoundly increased scar mass at three weeks which decreased in size toward control at six weeks.
  • In-situ hybridization demonstrated collagen expression (type I and III) no different than control at three weeks, but by six weeks elevated expression of type I was seen.
  • However, at six weeks rhTGF-beta2 significantly inhibited both the maximum load (p < 0.05) and energy absorbed (p < 0.05) with no change in stiffness.
  • Despite increased type I collagen expression and profound increase in early scar mass, rhTGF-beta2 did not improve the structural properties.
  • We hypothesize investigations of healing ligaments to cytokines should have biologic and biomechanical properties correlated in the same study at a minimum of two time points.
  • [MeSH-major] Collagen Type I / biosynthesis. Knee Injuries / drug therapy. Medial Collateral Ligament, Knee / metabolism. Medial Collateral Ligament, Knee / physiopathology. Transforming Growth Factor beta / therapeutic use
  • [MeSH-minor] Animals. Disease Models, Animal. Elasticity / drug effects. Hindlimb / drug effects. Hindlimb / metabolism. Hindlimb / physiopathology. Humans. In Situ Hybridization. Male. RNA, Messenger / metabolism. Rabbits. Range of Motion, Articular / drug effects. Range of Motion, Articular / physiology. Recombinant Proteins / therapeutic use. Transforming Growth Factor beta2. Weight-Bearing. Wound Healing / drug effects

  • MedlinePlus Health Information. consumer health - Knee Injuries and Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11918312.001).
  • [ISSN] 0736-0266
  • [Journal-full-title] Journal of orthopaedic research : official publication of the Orthopaedic Research Society
  • [ISO-abbreviation] J. Orthop. Res.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / AG06528; United States / NIGMS NIH HHS / GM / GM 40439; United States / NIAMS NIH HHS / AR / P30 AR41945
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Collagen Type I; 0 / RNA, Messenger; 0 / Recombinant Proteins; 0 / TGFB2 protein, human; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta2
  •  go-up   go-down


5. Mangel J, Buckstein R, Imrie K, Spaner D, Crump M, Tompkins K, Reis M, Perez-Ordonez B, Deodhare S, Romans R, Pennell N, Robinson JB, Hewitt K, Richardson P, Lima A, Pavlin P, Berinstein NL: Immunotherapy with rituximab following high-dose therapy and autologous stem-cell transplantation for mantle cell lymphoma. Semin Oncol; 2002 Feb;29(1S2):56-69
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunotherapy with rituximab following high-dose therapy and autologous stem-cell transplantation for mantle cell lymphoma.
  • Advanced-stage mantle cell lymphoma (MCL) is a disease for which no curative treatment strategy exists.
  • Results with standard combination chemotherapy, with or without an anthracycline, are disappointing, and new and better therapies are needed.
  • High-dose therapy and autologous stem-cell transplantation (ASCT) have been performed in patients with MCL both up front and at relapse with varying degrees of success.
  • Rituximab (Rituxan; Genentech, Inc, South San Francisco, CA, and IDEC Pharmaceuticals, San Diego, CA) has shown moderate response rates in patients with MCL.
  • We are currently investigating an aggressive protocol in patients with newly diagnosed, untreated MCL using a combination of two promising therapeutic modalities, high-dose therapy-ASCT and rituximab.
  • Since 1999, 13 patients with newly diagnosed MCL have been enrolled in this phase II clinical trial.
  • CHOP (cyclophosphamide/prednisone/vincristine/doxorubicin) is used as debulking chemotherapy.
  • Stem cells are mobilized with 5 days of granulocyte colony-stimulating factor 10 μg/kg/d, with a single infusion of rituximab 375 mg/m<sup>2</sup> used as an in vivo purge before stem-cell collection by large-volume leukapheresis.
  • So far, 12 patients (7 men/5 women) with a median age of 55 years (range, 41 to 65 years) have been transplanted.
  • Patients engrafted quickly, with a median of 11.5 days to neutrophil engraftment and 10 days to platelet independence.
  • Patients had modest transfusion requirements, requiring a median of four units of packed red blood cells and two and a half platelet transfusions.
  • Eight patients have received all eight maintenance rituximab treatments, and four have received only their first cycle.
  • With a median follow-up of 239 days from transplant (range, 61 to 727 days), all patients remain alive and well with no documented relapses.
  • Samples for molecular monitoring have been drawn from the stem-cell graft, and serially from the peripheral blood and bone marrow of patients at baseline, preapheresis, pretransplant, and post-transplant at 3-month intervals.
  • This data shows that ASCT followed by rituximab immunotherapy is feasible and safe in patients with MCL.
  • Although patient numbers are low and follow-up time is short, preliminary results are encouraging.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2002 W.B. Saunders Company. All rights reserved.
  • (PMID = 28140093.001).
  • [ISSN] 1532-8708
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


6. Rao R, Lee P, Fiskus W, Yang Y, Joshi R, Wang Y, Buckley K, Balusu R, Chen J, Koul S, Joshi A, Upadhyay S, Tao J, Sotomayor E, Bhalla KN: Co-treatment with heat shock protein 90 inhibitor 17-dimethylaminoethylamino-17-demethoxygeldanamycin (DMAG) and vorinostat: a highly active combination against human mantle cell lymphoma (MCL) cells. Cancer Biol Ther; 2009 Jul;8(13):1273-80
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Co-treatment with heat shock protein 90 inhibitor 17-dimethylaminoethylamino-17-demethoxygeldanamycin (DMAG) and vorinostat: a highly active combination against human mantle cell lymphoma (MCL) cells.
  • Here, we determined the effects of the more soluble, orally bio-available, geldanamycin analogue 17-NN-dimethyl ethylenediamine geldanamycin (DMAG, Kosan Biosciences Inc.) and/or vorinostat in cultured and primary human MCL cells.
  • While vorinostat induced accumulation in the G(1) phase, treatment with DMAG arrested MCL cells in the G(2)/M phase of the cell cycle.
  • Both agents dose-dependently induced apoptosis of MCL cells.
  • Vorinostat also induced hyperacetylation of hsp90 and disrupted the association of hsp90 with its co-chaperones p23 and cdc37, as well as with its client proteins CDK4 and c-RAF.
  • Treatment of MCL cells with vorinostat or 17-DMAG was associated with the inductionof p21 and p27, as well as with depletion of c-Myc, c-RAF, AKT and CDK4.
  • Compared to treatment with either agent alone, co-treatment with DMAG and vorinostat markedly attenuated the levels of cyclin D1 and CDK4, as well as of c-Myc, c-RAF and AKT.
  • Combined treatment with DMAG and vorinostat synergistically induced apoptosis of the cultured MCL cells, as well as induced more apoptosis of primary MCL cells than either agent alone.
  • Therefore, these findings support the rationale to determine the in vivo efficacy of co-treatment with vorinostat and DMAG against human MCL cells.

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Vorinostat .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2007 Jul 1;25(19):2770-7 [17563396.001]
  • [Cites] Leukemia. 2006 Oct;20(10):1905-8 [16932342.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2641-9 [17525289.001]
  • [Cites] Nat Rev Cancer. 2007 Oct;7(10):750-62 [17891190.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2007;:270-6 [18024640.001]
  • [Cites] Biochem J. 2008 Mar 15;410(3):439-53 [18290764.001]
  • [Cites] Blood. 2008 May 15;111(10):5142-51 [18339899.001]
  • [Cites] Curr Opin Hematol. 2008 Jul;15(4):415-21 [18536582.001]
  • [Cites] Cancer Res. 2008 Jun 15;68(12):4833-42 [18559531.001]
  • [Cites] Blood. 2008 Aug 1;112(3):822-9 [18483394.001]
  • [Cites] Blood. 2008 Sep 1;112(5):1886-93 [18591380.001]
  • [Cites] Clin Cancer Res. 2008 Oct 1;14(19):6106-15 [18829489.001]
  • [Cites] J Clin Oncol. 2008 Oct 20;26(30):4952-7 [18606983.001]
  • [Cites] Eur J Cancer. 2002 Feb;38(3):401-8 [11818206.001]
  • [Cites] Mol Cell. 2002 Feb;9(2):401-10 [11864612.001]
  • [Cites] J Immunol. 2003 Jul 1;171(1):88-95 [12816986.001]
  • [Cites] Br J Haematol. 2004 Jan;124(2):130-40 [14687022.001]
  • [Cites] J Biol Chem. 2003 Dec 26;278(52):52572-7 [14570880.001]
  • [Cites] Cell. 2004 Jan 9;116(1):87-98 [14718169.001]
  • [Cites] Adv Enzyme Regul. 1984;22:27-55 [6382953.001]
  • [Cites] Genes Dev. 1993 Mar;7(3):331-42 [8449399.001]
  • [Cites] EMBO J. 1994 May 1;13(9):2124-30 [8187765.001]
  • [Cites] Clin Cancer Res. 2004 Dec 1;10(23):8094-104 [15585645.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 28;101(52):18030-5 [15596714.001]
  • [Cites] Exp Hematol. 2005 Jan;33(1):53-61 [15661398.001]
  • [Cites] Mol Cell. 2005 Jan 21;17(2):237-49 [15664193.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):676-84 [15613699.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1768-76 [15514006.001]
  • [Cites] Cancer. 2005 Apr 25;105(2):110-8 [15712276.001]
  • [Cites] Mol Cell. 2005 May 27;18(5):601-7 [15916966.001]
  • [Cites] J Clin Oncol. 2005 Jun 10;23(17):3971-93 [15897549.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8567-72 [15937109.001]
  • [Cites] J Biol Chem. 2005 Jul 22;280(29):26729-34 [15937340.001]
  • [Cites] J Clin Oncol. 2005 Aug 10;23(23):5347-56 [15983389.001]
  • [Cites] Adv Immunol. 2005;87:163-208 [16102574.001]
  • [Cites] Clin Cancer Res. 2005 Sep 1;11(17):6382-9 [16144943.001]
  • [Cites] Blood. 2005 Oct 1;106(7):2506-12 [15972449.001]
  • [Cites] Mod Pathol. 2005 Oct;18(10):1343-9 [16056252.001]
  • [Cites] Nat Rev Cancer. 2005 Oct;5(10):761-72 [16175177.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10536-44 [16288046.001]
  • [Cites] Genes Chromosomes Cancer. 2006 Feb;45(2):203-10 [16258956.001]
  • [Cites] Eur J Haematol. 2006 Jan;76(1):42-50 [16343270.001]
  • [Cites] Nat Rev Cancer. 2006 Jan;6(1):38-51 [16397526.001]
  • [Cites] Hematol Oncol. 2006 Mar;24(1):22-7 [16402392.001]
  • [Cites] Nature. 2006 Apr 20;440(7087):1013-7 [16625188.001]
  • [Cites] Oncogene. 2006 Jul 13;25(30):4133-46 [16501598.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1668-76 [16645163.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1744-50 [16690963.001]
  • [Cites] Mol Cell. 2006 Sep 1;23(5):697-707 [16949366.001]
  • [Cites] Br J Haematol. 2006 Oct;135(1):68-71 [16925576.001]
  • [Cites] Clin Cancer Res. 2006 Oct 1;12(19):5869-78 [17020995.001]
  • [Cites] Genes Dev. 2007 Sep 1;21(17):2172-81 [17785525.001]
  • (PMID = 19440035.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA129962-01A1; United States / NCI NIH HHS / CA / R01 CA129962; United States / NCI NIH HHS / CA / R01 CA129962-01A1
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / Cell Cycle Proteins; 0 / HSP90 Heat-Shock Proteins; 0 / Hydroxamic Acids; 0 / Lactams, Macrocyclic; 001L2FE0M3 / 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin; 58IFB293JI / vorinostat
  • [Other-IDs] NLM/ NIHMS130612; NLM/ PMC2766923
  •  go-up   go-down


7. Determann O, Hoster E, Ott G, Wolfram Bernd H, Loddenkemper C, Leo Hansmann M, Barth TE, Unterhalt M, Hiddemann W, Dreyling M, Klapper W, European Mantle Cell Lymphoma Network and the German Low Grade Lymphoma Study Group: Ki-67 predicts outcome in advanced-stage mantle cell lymphoma patients treated with anti-CD20 immunochemotherapy: results from randomized trials of the European MCL Network and the German Low Grade Lymphoma Study Group. Blood; 2008 Feb 15;111(4):2385-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ki-67 predicts outcome in advanced-stage mantle cell lymphoma patients treated with anti-CD20 immunochemotherapy: results from randomized trials of the European MCL Network and the German Low Grade Lymphoma Study Group.
  • Clinical outcome of mantle cell lymphoma (MCL) is highly heterogeneous.
  • Tumor cell proliferation as assessed by the Ki-67 index has been shown to yield prognostic information on MCL in many studies using heterogeneously treated patient cohorts.
  • The prognostic value of the Ki-67 index in patients treated with anti-CD20 therapy has not been studied so far.
  • We analyzed the Ki-67 index at primary diagnosis in 249 advanced-stage MCL patients treated within randomized trials.
  • The 3 groups with different Ki-67 index of less than 10%, 10% to less than 30%, and 30% or more showed significantly different overall survival in patients treated with CHOP (P = .001) as well as in patients treated with CHOP in combination with anti-CD20 therapy (R-CHOP, P = .013).
  • Thus, the Ki-67 index remains an important prognostic marker in the era of anti-CD20 therapy.
  • The Euro-pean MCL study is registered at www.ClinicalTrials.gov as #NCT00016887.
  • [MeSH-major] Antigens, CD20 / immunology. Ki-67 Antigen / blood. Lymphoma, Mantle-Cell / drug therapy
  • [MeSH-minor] Biomarkers / blood. Europe. Germany. Humans. Immunotherapy. Multicenter Studies as Topic. Neoplasm Staging. Prognosis. Randomized Controlled Trials as Topic. Treatment Outcome

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18077791.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00016887
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Biomarkers; 0 / Ki-67 Antigen
  • [Investigator] Nitsche M; Weikersthal; Hahn M; Gensicke D; Schlimok S; Langer M; Possinger S; Ludwig M; Weh A; Rhode E; Dietrich KB; Schmiegel G; Musch R; Wörmann J; Pflüger D; Hänel N; Peter CT; Heike; Lange; Haas; Rösler; Fuchs WI; Dührsen N; Heit W; Saal H; Reiber S; Mertelsmann F; Fassbinder H; Heil S; Schliesser; Trümper G; Eimermacher L; Kraus H; Schmoll W; Spohn M; Hurtz R; Schmitz N; Zander K; Bokemeyer; Walter; Schmidt; Henne; Dietzfelbinger; Basler S; Pfreundschuh; Gasiorek; Höffken F; Bentz W; Mezger G; Mosthaf ZB; Siehl S; Löser US; Kneba; Eisenhauer N; Helmer N; Hallek R; Fokken; Aldaoud S; Mantovani M; Baumgarten; Heidenreich J; Liebau N; Uppenkamp H; Fetscher S; Heil TL; Franke JU; Kettner K; Huber F; Hehlmann L; Neubauer S; Bodenstein W; Becker KB; Götz J; Graeven K; Lunscken; Forstpointner D; Hentrich S; Abenhardt T; Berdel; Wehmeyer L; Ladda; Nürnberg; Heuser; Ehscheidt J; Wilhelm W; Böck B; Henning-Köhne M; Otremba Z; Wolff N; Theilmann S; Gmelin; Maschmeyer R; Kautzsch R; Andreesen K; Kreuser; Neeck KS; Freund; Hähling S; Seitz K; Mergenthaler S; Aulitzky M; Höring E; Heidemann K; Fiechtner; Biedermann K; Kölbel W; Clemens; Forstbauer A; Reiter; Brettner B; Vedder R; Katz M; Bock; Sandmann B; Einsele W; Schlag; Kreibich
  •  go-up   go-down


8. Tei K, Matsumoto T, Mifune Y, Ishida K, Sasaki K, Shoji T, Kubo S, Kawamoto A, Asahara T, Kurosaka M, Kuroda R: Administrations of peripheral blood CD34-positive cells contribute to medial collateral ligament healing via vasculogenesis. Stem Cells; 2008 Mar;26(3):819-30
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Administrations of peripheral blood CD34-positive cells contribute to medial collateral ligament healing via vasculogenesis.
  • Neoangiogenesis is a key process in the initial phase of ligament healing.
  • Adult human circulating CD34+ cells, an endothelial/hematopoietic progenitor-enriched cell population, have been reported to contribute to neoangiogenesis; however, the therapeutic potential of CD34+ cells for ligament healing is still unclear.
  • Therefore, we performed a series of experiments to test our hypothesis that ligament healing is supported by CD34+ cells via vasculogenesis.
  • Granulocyte colony-stimulating factor-mobilized peripheral blood (GM-PB) CD34+ cells with atelocollagen (CD34+ group), GM-PB mononuclear cells (MNCs) with atelocollagen (MNC group), or atelocollagen alone (control group) was locally transplanted after the creation of medial collateral ligament injury in immunodeficient rats.
  • Endogenous effect, assessed by capillary density and mRNA expression of vascular endothelial growth factor, was significantly higher in CD34+ cell group than the other groups.
  • In addition to the observation that, as assessed by real-time RT-PCR, gene expression of ligament-specific marker was significantly higher in the CD34+ group than in the other groups, ligament healing assessed by macroscopic, histological, and biomechanical examination was significantly enhanced by CD34+ cell transplantation compared with the other groups.
  • Our data strongly suggest that local transplantation of circulating human CD34+ cells may augment the ligament healing process by promoting a favorable environment through neovascularization.
  • [MeSH-major] Antigens, CD34 / metabolism. Cell- and Tissue-Based Therapy. Collateral Ligaments / pathology. Hematopoietic Stem Cell Transplantation. Neovascularization, Physiologic. Wound Healing
  • [MeSH-minor] Adult. Angiogenesis Inhibitors / pharmacology. Animals. Cell Differentiation / drug effects. Female. Granulocyte Colony-Stimulating Factor / pharmacology. Hematopoietic Stem Cell Mobilization. Hematopoietic Stem Cells / cytology. Hematopoietic Stem Cells / drug effects. Humans. Inflammation. Leukocytes, Mononuclear / cytology. Leukocytes, Mononuclear / drug effects. Phenotype. Rats. Rats, Nude

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18192236.001).
  • [ISSN] 1549-4918
  • [Journal-full-title] Stem cells (Dayton, Ohio)
  • [ISO-abbreviation] Stem Cells
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD34; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  •  go-up   go-down


9. Berinstein NL, Mangel J: Integrating Monoclonal Antibodies into the Management of Mantle Cell Lymphoma. Semin Oncol; 2004 Feb;31 Suppl 2:2-6

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integrating Monoclonal Antibodies into the Management of Mantle Cell Lymphoma.
  • Patients with mantle cell lymphoma (MCL) have a particularly poor prognosis when treated with standard chemotherapy, with a median overall survival of only 3 years.
  • These patients have therefore been considered for first-line treatment with more aggressive or experimental strategies, such as high-dose therapy (HDT) with autologous stem cell transplantation (ASCT).
  • While high rates of clinical remission have been achieved with HDT/ASCT, this procedure alone is not believed to be curative and different treatment strategies are being developed to improve outcomes in this group of patients.
  • Single-agent rituximab is active in both newly diagnosed and relapsed MCL and therefore the addition of rituximab to chemotherapy regimens and/or HDT/ASCT may enhance their efficacy.
  • Outside the transplantation setting, rituximab plus chemotherapy has been shown to be highly active in MCL, and preliminary data from randomized trials suggest that the combination may yield superior results compared with chemotherapy alone.
  • The addition of rituximab to transplantation protocols appears to be a very promising strategy for patients with MCL, given as an in vivo purge before HDT/ASCT and/or as posttransplant maintenance therapy.
  • Two phase II clinical trials with rituximab given as an in vivo purge during stem cell mobilization and as posttransplant immunotherapy in patients with previously untreated MCL have generated very promising data.
  • Rituximab is an important addition to cytotoxic therapy and with HDT/ASCT represents a highly active therapy that may be superior to conventional treatment or HDT/ASCT alone in MCL.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28140105.001).
  • [ISSN] 1532-8708
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


10. Miglietta L, Franzone P, Centurioni MG, Boni L, Tacchini L, Cosso M, Boccardo F, Ferrarini M, Bruzzone M: A phase II trial with cisplatin-paclitaxel cytotoxic treatment and concurrent external and endocavitary radiation therapy in locally advanced or recurrent cervical cancer. Oncology; 2006;70(1):19-24
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II trial with cisplatin-paclitaxel cytotoxic treatment and concurrent external and endocavitary radiation therapy in locally advanced or recurrent cervical cancer.
  • BACKGROUND: Five randomized studies have demonstrated a beneficial effect of adding cisplatin-based chemotherapy to radiation therapy in the treatment of cervical carcinoma.
  • In the present phase II study, we evaluated the response and toxicity of cisplatin-Taxol chemotherapy combined with concomitant radiotherapy in patients with locally advanced cervical carcinoma (LACC) and locally recurrent cervical carcinoma (LRCC).
  • PATIENTS AND METHODS: In 2000, this phase II study was initiated with a chemotherapy regimen of cisplatin (75 mg/m(2)) and Taxol (175 mg/m(2)) every 21 days, for four cycles, concomitant with external radiotherapy and high-dose-rate brachytherapy.
  • Pelvic radiotherapy was started 2 weeks after the first chemotherapy cycle, while the first brachytherapy insertion was carried out during the fourth chemotherapy cycle.
  • SCC marker was determined before treatment and after every chemotherapy cycle.
  • Two patients with LACC experienced distant recurrence 22 and 24 months after complete response, respectively, and 1 patient with LRCC had local progression 6 months after the end of radiotherapy.
  • Although generally tolerable, neutropenia grade 3-4 in 4 patients and anemia grade 3 in 2 patients were observed, and 1 patient experienced grade 2 neurotoxicity; toxicity due to radiotherapy was moderate.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brachytherapy. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / radiotherapy. Uterine Cervical Neoplasms / drug therapy. Uterine Cervical Neoplasms / radiotherapy
  • [MeSH-minor] Adult. Aged. Carcinoma / drug therapy. Carcinoma / radiotherapy. Carcinoma / surgery. Chemotherapy, Adjuvant. Cisplatin / administration & dosage. Drug Administration Schedule. Feasibility Studies. Female. Humans. Middle Aged. Neoplasm Staging. Paclitaxel / administration & dosage. Prospective Studies. Radiotherapy, Adjuvant / methods. Treatment Outcome


11. Evans CJ, Phillips RM, Jones PF, Loadman PM, Sleeman BD, Twelves CJ, Smye SW: A mathematical model of doxorubicin penetration through multicellular layers. J Theor Biol; 2009 Apr 21;257(4):598-608
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A mathematical model of doxorubicin penetration through multicellular layers.
  • Inadequate drug delivery to tumours is now recognised as a key factor that limits the efficacy of anticancer drugs.
  • Extravasation and penetration of therapeutic agents through avascular tissue are critically important processes if sufficient drug is to be delivered to be therapeutic.
  • The purpose of this study is to develop an in silico model that will simulate the transport of the clinically used cytotoxic drug doxorubicin across multicell layers (MCLs) in vitro.
  • Three cell lines were employed: DLD1 (human colon carcinoma), MCF7 (human breast carcinoma) and NCI/ADR-Res (doxorubicin resistant and P-glycoprotein [Pgp] overexpressing ovarian cell line).
  • The concentration of drug appearing in the bottom chamber was determined as a function of time by HPLC-MS/MS.
  • The rate of drug penetration was inversely proportional to the thickness of the MCL.
  • A mathematical model based upon the premise that the transport of doxorubicin across cell membrane bilayers occurs by a passive "flip-flop" mechanism of the drug between two membrane leaflets was constructed.
  • The mathematical model treats the transwell apparatus as a series of compartments and the MCL is treated as a series of cell layers, separated by small intercellular spaces.
  • This model demonstrates good agreement between predicted and actual drug penetration in vitro and may be applied to the prediction of drug transport in vivo, potentially becoming a useful tool in the study of optimal chemotherapy regimes.
  • [MeSH-minor] Biological Transport. Cell Membrane / metabolism. Chromatography, High Pressure Liquid / methods. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Female. Humans. Neoplasm Proteins / metabolism. P-Glycoprotein / metabolism. Tumor Cells, Cultured

  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] J Theor Biol. 2011 Mar 21;273(1):235
  • (PMID = 19183560.001).
  • [ISSN] 1095-8541
  • [Journal-full-title] Journal of theoretical biology
  • [ISO-abbreviation] J. Theor. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Neoplasm Proteins; 0 / P-Glycoprotein; 80168379AG / Doxorubicin
  •  go-up   go-down


12. Dreyling M, Hoster E, Bea S, Hartmann E, Horn H, Hutter G, Salaverria I, Pott C, Trneny M, Le Gouill S, Cortelazzo S, Szymczyk M, Jurczak W, Shpilberg O, Ribrag V, Hermine O, European MCL Network: Update on the molecular pathogenesis and clinical treatment of Mantle Cell Lymphoma (MCL): minutes of the 9th European MCL Network conference. Leuk Lymphoma; 2010 Sep;51(9):1612-22
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Update on the molecular pathogenesis and clinical treatment of Mantle Cell Lymphoma (MCL): minutes of the 9th European MCL Network conference.
  • Mantle cell lymphoma (MCL) is a distinct subtype of malignant lymphoma which is characterized by the chromosomal translocation t(11;14)(q13;q32), resulting in constitutional overexpression of cyclin D1 and cell cycle dysregulation in virtually all cases.
  • Clinically, MCL shows an aggressive clinical course with a continuous relapse pattern and a median survival of only 3-5 years.
  • However, recently a subset of 15% long-term survivors has been identified with a rather indolent clinical course, even after conventional treatment strategies only.
  • Advanced stage disease is usually apparent already at first clinical manifestation; thus, conventional chemotherapy is only palliative, and the median duration of remissions is only 1-2 years.
  • Emerging strategies including proteasome inhibitors, immune modulatory drugs (IMiDs), mTOR inhibitors, and others are based on the dysregulated control of cell cycle machinery and impaired apoptotic pathways.
  • Monotherapy of these compounds achieves efficacy comparable to conventional chemotherapy in relapsed MCL, and combination strategies are currently being investigated in numerous trials; however, their introduction into clinical practice and current treatment algorithms remain a challenge.
  • In 2000 the European MCL Network ( http://www.european-mcl.net ) was founded, consisting of 15 national lymphoma study groups supplemented by experts in histopathology and molecular genetics.
  • During the past decade, the European consortium has successfully initiated the largest phase III trials in MCL worldwide, with a current annual recruitment of almost 200 patients per year in first-line studies.
  • In detail, in prospective randomized studies, the addition of a B-lymphocyte specific antibody doubled the median progression-free survival from 14 to 28 months, and a dose-intensified consolidation with high-dose radiochemotherapy and subsequent autologous stem cell transplant resulted in superior response duration (3.7 vs. 1.6 years) and even improved overall survival in a recent analysis.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Mantle-Cell / etiology. Lymphoma, Mantle-Cell / therapy. Stem Cell Transplantation
  • [MeSH-minor] Clinical Trials as Topic. Combined Modality Therapy. Congresses as Topic. Humans


13. Ghobrial IM, McCormick DJ, Kaufmann SH, Ansell SM, Novak AJ, Stenson MJ, Krajnik KL, Witzig TE: Proteomic analysis of patients with mantle cell lymphoma identifies Hsp90, and other proteins as potential target(s) for drug therapy. J Clin Oncol; 2004 Jul 15;22(14_suppl):6530

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proteomic analysis of patients with mantle cell lymphoma identifies Hsp90, and other proteins as potential target(s) for drug therapy.
  • : 6530 Background: We employed antibody protein microarrays to measure changes in the patterns of protein expression between normal B-lymphocytes and those from patients with mantle cell lymphoma (MCL).
  • METHODS: The pattern of protein expression in MCL patients was measured on antibody protein microarrays (BD Clonetech, CA) with 512 monoclonal antibodies.
  • CD19+ mononuclear cells were purified from 6 patients with MCL.
  • Another patient with lymphoplasmacytic lymphoma (LPL) was performed for comparison to confirm that the pattern of expression is unique to MCL.
  • A control experiment of tonsil B-cell extracts was performed to ensure the absence of non-specific protein expression patterns.
  • Immunoblotting experiments with monoclonal anti-human Hsp90 were also performed in 10 different MCL patients.
  • RESULTS: Of the 6 MCL patients, 1 patient was heavily pretreated with chemotherapy and autologous stem cell transplantation and showed a distinct protein pattern from the other MCL patients.
  • The patient with LPL had a different protein expression pattern compared to patients with MCL.
  • The common proteins that were overexpressed in MCL patients included: chaperone proteins (Hsp90, Hsp10), cell cycle regulators (RCC-1, p73a, MDM2, CDC25C), apoptosis regulators (caspase 7, Smac/DIABLO), and kinase regulators (PP5, AKAP450).
  • We confirmed the abundant expression of Hsp90 by immunoblotting in 10 different MCL patients.
  • CONCLUSION: Hsp90 is highly expressed in patients with MCL, along with other possible candidates.
  • Funded in part by NCI cancer center CA15083-29C1 and CA97274 No significant financial relationships to disclose.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28016943.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


14. Ruan J, Martin P, Coleman M, Furman R, Glynn P, Joyce M, Cheung K, Shore T, Schuster M, Leonard J: Durable responses with the antiangiogenic metronomic regimen RT-PEPC in elderly patients with recurrent mantle cell lymphoma (MCL). J Clin Oncol; 2009 May 20;27(15_suppl):8525

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Durable responses with the antiangiogenic metronomic regimen RT-PEPC in elderly patients with recurrent mantle cell lymphoma (MCL).
  • : 8525 Background: Targeting tumor microenvironment and angiogenesis is a novel therapeutic strategy in lymphoma.
  • Two putative anti-angiogenic regimens, RT (rituximab with thalidomide) and PEPC oral metronomic chemotherapy (prednisone, etoposide, procarbazine and cyclophosphamide) are clinically active.
  • We report phase II safety, activity, and angiogenic profiling data with the novel combination RT-PEPC in elderly patients with recurrent MCL.
  • Translational studies assessed the angiogenic phenotypes of tumor cells, and dynamic levels of circulating endothelial and hematopoietic progenitors in response to treatment.
  • The median number of prior therapies was two (range 1 to 7), and 15 pts (60%) progressed on bortezomib.
  • QoL was maintained or improved on treatment.
  • Correlative studies demonstrated pre-therapy autocrine angiogenic loop in tumor cells evidenced by expression of VEGFA and VEGFR1.
  • Circulating levels of hematopoietic and endothelial progenitor cells decreased on rx in responders.
  • CONCLUSIONS: RT-PEPC has significant and durable clinical activity in MCL, with manageable toxicity and maintained QoL.
  • Novel low-intensity anti-angiogenic approaches warrant further evaluation in MCL and other NHL subtypes, potentially as initial therapy in elderly patients.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27960902.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


15. Rule S, Smith P, Qian W, Gambell J, Curtis N, Johnson P, Linch D: Application of the mantle international prognostic index (MIPI) to patients with mantle cell lymphoma treated with fludarabine/cyclophosphamide: Results from a UK NCRI Lymphoma Group study. J Clin Oncol; 2009 May 20;27(15_suppl):8555

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Application of the mantle international prognostic index (MIPI) to patients with mantle cell lymphoma treated with fludarabine/cyclophosphamide: Results from a UK NCRI Lymphoma Group study.
  • : 8555 Background: Mantle cell lymphoma (MCL) remains an incurable malignancy with conventional chemotherapeutic options with little randomised evidence to help direct therapy.
  • The International Prognostic Index (IPI) for diffuse large cell lymphoma or Follicular Lymphoma International Prognostic Index (FLIPI) showed poor separation of survival curves in MCL patients.
  • A new prognostic index (MIPI) based on age, performance status, lactate dehydrogenase (LDH), and leukocyte count was developed for patients with advanced stage MCL.
  • Data from a randomised phase II NCRI trial designed to assess the effect of adding rituximab to an all oral chemotherapy regimen has been used to validate the MIPI.
  • METHODS: Patients with advanced stage, newly diagnosed MCL were randomised to receive either oral fludarabine 40mg/m<sup>2</sup> and cyclophosphamide 250mg/m<sup>2</sup> daily x 3 repeated every 28 days (FC) or FC with standard dose rituximab (375mg/m<sup>2</sup> on day 1 of every cycle) (FCR).
  • Patients could receive up to 8 cycles of treatment but no consolidation therapy was permitted.
  • The primary outcome measures were response rate and the feasibility of a phase III randomised study.
  • Median age 64 (36-88) with a significant male predominance.
  • However MIPI does not discriminate for PFS suggesting that those patients with high scores have an inferior response to subsequent therapy post relapse after FC based therapy.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27960988.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


16. Goy A, Younes A, McLaughlin P, Pro B, Romaguera J, Hagemeister F, Fayad L, Trehu EG, Schenkein D, Rodriguez MA: Update on a phase (ph) 2 study of bortezomib in patients (pts) with relapsed or refractory indolent or aggressive non-Hodgkin's lymphomas (NHL). J Clin Oncol; 2004 Jul 15;22(14_suppl):6581

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 6581 Background: Proteasome inhibition disrupts many cell cycle checkpoints and pathways that lead to apoptosis.
  • Pts ≥ 16 yr, with relapsed or refractory mantle cell (MCL, gp A) or other B cell lymphomas (gp B) were eligible.
  • There were 25 pts in gp A and 20 pts in gp B, including 10 diffuse large cell lymphoma (DLCL), 4 follicular lymphoma (FL), 3 transformed (t) FL, 2 small lymphocytic lymphoma (SLL), 1 Waldenström's macroglobulinemia (WM).
  • Gp A had 3 median prior therapies (range 1-6); gp B had 4 (range 1-12).
  • In gp B, there were 8 ev DLCL with 1 PR (DOR 4 mo), 1 NC, 6 POD; 4 ev FL with 2 MR, 1 NC, 1 POD; 1 ev tFL with POD; 2 ev SLL with 1 NC, 1 POD; 1 WM pt had PR.
  • CONCLUSIONS: This study showed remarkable activity of Vc in MCL and encouraging results in other B cell lymphomas.
  • Future studies will include combinations of Vc with other chemotherapy and/or biological agents.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28016185.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


17. Delarue R, Haioun C, Brice P, Delmer A, Ribrag V, Van Hoof A, Casasnovas O, Tilly H, Salles G, Hermine O: CHOP and DHAP plus rituximab followed by autologous stem cell transplantation (ASCT) in mantle cell lymphoma (MCL): A pilot study from the GELA. J Clin Oncol; 2004 Jul 15;22(14_suppl):6529

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CHOP and DHAP plus rituximab followed by autologous stem cell transplantation (ASCT) in mantle cell lymphoma (MCL): A pilot study from the GELA.
  • : 6529 Background: Sequential chemotherapy by CHOP and DHAP regimens followed by ASCT improves complete response (CR) rate and EFS in younger patients with MCL (Lefrère et al, Leukemia, 2002).
  • Since Rituximab (R) may induce significant response in relapsing MCL, we conduct a pilot, multicentric study to determine the impact of the CHOP/DHAP protocol plus R followed by ASCT as a first line therapy in the treatment of MCL at advanced stage.
  • METHODS: Patients under 66 years with histologically proven, stage III-IV MCL were included.
  • Treatment consisted of two courses of CHOP, one R-CHOP (Rituximab : 375 mg/m<sup>2</sup>) and three R-DHAP.
  • Responding pts were eligible for an ASCT after high dose therapy with TBI (10 Gy), Aracytine (6g/m<sup>2</sup>) and Melphalan (140 mg/m<sup>2</sup>) (TAM 6) or BEAM if TBI could not be performed.
  • Fourty-eight pts are evaluable for treatment response.
  • Fourty patients have completed the three courses of R-DHAP.
  • Thirty patients were autografted with a TAM 6 (28 pts) or a BEAM regimen (2 pts).
  • Currently, with a median follow up of 25 months, 28/30 pts were in CR 1 and only one relapse was observed.
  • CONCLUSIONS: Chemotherapy with DHAP followed by a Aracytine containing regimen provide a high response rate in untreated MCL.
  • Multicentric European study is currently ongoing to test this approach against R-CHOP induction therapy.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28016908.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


18. Braun E, Katz D, Venugopal P, Larson M, Shammo J, Fung H, Gregory S: Safety analysis of radioimmunotherapy (RIT) in patients with relapsed or refractory low grade, follicular or transformed non-Hodgkin's lymphoma and mantle cell lymphoma based on age at time of therapy. J Clin Oncol; 2009 May 20;27(15_suppl):e19529

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Safety analysis of radioimmunotherapy (RIT) in patients with relapsed or refractory low grade, follicular or transformed non-Hodgkin's lymphoma and mantle cell lymphoma based on age at time of therapy.
  • : e19529 Background: Radioimmunotherapy is a therapeutic option for relapsed or refractory indolent, follicular and transformed non Hodgkin's lymphoma and mantle cell lymphoma.
  • Although prolongued myelotoxicity has been described with use of iodine I 131 tositumomab (TOSI) and yttrium 90 ibritumomab tiuxetan (IBRI), analysis of toxicity according to patients' age at therapy still lacks.
  • METHODS: Utilizing the Rush University Medical Center database 61 subjects who received RIT between November/2003 and June/2008, either with TOSI or IBRI were divided in 2 groups according to age at time of therapy.
  • Parameters compared between groups were: Time to nadir of lowest absolute neutrophil count (ANC), time to recovery ANC above 1000/mcL, time to nadir of lowest hemoglobin levels, time to recovery to hemoglobin levels above 8g/dL, time to lowest platelet count and time to recovery to platelet count above 100,000/mcL.
  • Incidence o myelodysplastic syndrome (MDS) was also compared between groups.
  • Groups characteristics such as sex, type of RIT, presence of disease in bone marrow, FLIPI/IPI and use of G-CSF were noted.
  • RESULTS: There was no significant statistical difference between groups in time (number of days) to achieve nadir of ANC (group 1 85.3±208; group 2 50.3±19.9), nadir of hemoglobin levels (group 1 106±60.6; group 2 84±57.0) and time to nadir of platelet level (group 1 53.5±70.7; group 2 41.8±9.6).
  • There was no statistical significant difference between groups in duration of cytopenias, except for time for platelet recovery which was significant longer in group 2 using the Pearson Correlation analysis. (p=0.008). (Days for platelets recovery to levels above 100,000/mcL group 1 29.4±27.7; group 2 108.8 ±207.3).
  • One patient in group 1 and three patients on group 2 were diagnosed with MDS but were also treated with different chemotherapy regimens.
  • CONCLUSIONS: RIT should be considered a safe therapeutic modality in patients with refractory or relapsed indolent, follicular, NHL, transformed and Mantle Cell lymphoma regardless of age.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27960911.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


19. Schaffel R, Hedvat C, Teruya-Feldstein J, Portlock CS, Moskowitz CH, Zelenetz AD: Prognostic value of quantitative image analysis (QIA) for determination of proliferative index in mantle cell lymphoma (MCL) treated with sequential chemotherapy followed by high-dose therapy and autologous stem cell rescue (HDT/ASCR). J Clin Oncol; 2009 May 20;27(15_suppl):e19522

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic value of quantitative image analysis (QIA) for determination of proliferative index in mantle cell lymphoma (MCL) treated with sequential chemotherapy followed by high-dose therapy and autologous stem cell rescue (HDT/ASCR).
  • : e19522 Background: Gene expression studies have demonstrated that the proliferation signature is the most important factor in determination of outcome in MCL.
  • We tested the agreement between manual counting (MC) and QIA and its prognostic value in patients with MCL.
  • METHODS: 105 patients with MCL underwent therapy for de novo MCL, of these, 66 had slides stained with MIB-1 for the analysis.
  • The survival analysis was restricted to 47 patients that were treated with sequential therapy followed by upfront consolidation with HDT/ASCR.
  • In a Cox regression analysis, both OS and EFS were significantly associated with PI and not associated with either MIPI or inclusion of rituximab during therapy.
  • CONCLUSIONS: Digital image analysis of MIB-1/Ki67 staining is highly reproducible and further validates the prognostic significance of a high PI in MCL using a threshold of 30%.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27960939.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


20. Buckstein R, Crump M, Shaked Y, Foden C, Nayar R, Taylor D, Bertolini F, Baruchel S, Man S, Kerbel R: Palliation of relapsed aggressive histology NHL with high-dose celecoxib and 'metronomic' low-dose cyclophosphamide. J Clin Oncol; 2004 Jul 15;22(14_suppl):3016

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 3016 Background: Relapsed aggressive Non-Hodgkin's Lymphoma (NHL) has a poor prognosis; and new treatments are needed.
  • Low dose chronic chemotherapy (metronomic chemotherapy, MC) inhibits angiogenesis in vitro.
  • Since COX-2 may promote neoplasia and tumour angiogenesis, selective COX-2 inhibitors may have anti-tumour effects in NHL.We assessed response to MC and COX-2 inhibition and toxicity in patients (pts) with relapsed aggressive NHL following anthracycline based chemotherapy.
  • METHODS: Pts with measureable disease and normal renal function received cyclophosphamide 50 mg po qd + celecoxib 400 mg po bid.
  • Pts were assessed clinically monthly x 6 then q 2 mos; CT scans q 3 mos, serial plasma VEGF and TSP-1 levels.
  • Pharmacokinetics (PK)and serial LN biopsies for COX-2 IHC were performed in selected pts.
  • RESULTS: To date 21 of a planned 32 pts have been treated; 17 are evaluable for response.
  • HISTOLOGY: 17 DLBCL, 2 MCL, 2 transformed (CLL+FL).
  • Median # of previous chemotherapy regimens: 3 (range 1-6); prior ASCT: 7.
  • Median time to death or last follow-up: 8.5 mos (range 1.8-17); 6/17 pts responded (1 CRu, 5 PR,ORR 35%) at a median time of 4.6 mos, and 4 remain in PR at 18, 14, 12 and 3 mos.
  • Two pts have SD and 10 have progressed at a median time of 1.9 mos (range <1-9); 7 have died of NHL.
  • Adverse events(# pts): grade 3-4 ANC (2), grade 3 plt (3), grade 3 hypertension(1), grade 3 headache(1) and grade 3 drug rash(1).
  • Lab correlates (COX-2 IHC, PK, serum VEGF, TSP-1 and blood CEC and CEP levels will be presented.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28015166.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


21. O'Connor OA: Marked clinical activity of the novel proteasome inhibitor bortezomib in patients with relapsed follicular (RL) and mantle cell lymphoma (MCL). J Clin Oncol; 2004 Jul 15;22(14_suppl):6582

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Marked clinical activity of the novel proteasome inhibitor bortezomib in patients with relapsed follicular (RL) and mantle cell lymphoma (MCL).
  • : 6582 Background: Targeting of the ubiquitin proteasome pathway has proven to be a valid and efficacious approach for the treatment of several hematologic malignancies.
  • METHODS/RESULTS: To date, we have treated 25 previously treated patients with relapsed or refractory indolent lymphomas, including: 3 patients with small lymphocytic lymphoma; 9 patients with FL; 11 patients with MCL; and 2 patients with marginal zone lymphoma.
  • All but one patient had received some form of treatment prior to receiving bortezomib, including: CHOP +/- R (60%); CVP +/- R (20%); or some other purine analog based treatment program (15%), with some patients having received prior high dose chemotherapy with peripheral blood stem cell transplant (12%) or radioimmunotherapy (8%).
  • Patients were treated at a dose of 1.5 mg/m<sup>2</sup> twice weekly for two consecutive weeks with a one-week rest period.
  • No Grade III or IV toxicities were observed, save one patient that developed a grade 3 sensory and motor neuropathy.
  • Re-staging studies were routinely performed after two complete cycles of therapy.
  • The two patients with marginal zone lymphoma achieved a PR after 2 cycles of therapy, lasting now 3+ and 6+ months each..
  • Of the 10 evaluable patients with mantle cell lymphoma, 5 achieved a partial remission (response rate of 50%), with this response lasting 1+, 1+, 3+ 6 and 19 months.
  • CONCLUSIONS: These data continue to support the biological activity of bortezomib in patients with select sub-types of indolent NHL.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28016179.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


22. Drach J, Kaufmann H, Woehrer S, Chott A, Zielinski CC, Raderer M: Durable remissions after rituximab plus thalidomide for relapsed/refractory mantle cell lymphoma. J Clin Oncol; 2004 Jul 15;22(14_suppl):6583

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Durable remissions after rituximab plus thalidomide for relapsed/refractory mantle cell lymphoma.
  • : 6583 Background: Mantle cell lymphoma (MCL) remains difficult to treat by conventional treatment approaches.
  • Since the microenvironment plays an important role for growth and survival of malignant B-cells, we hypothesized that a treatment strategy targeting both the tumor cell and the microenvironment could be active in MCL.
  • METHODS: A phase 2 clinical trial was performed to evaluate the toxicity and efficacy of rituximab plus thalidomide (R+THAL) in patients (pts) with CD20 positive relapsed MCL (previously treated by CHOP or a CHOP-like regimen).
  • R was administered at 375 mg/m<sup>2</sup> on days 1, 8, 15, and 22; THAL was given at a daily dose of 200mg starting on day 1 and a dose escalation to 400mg on day 15 (continued until progression or relapse).
  • RESULTS: 16 pts with MCL were treated (8 pts at first relapse including 2 pts after autologous transplantation, 5 pts at ≥ second relapse, 1 pt with primary CHOP-resistant MCL).
  • Median age of pts was 67 (range, 45 to 76) years, and time from initial diagnosis ranged between 6 and 53 (median, 21) months.
  • In 7 pts, grade 2 fever and chills (grade 1-2) associated with administration of R were observed.
  • One pt experienced severe neutropenia associated with THAL causing discontinuation of treatment, and thromboembolic events were observed in 2 pts.
  • Tumor responses occured both at nodular and extranodular MCL manifestations.
  • Median time to progression (TTP) was 20 months.
  • In pts achieving a CR, TTP was longer than the preceding TTP after chemotherapy (27+, 21, 20, 29 months versus 3, 15, 17, 22 months, respectively).
  • CONCLUSIONS: R+THAL has marked anti-tumor activity and low toxicity in pts with relapsed/resistant MCL, even after high-dose therapy.
  • Thus, a clinical trial with R-CHOP-THAL as frontline therapy for pts with MCL has been initiated.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 28016180.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


23. Zec ML, Thistlethwaite P, Frank CB, Shrive NG: Characterization of the fatigue behavior of the medial collateral ligament utilizing traditional and novel mechanical variables for the assessment of damage accumulation. J Biomech Eng; 2010 Jan;132(1):011001
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of the fatigue behavior of the medial collateral ligament utilizing traditional and novel mechanical variables for the assessment of damage accumulation.
  • Ligaments are regularly subjected to repetitive loading in vivo.
  • The aims of this study were as follows: (a) to demonstrate that damage does accumulate in ligament tissue subjected to repetitive loading and (b) to evaluate existing and new methods for characterizing fatigue damage accumulation.
  • It was hypothesized that ligaments would accumulate damage with repetitive loading as evidenced by failure at stresses well below ultimate tensile strength, creep curve discontinuities, and by reductions in stiffness during loading.
  • Eight normal medial collateral ligaments from female New Zealand white rabbits were cycled in tension, between 0 MPa and 28 MPa, to failure or until 259,200 cycles, whichever came first.
  • Medial collateral ligaments that did not fail were subsequently loaded to failure.
  • Displacement rates (dl(max)/dt) as well as primary, secondary, and tertiary creeps were monitored as indices of damage accumulation and impending mechanical failure.
  • Additionally, the relative utilities of tangent, secant, and chord stiffness parameters were critically evaluated.
  • Three out of eight ligaments failed during testing, demonstrating that ligaments can fail in fatigue under moderate tensile stress in vitro.
  • The evaluation of displacement rates (dl(max)/dt), as well as primary through tertiary creep patterns, were not well suited to predicting failure in normal ligaments until rupture was all but imminent.
  • Secant stiffness dropped in a predictable fashion, providing a global indicator of tissue stiffness, but did not provide any insight into fiber mechanics.
  • Chord stiffness, on the other hand, appeared to be sensitive to fiber recruitment patterns.
  • The second derivative of force-displacement data proved to be a useful means of (a) objectively defining the start of the linear region and (b) inferring changes in fiber recruitment patterns within ligament tissue.
  • Tangent, secant, and chord stiffnesses highlight different attributes of ligament responses to loading; hence these parameters cannot be used interchangeably.
  • [MeSH-major] Cumulative Trauma Disorders / etiology. Cumulative Trauma Disorders / physiopathology. Medial Collateral Ligament, Knee / injuries. Medial Collateral Ligament, Knee / physiopathology. Models, Biological

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20524739.001).
  • [ISSN] 1528-8951
  • [Journal-full-title] Journal of biomechanical engineering
  • [ISO-abbreviation] J Biomech Eng
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


24. Gomez-Bougie P, Oliver L, Le Gouill S, Bataille R, Amiot M: Melphalan-induced apoptosis in multiple myeloma cells is associated with a cleavage of Mcl-1 and Bim and a decrease in the Mcl-1/Bim complex. Oncogene; 2005 Dec 1;24(54):8076-9
Hazardous Substances Data Bank. MELPHALAN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Melphalan-induced apoptosis in multiple myeloma cells is associated with a cleavage of Mcl-1 and Bim and a decrease in the Mcl-1/Bim complex.
  • Multiple myeloma (MM) is a rapidly fatal plasma-cell malignancy that evolves mainly in the bone marrow.
  • In the current study, we demonstrate that melphalan induces a drastic downregulation of Mcl-1L, Bcl-x(L) and BimEL in human melphalan-sensitive myeloma cells while the most potent proapoptotic isoforms, BimL and S, are affected to a lesser extent.
  • Moreover, Mcl-1L and BimEL disappearance is associated with the generation of proapoptotic cleaved forms generated by a caspase cleavage.
  • In myeloma cells, we have previously shown that Mcl-1 neutralizes the proapoptotic function of Bim and therefore, prevents the activation of death effectors.
  • In this study, we demonstrate that melphalan disrupts the Mcl-1/Bim complex whereas the Bcl-2/Bim complex is not modified.
  • The disappearance of full length Mcl-1 allows the release of Bim isoforms, particularly L and S, which can exert their proapoptotic function and leads to Bax activation and cytochrome c release.
  • Thus, we can hypothesize that the cleaved 26 kDa proapoptotic Mcl-1 and the 19 and 12 kDa of Bim, generated during melphalan treatment could contribute to the amplification loop of apoptosis.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Apoptosis Regulatory Proteins / metabolism. Melphalan / pharmacology. Membrane Proteins / metabolism. Multiple Myeloma / drug therapy. Neoplasm Proteins / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] Down-Regulation. Gene Expression Regulation, Neoplastic / drug effects. Humans. Myeloid Cell Leukemia Sequence 1 Protein. Protein Isoforms / genetics. Protein Isoforms / metabolism. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Multiple myeloma.
  • MedlinePlus Health Information. consumer health - Multiple Myeloma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16091744.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Membrane Proteins; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Protein Isoforms; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; Q41OR9510P / Melphalan
  •  go-up   go-down


25. Chan YS, Chen AC, Yuan LJ, Lin SS, Yang CY, Lee MS, Ueng SW: Effects of hyperbaric oxygen and platelet derived growth factor on medial collateral ligament fibroblasts. Undersea Hyperb Med; 2007 May-Jun;34(3):181-90
Hazardous Substances Data Bank. OXYGEN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of hyperbaric oxygen and platelet derived growth factor on medial collateral ligament fibroblasts.
  • PURPOSE: This study investigated hyperbaric oxygen (HBO2) and platelet-derived growth factor-BB (PDGF-BB) to determine their combined effects on fibroblasts from rabbit medial collateral ligament (MCL).
  • METHOD: Cells were divided into four groups: (I) Control, (II) HBO2 treatment, (III) PDGF-BB treatment and (IV) HBO2 combined with PDGF-BB treatment.
  • Measurement of cell growth was based on increase in cell number.
  • Cell cycle modulations were analyzed by fluorescence-activated cell sorter (FACS).
  • Quantity of Type I and Type III collagen was determined by western blotting and image analyzer.
  • RESULTS: Treatment doses of HBO2 alone or PDGF-bb alone dependently increased cell growth.
  • A combination of HBO2 treatment plus PDGF-bb treatment had an additive effect on cell growth in comparison with HBO2 treatment alone or PDGF-bb treatment alone.
  • FACS analysis revealed that HBO2 alone, PDGF-bb alone and PDGF-bb plus HBO2 treatment increase the percentage of cells accumulated in S-phase.
  • Western blotting analysis revealed that Type III collagen content was decreased significantly after HBO2 treatment alone or HBO2 plus PDGF-bb treatment but not in PDGF-bb treatment alone.
  • In contrast, although Type I collagen content was increased after HBO2 treatment, the increase in Type I collagen (increase /original) was not statistically significant.
  • CONCLUSION: HBO2 or HBO2 plus PDGF-bb treatment decreases the Type III collagen/Type I collagen content, which could result in mechanically stronger collagen fibrils.
  • We propose HBO2 therapy as a potentially effective treatment for MCL healing.
  • [MeSH-major] Fibroblasts / drug effects. Hyperbaric Oxygenation. Medial Collateral Ligament, Knee / cytology. Oxygen / pharmacology. Platelet-Derived Growth Factor / pharmacology
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Proliferation / drug effects. Cells, Cultured. Collagen Type I / metabolism. Collagen Type III / metabolism. Proto-Oncogene Proteins c-sis. Rabbits

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17672174.001).
  • [ISSN] 1066-2936
  • [Journal-full-title] Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, Inc
  • [ISO-abbreviation] Undersea Hyperb Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Collagen Type I; 0 / Collagen Type III; 0 / Platelet-Derived Growth Factor; 0 / Proto-Oncogene Proteins c-sis; 0 / platelet-derived growth factor BB; S88TT14065 / Oxygen
  •  go-up   go-down


26. Kojima K, Konopleva M, Tsao T, Andreeff M, Ishida H, Shiotsu Y, Jin L, Tabe Y, Nakakuma H: Selective FLT3 inhibitor FI-700 neutralizes Mcl-1 and enhances p53-mediated apoptosis in AML cells with activating mutations of FLT3 through Mcl-1/Noxa axis. Leukemia; 2010 Jan;24(1):33-43
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selective FLT3 inhibitor FI-700 neutralizes Mcl-1 and enhances p53-mediated apoptosis in AML cells with activating mutations of FLT3 through Mcl-1/Noxa axis.
  • Treatment using Fms-like tyrosine kinase-3 (FLT3) inhibitors is a promising approach to overcome the dismal prognosis of acute myeloid leukemia (AML) with activating FLT3 mutations.
  • Current trials are combining FLT3 inhibitors with p53-activating conventional chemotherapy.
  • We found that FI-700 immediately reduced antiapoptotic Mcl-1 levels and enhanced Nutlin-induced p53-mediated mitochondrial apoptosis in FLT3/internal tandem duplication cells through the Mcl-1/Noxa axis.
  • FI-700 induced proteasome-mediated degradation of Mcl-1, resulting in the reduced ability of Mcl-1 to sequester proapoptotic Bim.
  • Nutlin-3 induced Noxa, which displaced Bim from Mcl-1.
  • [MeSH-major] Apoptosis / drug effects. Leukemia, Myeloid, Acute / drug therapy. Mutation. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Proto-Oncogene Proteins c-bcl-2 / physiology. Pyridines / pharmacology. Pyrimidines / pharmacology. Tumor Suppressor Protein p53 / physiology. fms-Like Tyrosine Kinase 3 / genetics
  • [MeSH-minor] Cell Line, Tumor. Doxorubicin / pharmacology. G1 Phase / drug effects. Humans. Imidazoles / pharmacology. Myeloid Cell Leukemia Sequence 1 Protein. Piperazines / pharmacology. Proteasome Endopeptidase Complex / physiology. bcl-2-Associated X Protein / metabolism

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19946262.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / FI-700; 0 / Imidazoles; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / PMAIP1 protein, human; 0 / Piperazines; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyridines; 0 / Pyrimidines; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 0 / nutlin 3; 80168379AG / Doxorubicin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  •  go-up   go-down


27. Brunelle JK, Ryan J, Yecies D, Opferman JT, Letai A: MCL-1-dependent leukemia cells are more sensitive to chemotherapy than BCL-2-dependent counterparts. J Cell Biol; 2009 Nov 2;187(3):429-42
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MCL-1-dependent leukemia cells are more sensitive to chemotherapy than BCL-2-dependent counterparts.
  • Myeloid cell leukemia sequence 1 (MCL-1) and B cell leukemia/lymphoma 2 (BCL-2) are anti-apoptotic proteins in the BCL-2 protein family often expressed in cancer.
  • To compare the function of MCL-1 and BCL-2 in maintaining cancer survival, we constructed complementary mouse leukemia models based on Emu-Myc expression in which either BCL-2 or MCL-1 are required for leukemia maintenance.
  • We show that the principal anti-apoptotic mechanism of both BCL-2 and MCL-1 in these leukemias is to sequester pro-death BH3-only proteins rather than BAX and BAK.
  • We find that the MCL-1-dependent leukemias are more sensitive to a wide range of chemotherapeutic agents acting by disparate mechanisms.
  • In common across these varied treatments is that MCL-1 protein levels rapidly decrease in a proteosome-dependent fashion, whereas those of BCL-2 are stable.
  • We demonstrate for the first time that two anti-apoptotic proteins can enable tumorigenesis equally well, but nonetheless differ in their influence on chemosensitivity.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Leukemia / metabolism. Proto-Oncogene Proteins c-bcl-2 / physiology
  • [MeSH-minor] Animals. Apoptosis / genetics. Apoptosis / physiology. Apoptosis Regulatory Proteins / metabolism. Disease Models, Animal. Genes, myc. Half-Life. Lymphoma / genetics. Lymphoma / metabolism. Lymphoma / pathology. Membrane Proteins / metabolism. Mice. Myeloid Cell Leukemia Sequence 1 Protein. Proto-Oncogene Proteins / metabolism. Tumor Suppressor Proteins / metabolism

  • MedlinePlus Health Information. consumer health - Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Annu Rev Immunol. 2001;19:595-621 [11244048.001]
  • [Cites] Genes Dev. 2000 Aug 15;14(16):2060-71 [10950869.001]
  • [Cites] Mol Cell. 2001 Mar;7(3):683-94 [11463392.001]
  • [Cites] Mol Cell. 2001 Sep;8(3):705-11 [11583631.001]
  • [Cites] Cell Death Differ. 2002 May;9(5):505-12 [11973609.001]
  • [Cites] Blood. 2002 Jul 1;100(1):194-9 [12070027.001]
  • [Cites] Cancer Cell. 2002 Apr;1(3):289-98 [12086865.001]
  • [Cites] Cancer Cell. 2002 Sep;2(3):183-92 [12242151.001]
  • [Cites] Genes Dev. 2003 Jun 15;17(12):1475-86 [12783855.001]
  • [Cites] Cell. 2004 Jan 23;116(2):205-19 [14744432.001]
  • [Cites] J Biol Chem. 2004 Feb 6;279(6):4305-12 [14627695.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 20;101(16):6164-9 [15079075.001]
  • [Cites] Cancer Cell. 2004 Sep;6(3):241-9 [15380515.001]
  • [Cites] Nature. 1985 Dec 12-18;318(6046):533-8 [3906410.001]
  • [Cites] Nature. 1990 Nov 22;348(6299):331-3 [2250704.001]
  • [Cites] Cell. 1992 Apr 3;69(1):119-28 [1555236.001]
  • [Cites] Nature. 1992 Oct 8;359(6395):552-4 [1406975.001]
  • [Cites] Nature. 1992 Oct 8;359(6395):554-6 [1406976.001]
  • [Cites] Cancer Res. 1994 Dec 15;54(24):6348-52 [7987827.001]
  • [Cites] Nature. 1996 Jan 4;379(6560):88-91 [8538748.001]
  • [Cites] Nature. 1996 Feb 8;379(6565):554-6 [8596636.001]
  • [Cites] Mol Cell. 2005 Feb 18;17(4):525-35 [15721256.001]
  • [Cites] Genes Dev. 2005 Jun 1;19(11):1294-305 [15901672.001]
  • [Cites] Mol Cell. 2006 Mar 17;21(6):749-60 [16543145.001]
  • [Cites] Cancer Cell. 2006 May;9(5):351-65 [16697956.001]
  • [Cites] J Clin Invest. 2007 Jan;117(1):112-21 [17200714.001]
  • [Cites] Science. 2007 Feb 9;315(5813):856-9 [17289999.001]
  • [Cites] Cell Death Differ. 2007 Mar;14(3):616-24 [16977331.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Apr 10;104(15):6217-22 [17389404.001]
  • [Cites] Cancer Cell. 2007 Aug;12(2):171-85 [17692808.001]
  • [Cites] Genes Dev. 2007 Dec 15;21(24):3232-7 [18055695.001]
  • [Cites] Nat Rev Cancer. 2008 Feb;8(2):121-32 [18202696.001]
  • [Cites] J Cell Biol. 2008 Jan 28;180(2):341-55 [18209102.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Nov 18;105(46):17961-6 [19004807.001]
  • [Cites] Oncogene. 2009 Mar 5;28(9):1274-9 [19137012.001]
  • [Cites] Cell Death Differ. 2009 May;16(5):684-96 [19148184.001]
  • [Cites] Genes Dev. 1999 Oct 15;13(20):2658-69 [10541552.001]
  • [Cites] Blood. 2001 Jun 15;97(12):3902-9 [11389033.001]
  • (PMID = 19948485.001).
  • [ISSN] 1540-8140
  • [Journal-full-title] The Journal of cell biology
  • [ISO-abbreviation] J. Cell Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA068484; United States / NCI NIH HHS / CA / R01 CA129974; United States / NCI NIH HHS / CA / R01 CA129974; United States / NCI NIH HHS / CA / U01 CA105423
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Bcl-2-like protein 11; 0 / Mcl1 protein, mouse; 0 / Membrane Proteins; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / PUMA protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC2779245
  •  go-up   go-down


28. Sohn SK, Baek JH, Kim DH, Jung JT, Kwak DS, Park SH, Suh JS, Lee KB: Successful allogeneic stem-cell transplantation with prophylactic stepwise G-CSF primed-DLIs for relapse after autologous transplantation in mantle cell lymphoma: a case report and literature review on the evidence of GVL effects in MCL. Am J Hematol; 2000 Sep;65(1):75-80
Genetic Alliance. consumer health - Transplantation.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful allogeneic stem-cell transplantation with prophylactic stepwise G-CSF primed-DLIs for relapse after autologous transplantation in mantle cell lymphoma: a case report and literature review on the evidence of GVL effects in MCL.
  • Mantle cell lymphoma (MCL) is a distinctive clinicopathologic entity and represents 2-8% of all non-Hodgkin's lymphomas.
  • The median survival of patients with MCL is only 3 years, and none of the available conventional chemotherapy regimens appears curative.
  • Encouraging results have been reported with high-dose chemotherapy with autologous stem-cell transplantation (autoSCT).
  • However, a plateau in disease-free survival was not observed in relapsed MCL on the autoSCT trials.
  • Donor lymphocyte infusions (DLIs), by virtue of a GVL effect, have been shown to induce durable remissions in a few cases with refractory MCL that recur after alloSCT.
  • In this article, we review the literature on the evidence of the GVL effects in MCL and describe a patient with relapsed MCL shortly after high-dose chemotherapy with autoSCT.
  • G-CSF-primed cryopreserved DLIs were then infused on D+64 and D+92 to enhance the GVL effect.
  • Grade 3 intestinal GVHD developed 20 days after the 2(nd) DLI and was partially controlled with the combination of cyclosporin, prednisone, and mycophenolate mofetil.
  • Our findings suggest that alloSCT followed by prophylactic DLIs may offer a curative approach to refractory MCL.
  • [MeSH-major] Graft vs Tumor Effect. Granulocyte Colony-Stimulating Factor / pharmacology. Hematopoietic Stem Cell Transplantation. Intestinal Neoplasms / therapy. Lymphocyte Transfusion. Lymphoma, Mantle-Cell / therapy
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blood Donors. Humans. Male. Recurrence. Transplantation, Homologous. Treatment Outcome

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • (PMID = 10936869.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Number-of-references] 33
  •  go-up   go-down


29. Croft SL, Yardley V: Chemotherapy of leishmaniasis. Curr Pharm Des; 2002;8(4):319-42
HIV InSite. treatment guidelines - Pneumocystosis and HIV .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotherapy of leishmaniasis.
  • Leishmaniasis, in its variety of visceral (VL), cutaneous (CL) and mucocutaneous (MCL) forms, directly affects about 2 million people per annum, with approximately 350 million individuals at risk worldwide.
  • No vaccines exist for either VL, CL or MCL and chemotherapy is inadequate and expensive.
  • Current regimes use pentavalent antimony as primary therapy, which must be administered parenterally.
  • Should this fail, a number of other drugs may be employed, depending upon the species of Leishmania concerned and the resources available to the health professionals involved.
  • Recommended secondary treatment employs a variety of drugs, again depending on the nature of the infection.
  • The newer formulations of this drug are too expensive to use for the majority of endemic countries.
  • Pentamidine and paromomycin are used in some instances, and a new anti-leishmanial, miltefosine, may be used in the future.
  • In short, there remains a pressing need for new anti-leishmanials and this chapter reviews the current status of chemotherapy, the various avenues being investigated by researchers and their potential application in the future.
  • [MeSH-major] Antiprotozoal Agents / therapeutic use. Leishmania / drug effects. Leishmaniasis, Cutaneous / drug therapy. Leishmaniasis, Visceral / drug therapy

  • Genetic Alliance. consumer health - Leishmaniasis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11860369.001).
  • [ISSN] 1381-6128
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antiprotozoal Agents
  • [Number-of-references] 315
  •  go-up   go-down


30. Dreyling M, Lenz G, Hoster E, Van Hoof A, Gisselbrecht C, Schmits R, Metzner B, Truemper L, Reiser M, Steinhauer H, Boiron JM, Boogaerts MA, Aldaoud A, Silingardi V, Kluin-Nelemans HC, Hasford J, Parwaresch R, Unterhalt M, Hiddemann W: Early consolidation by myeloablative radiochemotherapy followed by autologous stem cell transplantation in first remission significantly prolongs progression-free survival in mantle-cell lymphoma: results of a prospective randomized trial of the European MCL Network. Blood; 2005 Apr 1;105(7):2677-84
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Early consolidation by myeloablative radiochemotherapy followed by autologous stem cell transplantation in first remission significantly prolongs progression-free survival in mantle-cell lymphoma: results of a prospective randomized trial of the European MCL Network.
  • Mantle-cell lymphoma (MCL) is characterized by poor prognosis with a median survival of only 3 to 4 years.
  • To improve clinical outcome, the European MCL Network initiated a randomized trial comparing consolidation with myeloablative radiochemotherapy followed by autologous stem cell transplantation (ASCT) to alpha-interferon maintenance (IFN alpha) in first remission.
  • Patients 65 years of age or younger with advanced-stage MCL were assigned to ASCT or IFN alpha after achievement of complete or partial remission by a cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP)-like induction therapy.
  • Patients in the ASCT arm experienced a significantly longer progression-free survival (PFS) with a median of 39 months compared with 17 months for patients in the IFN alpha arm (P = .0108).
  • Early consolidation by myeloablative radiochemotherapy followed by ASCT is feasible and results in a significant prolongation of PFS in advanced-stage MCL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Hematopoietic Stem Cell Transplantation. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / radiotherapy. Prednisone / administration & dosage. Vincristine / administration & dosage. Whole-Body Irradiation
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Disease-Free Survival. Europe. Female. Humans. Male. Middle Aged. Remission Induction. Survival Analysis. Transplantation, Autologous

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Steroids.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15591112.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
  •  go-up   go-down


31. Schulz H, Bohlius J, Skoetz N, Trelle S, Kober T, Reiser M, Dreyling M, Herold M, Schwarzer G, Hallek M, Engert A: Chemotherapy plus Rituximab versus chemotherapy alone for B-cell non-Hodgkin's lymphoma. Cochrane Database Syst Rev; 2007;(4):CD003805
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotherapy plus Rituximab versus chemotherapy alone for B-cell non-Hodgkin's lymphoma.
  • BACKGROUND: Rituximab has been shown to improve response rates and progression free survival when added to chemotherapy in patients with indolent and mantle cell lymphoma.
  • However, the impact of R on overall survival (OS) when given in combination with chemotherapy (R-chemo) has remained unclear so far.
  • OBJECTIVES: We thus performed a comprehensive systematic review in this group of patients to compare R-chemo with chemotherapy alone with respect to OS.
  • Other endpoints were overall response rate (ORR), toxicity and disease control as assessed by measures such as time to treatment failure (TTF), event free-survival (EFS), progression free-survival (PFS) and time to progression (TTP).
  • SELECTION CRITERIA: Only randomised controlled trials (RCT) comparing R-chemo with chemotherapy alone in patients with newly diagnosed or relapsed indolent lymphoma and mantle cell lymphoma (MCL) were included.
  • MAIN RESULTS: Seven randomised controlled trials involving 1943 patients with follicular lymphoma, mantle cell lymphoma, or other indolent lymphomas were included in the meta-analysis.
  • Patients treated with R-chemo had better overall survival (hazard ratio [HR] for mortality 0.65; 95% confidence interval (CI) 0.54 to 0.78), overall response (relative risk of tumour response 1.21; 95% CI 1.16 to 1.27), and disease control (HR of disease event 0.62; 95% CI 0.55 to 0.71) than patients treated with chemotherapy alone.
  • R-chemo improved overall survival in patients with follicular lymphoma (HR for mortality 0.63; 95% CI 0.51 to 0.79) and in patients with mantle cell lymphoma (HR for mortality 0.60; 95% CI 0.37 to 0.98).
  • AUTHORS' CONCLUSIONS: The systematic review demonstrated improved OS for patients with indolent lymphoma, particularly in the subgroups of follicular and in mantle cell lymphoma when treated with R-chemo compared to chemotherapy alone.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, B-Cell / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Humans. Lymphoma, Mantle-Cell / drug therapy. Randomized Controlled Trials as Topic. Rituximab. Survival Analysis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17943799.001).
  • [ISSN] 1469-493X
  • [Journal-full-title] The Cochrane database of systematic reviews
  • [ISO-abbreviation] Cochrane Database Syst Rev
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 67
  •  go-up   go-down


32. Coleman M, Martin P, Ruan J, Furman R, Niesvizky R, Elstrom R, George P, Leonard J, Kaufmann T: Low-dose metronomic, multidrug therapy with the PEP-C oral combination chemotherapy regimen for mantle cell lymphoma. Leuk Lymphoma; 2008 Mar;49(3):447-50
Hazardous Substances Data Bank. PROCARBAZINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low-dose metronomic, multidrug therapy with the PEP-C oral combination chemotherapy regimen for mantle cell lymphoma.
  • The prednisone, etoposide, procarbazine and cyclophosphamide (PEP-C) oral combination chemotherapy regimen (prednisone 20 mg, cyclophosphamide 50 mg, etoposide 50 mg, and procarbazine 50 mg with an oral anti-emetic) was employed at our center to treat 22 patients with heavily pretreated, recurrent mantle cell lymphoma (MCL).
  • All medications were administered daily until leukocytes fell to <3.0 x 10(9)/L whereupon treatment was withheld until recovery from the nadir.
  • Therapy was then reinstituted on a daily, alternate day, or fractionated basis (e.g.
  • Median time on therapy was 17 months.
  • Our findings demonstrate that low-dose oral agents administered in combination for continuous, prolonged periods with minimal drug-free intervals (metronomic therapy) may represent a novel, effective, easily tolerated approach to MCL and that this treatment approach warrants further exploration.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Lymphoma, Mantle-Cell / drug therapy
  • [MeSH-minor] Cyclophosphamide / administration & dosage. Etoposide / administration & dosage. Humans. Leukocyte Count. Middle Aged. Prednisone / administration & dosage. Procarbazine / administration & dosage. Recurrence. Retrospective Studies. Treatment Outcome

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18297520.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 35S93Y190K / Procarbazine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone
  •  go-up   go-down


33. Takasaki H, Hashimoto C, Takemura S, Motomura S, Ishigatsubo Y: [Clinical study of sequential high-dose chemotherapy with in vivo rituximab-purged stem cell autografting for mantle cell lymphoma]. Rinsho Ketsueki; 2010 Jan;51(1):57-62
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical study of sequential high-dose chemotherapy with in vivo rituximab-purged stem cell autografting for mantle cell lymphoma].
  • Sequential high-dose chemotherapy with in vivo rituximab-purged stem cell autografting was designed for previously untreated mantle cell lymphoma (MCL).
  • Between November 2001 and August 2008, five patients younger than 65 years of age with MCL at diagnosis were enrolled in this study.
  • Initial chemotherapy consisted of 3 cycles of CHOP regimen followed by four courses of high-dose chemotherapy.
  • One patient relapsed 3.2 years after treatment.
  • The principal toxicity in the study was hematologic but there were no treatment-related deaths.
  • Intensive high-dose sequential chemotherapy with in vivo purged stem cell support can achieve long-term disease-free survival for MCL.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Mantle-Cell / drug therapy. Stem Cell Transplantation. Transplantation Conditioning
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Disease-Free Survival. Doxorubicin / administration & dosage. Female. Humans. Male. Melphalan / administration & dosage. Middle Aged. Mitoxantrone / administration & dosage. Prednisolone / administration & dosage. Pulse Therapy, Drug. Rituximab. Transplantation, Autologous. Treatment Outcome. Vincristine / administration & dosage

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. MELPHALAN .
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20134141.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 04079A1RDZ / Cytarabine; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; BZ114NVM5P / Mitoxantrone; Q41OR9510P / Melphalan; VAP-cyclo protocol
  •  go-up   go-down


34. Mangel J, Leitch HA, Connors JM, Buckstein R, Imrie K, Spaner D, Crump M, Pennell N, Boudreau A, Berinstein NL: Intensive chemotherapy and autologous stem-cell transplantation plus rituximab is superior to conventional chemotherapy for newly diagnosed advanced stage mantle-cell lymphoma: a matched pair analysis. Ann Oncol; 2004 Feb;15(2):283-90
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intensive chemotherapy and autologous stem-cell transplantation plus rituximab is superior to conventional chemotherapy for newly diagnosed advanced stage mantle-cell lymphoma: a matched pair analysis.
  • BACKGROUND: The outcome of 20 patients with newly diagnosed mantle-cell lymphoma (MCL) treated on a prospective trial of autologous stem-cell transplantation (ASCT) and rituximab immunotherapy was compared with the outcome of 40 matched historical control patients treated with standard combination chemotherapy.
  • PATIENTS AND METHODS: Control patients with MCL were identified from a lymphoma database, and pairs were matched with patients receiving ASCT-rituximab for stage of disease, gender and age (+/-5 years).
  • Of 40 patients treated with conventional chemotherapy, with a median follow-up of 80 months, 33 have relapsed or progressed and 29 have died.
  • Overall (OS) and progression-free (PFS) survival were superior in patients treated with ASCT-rituximab compared with those treated with conventional chemotherapy (PFS at 3 years, 89% versus 29%, P <0.00001; OS at 3 years, 88% versus 65%, P = 0.052).
  • CONCLUSIONS: This matched-pair analysis suggests that patients with advanced-stage MCL treated with ASCT-rituximab had statistically significantly better PFS and a trend toward better OS than patients treated with conventional chemotherapy.
  • Longer follow-up will determine response duration and the true impact of this treatment strategy on PFS and OS.

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14760123.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  •  go-up   go-down


35. Li R, Zang Y, Li C, Patel NS, Grandis JR, Johnson DE: ABT-737 synergizes with chemotherapy to kill head and neck squamous cell carcinoma cells via a Noxa-mediated pathway. Mol Pharmacol; 2009 May;75(5):1231-9
Hazardous Substances Data Bank. BORTEZOMIB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ABT-737 synergizes with chemotherapy to kill head and neck squamous cell carcinoma cells via a Noxa-mediated pathway.
  • Overexpression of Bcl-X(L), an antiapoptotic Bcl-2 family member, occurs in a majority of head and neck squamous cell carcinomas (HNSCCs) and correlates with chemotherapy resistance in this disease.
  • As a single agent, ABT-737 was largely ineffective at promoting HNSCC cell death.
  • By contrast, ABT-737 strongly synergized with the chemotherapy drugs cisplatin and etoposide to promote HNSCC cell death and loss of clonogenic survival.
  • Synergism between ABT-737 and chemotherapy was associated with synergistic activation of caspase-3 and cleavage of poly(ADP-ribose) polymerase.
  • Treatment with ABT-737 plus chemotherapy resulted in dramatic up-regulation of proapoptotic Noxa protein, and small interfering RNA (siRNA)-mediated inhibition of Noxa up-regulation partially attenuated cell death by the synergistic combination.
  • Treatment with cisplatin or etoposide, alone or in combination with ABT-737, resulted in substantial down-regulation of Mcl-1L, a known inhibitor of ABT-737 action.
  • Further down-regulation of Mcl-1L using siRNA failed to enhance killing by the cisplatin/ABT-737 synergistic combination, indicating that chemotherapy treatment of HNSCC cells is sufficient to remove this impediment to ABT-737.
  • Together, our results demonstrate potent synergy between ABT-737 and chemotherapy drugs in the killing of HNSCC cells and reveal an important role for Noxa in mediating synergism by these agents.

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • MedlinePlus Health Information. consumer health - Head and Neck Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 2001 Dec 27;345(26):1890-900 [11756581.001]
  • [Cites] J Biol Chem. 2006 Oct 20;281(42):31440-7 [16928686.001]
  • [Cites] Cancer Cell. 2002 Sep;2(3):183-92 [12242151.001]
  • [Cites] Cell. 2004 Jan 23;116(2):205-19 [14744432.001]
  • [Cites] Adv Enzyme Regul. 1984;22:27-55 [6382953.001]
  • [Cites] Clin Cancer Res. 1998 Nov;4(11):2913-21 [9829760.001]
  • [Cites] Mol Carcinog. 1999 Oct;26(2):119-29 [10506755.001]
  • [Cites] Mol Cell. 2005 Feb 4;17(3):393-403 [15694340.001]
  • [Cites] Mol Cell. 2005 Feb 18;17(4):525-35 [15721256.001]
  • [Cites] Nature. 2005 Jun 2;435(7042):677-81 [15902208.001]
  • [Cites] Mol Cancer Ther. 2005 Jul;4(7):1096-104 [16020667.001]
  • [Cites] Cancer Biol Ther. 2005 Jul;4(7):720-7 [15917659.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2005 Dec 1;63(5):1400-12 [16005577.001]
  • [Cites] N Engl J Med. 2006 Feb 9;354(6):567-78 [16467544.001]
  • [Cites] Neoplasia. 2006 Mar;8(3):163-72 [16611409.001]
  • [Cites] Lancet Oncol. 2006 Jul;7(7):565-74 [16814208.001]
  • [Cites] Cell Death Differ. 2006 Aug;13(8):1419-21 [16645636.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Oct 3;103(40):14907-12 [16997913.001]
  • [Cites] Cancer Cell. 2006 Nov;10(5):375-88 [17097560.001]
  • [Cites] Cancer Cell. 2006 Nov;10(5):389-99 [17097561.001]
  • [Cites] J Clin Invest. 2007 Jan;117(1):112-21 [17200714.001]
  • [Cites] Cancer Res. 2007 Jan 15;67(2):782-91 [17234790.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):621-9 [17255285.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1176-83 [17283153.001]
  • [Cites] Science. 2007 Feb 9;315(5813):856-9 [17289999.001]
  • [Cites] Head Neck. 2007 Feb;29(2):163-88 [17312569.001]
  • [Cites] Oncogene. 2007 Apr 5;26(16):2374-80 [17016430.001]
  • [Cites] Oncogene. 2007 Jun 7;26(27):3972-9 [17173063.001]
  • [Cites] Blood. 2007 Sep 15;110(6):2057-66 [17536015.001]
  • [Cites] Int J Cancer. 2007 Dec 1;121(11):2387-94 [17688235.001]
  • [Cites] Neoplasia. 2007 Oct;9(10):801-11 [17971900.001]
  • [Cites] Clin Cancer Res. 2007 Dec 1;13(23):7191-8 [18056200.001]
  • [Cites] Cancer Res. 2008 Apr 15;68(8):2944-51 [18413764.001]
  • [Cites] J Natl Cancer Inst. 2008 Apr 16;100(8):580-95 [18398104.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3421-8 [18451170.001]
  • [Cites] Mol Cancer Ther. 2008 Jun;7(6):1647-55 [18566236.001]
  • [Cites] J Biol Chem. 2008 Sep 5;283(36):25003-13 [18599488.001]
  • [Cites] Blood. 2008 Oct 1;112(7):2906-16 [18591385.001]
  • [Cites] Laryngoscope. 2002 Apr;112(4):638-44 [12150516.001]
  • (PMID = 19246337.001).
  • [ISSN] 1521-0111
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097190; United States / NCI NIH HHS / CA / P50-CA097190-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABT-737; 0 / Antineoplastic Agents; 0 / Biphenyl Compounds; 0 / Boronic Acids; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Nitrophenols; 0 / PMAIP1 protein, human; 0 / Piperazines; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / Sulfonamides; 0 / bcl-X Protein; 69G8BD63PP / Bortezomib; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC2672802
  •  go-up   go-down


36. Thieblemont C, Antal D, Lacotte-Thierry L, Delwail V, Espinouse D, Michallet AS, Traulle C, Bouafia-Sauvy F, Giraud C, Salles G, Guilhot F, Coiffier B: Chemotherapy with rituximab followed by high-dose therapy and autologous stem cell transplantation in patients with mantle cell lymphoma. Cancer; 2005 Oct 1;104(7):1434-41
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotherapy with rituximab followed by high-dose therapy and autologous stem cell transplantation in patients with mantle cell lymphoma.
  • BACKGROUND: The authors evaluated the efficacy of chemotherapy combined with rituximab followed by high-dose therapy (HDT) plus autologous stem cell transplantation in patients with mantle cell lymphoma (MCL).
  • METHODS: This was a retrospective analysis of 34 patients who were treated in 2 departments of hematology, including 29 patients (85%) who received first-line treatment.
  • Rituximab was administered as 4 injections just before harvest in 25 patients (73%) or simultaneously with chemotherapy in 9 patients (27%).
  • RESULTS: After induction therapy, all patients except one reached a response: There were 14 (41%) complete responses (CR) and 19 (56%) partial responses (PR).
  • Stem cell harvest was successful in all patients but 2, with a median number of 5.9 CD34-positive cells per 10(6)/kg.
  • With a median follow-up at 2.6 years, the estimated median time to disease progression was 3.4 years.
  • Rituximab treatment before harvest did not delay hematopoietic reconstitution: The median time it took patients to recover absolute neutrophil count to > 0.5 G/L was 10 days.
  • CONCLUSIONS: Chemotherapy combined with rituximab followed by HDT improved the overall survival and progression-free survival in patients MCL without adding toxicities.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Lymphoma, Mantle-Cell / mortality. Lymphoma, Mantle-Cell / therapy. Stem Cell Transplantation / methods
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal, Murine-Derived. Combined Modality Therapy. Female. Follow-Up Studies. Graft Survival. Humans. Infusions, Intravenous. Male. Middle Aged. Pulse Therapy, Drug. Remission Induction. Retrospective Studies. Risk Assessment. Rituximab. Severity of Illness Index. Survival Rate. Transplantation, Autologous. Treatment Outcome

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16104036.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab
  •  go-up   go-down


37. Wirth T, Kühnel F, Fleischmann-Mundt B, Woller N, Djojosubroto M, Rudolph KL, Manns M, Zender L, Kubicka S: Telomerase-dependent virotherapy overcomes resistance of hepatocellular carcinomas against chemotherapy and tumor necrosis factor-related apoptosis-inducing ligand by elimination of Mcl-1. Cancer Res; 2005 Aug 15;65(16):7393-402
MedlinePlus Health Information. consumer health - Liver Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Telomerase-dependent virotherapy overcomes resistance of hepatocellular carcinomas against chemotherapy and tumor necrosis factor-related apoptosis-inducing ligand by elimination of Mcl-1.
  • Hepatocellular carcinomas (HCC) are drug-resistant tumors that frequently possess high telomerase activity.
  • It was therefore the aim of our study to investigate the potential of telomerase-dependent virotherapy in multimodal treatment of HCC.
  • Neither tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) or chemotherapy alone nor the combined treatment with both agents resulted in significant destruction of HCC cells.
  • Application of hTERT-Ad at low titers was also not capable to destroy HCC cells, but telomerase-dependent virotherapy overcame the resistance of HCC against TRAIL and chemotherapy.
  • The synergistic effects are explained by a strong down-regulation of Mcl-1 expression through hTERT-Ad that sensitizes HCC for TRAIL- and chemotherapy-mediated apoptosis.
  • To investigate whether down-regulation of Mcl-1 alone is sufficient to explain synergistic effects observed with virotherapy, Mcl-1 expression was inhibited by RNA interference.
  • Treatment with Mcl-1-siRNA significantly enhanced caspase-3 activity after chemotherapy and TRAIL application, confirming that elimination of Mcl-1 is responsible for the drug sensitization by hTERT-Ad.
  • Consistent with these results, heterologous overexpression of Mcl-1 significantly reduced the sensitization of hTERT-Ad transduced cells against apoptosis-inducing agents.
  • Chemotherapy did not interfere with quantitative hTERT-Ad production in HCC cells.
  • Whereas hTERT-Ad virotherapy alone was only capable to inhibit the growth of Hep3B xenografts, virochemotherapy resulted in vast destruction of the drug-resistant HCC.
  • In conclusion our data indicate that telomerase-dependent virotherapy is an attractive strategy to overcome the natural resistance of HCC against anticancer drugs by elimination of Mcl-1.
  • [MeSH-major] Carcinoma, Hepatocellular / therapy. Liver Neoplasms / therapy. Membrane Glycoproteins / pharmacology. Neoplasm Proteins / antagonists & inhibitors. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Telomerase / metabolism. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Adenoviridae / genetics. Adenoviridae / metabolism. Adenovirus E1A Proteins / biosynthesis. Adenovirus E1A Proteins / genetics. Animals. Apoptosis Regulatory Proteins. Cell Line, Tumor. Combined Modality Therapy. Down-Regulation. Drug Resistance, Neoplasm. Drug Synergism. Humans. Male. Mice. Mice, Nude. Myeloid Cell Leukemia Sequence 1 Protein. TNF-Related Apoptosis-Inducing Ligand. Xenograft Model Antitumor Assays

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16103092.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenovirus E1A Proteins; 0 / Apoptosis Regulatory Proteins; 0 / Mcl1 protein, mouse; 0 / Membrane Glycoproteins; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tnfsf10 protein, mouse; 0 / Tumor Necrosis Factor-alpha; EC 2.7.7.49 / Telomerase
  •  go-up   go-down


38. Evens AM, Winter JN, Hou N, Nelson BP, Rademaker A, Patton D, Singhal S, Frankfurt O, Tallman MS, Rosen ST, Mehta J, Gordon LI: A phase II clinical trial of intensive chemotherapy followed by consolidative stem cell transplant: long-term follow-up in newly diagnosed mantle cell lymphoma. Br J Haematol; 2008 Feb;140(4):385-93
Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II clinical trial of intensive chemotherapy followed by consolidative stem cell transplant: long-term follow-up in newly diagnosed mantle cell lymphoma.
  • Mantle cell lymphoma (MCL) is associated with high relapse rates and poor survival when treated with conventional chemotherapy, with or without rituximab.
  • We report the long-term follow-up of a phase II clinical trial using a new intensive multiagent chemotherapeutic regimen [cyclophosphamide, teniposide, doxorubicin and prednisone (CTAP) alternating with vincristine and high-dose methotrexate and cytarabine (VMAC)] in newly diagnosed MCL.
  • Following 4-6 cycles of CTAP/VMAC induction, patients aged < or =65 years proceeded to consolidative autologous haematopoietic stem cell transplantation (auto-HSCT), while patients < or =55 years who had a HLA-identical sibling received allogeneic-HSCT (busulfan/cyclophosphamide conditioning for both).
  • Twenty-five untreated MCL patients enrolled on the protocol between 1997 and 2002.
  • Among evaluable patients, overall response rate (ORR) was 74% following induction chemotherapy.
  • Therapy was well-tolerated with 4% treatment-related mortality (including HSCT).
  • CTAP/VMAC induction followed by consolidative auto-HSCT for newly diagnosed MCL is associated with high ORR and durable survival.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Lymphoma, Mantle-Cell / drug therapy
  • [MeSH-minor] Adult. Aged. Epidemiologic Methods. Female. Humans. Interferon-alpha / therapeutic use. Interleukin-2 / therapeutic use. Male. Middle Aged. Neoplasm Staging. Prognosis. Treatment Outcome

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Br J Haematol. 2008 Jul;142(3):482-4 [18510683.001]
  • (PMID = 18162124.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K23 CA109613-A1
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Interleukin-2
  •  go-up   go-down


39. Hitz F, Martinelli G, Zucca E, von Moos R, Mingrone W, Simcock M, Peterson J, Cogliatti SB, Bertoni F, Zimmermann DR, Ghielmini M, Swiss Group for Clinical Cancer Research (SAKK), Bern, Switzerland: A multicentre phase II trial of gemcitabine for the treatment of patients with newly diagnosed, relapsed or chemotherapy resistant mantle cell lymphoma: SAKK 36/03. Hematol Oncol; 2009 Sep;27(3):154-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A multicentre phase II trial of gemcitabine for the treatment of patients with newly diagnosed, relapsed or chemotherapy resistant mantle cell lymphoma: SAKK 36/03.
  • Mantle cell lymphoma (MCL) has a poor prognosis with often short and incomplete remissions.
  • We aimed to test the efficacy and tolerability of gemcitabine in treating MCL.
  • Gemcitabine was given in doses of 1000 mg/m(2) as a 30 min infusion on days 1 and 8 of each 3 week cycle for a maximum of nine cycles.
  • Eighteen patients with a median age of 70 years were recruited.
  • MCL was newly diagnosed in half of patients and relapsed in the remainder.
  • Most haematological adverse events occurred during the first chemotherapy cycle.
  • Three patients developed non-haematological serious adverse events: dyspnea, glomerular microangiopathy with haemolytic uremic syndrome (HUS) and hyperglycaemia.
  • The median time-to-progression and treatment response duration (TRD) was 8.0 (95% confidence interval: 5.5, 9.3) and 10.6 (95% confidence interval: 5.5, 10.9) months, respectively.
  • We conclude that Gemcitabine is well tolerated, moderately active and can induce disease stabilization in patients with MCL.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Antimetabolites, Antineoplastic / therapeutic use. Deoxycytidine / analogs & derivatives. Lymphoma, Mantle-Cell / drug therapy

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19274614.001).
  • [ISSN] 1099-1069
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
  •  go-up   go-down


40. Fox E, Widemann BC, Hawkins DS, Jayaprakash N, Dagher R, Aikin AA, Bernstein D, Long L, Mackall C, Helman L, Steinberg SM, Balis FM: Randomized trial and pharmacokinetic study of pegfilgrastim versus filgrastim after dose-intensive chemotherapy in young adults and children with sarcomas. Clin Cancer Res; 2009 Dec 1;15(23):7361-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Randomized trial and pharmacokinetic study of pegfilgrastim versus filgrastim after dose-intensive chemotherapy in young adults and children with sarcomas.
  • PURPOSE: To compare the effectiveness, tolerance, and pharmacokinetics of a single dose of pegfilgrastim to daily filgrastim in children and young adults with sarcomas treated with dose-intensive combination chemotherapy.
  • EXPERIMENTAL DESIGN: Patients were randomized to receive a single dose of 100 mcg/kg of pegfilgrastim s.c. or 5 mcg/kg/day of filgrastim s.c., daily until neutrophil recovery after two treatment cycles with vincristine, doxorubicin, and cyclophosphamide (VDC) and two cycles of etoposide and ifosfamide (IE).
  • The duration of severe neutropenia (absolute neutrophil count, < or =500/mcL) during cycles 1 to 4 and cycle duration for all cycles were compared.
  • Pharmacokinetics of pegfilgrastim and filgrastim and CD34+ stem cell mobilization were studied on cycle 1.
  • The median (range) duration of absolute neutrophil count of <500/mcL was 5.5 (3-8) days for pegfilgrastim and 6 (0-9) days for filgrastim (P = 0.76) after VDC, and 1.5 (0-4) days for pegfilgrastim and 3.75 (0-6.5) days for filgrastim (P = 0.11) after IE.
  • CONCLUSION: A single dose per cycle of pegfilgrastim was well tolerated and may be as effective as daily filgrastim based on the duration of severe neutropenia and number of episodes of febrile neutropenia and documented infections after dose-intensive treatment with VDC and IE.

  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Filgrastim .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Pediatr Hematol Oncol. 2005 Nov;27(11):627-9 [16282899.001]
  • [Cites] J Pediatr Hematol Oncol. 2005 Aug;27(8):449-51 [16096530.001]
  • [Cites] J Clin Oncol. 2006 Jul 1;24(19):3187-205 [16682719.001]
  • [Cites] J Clin Pharmacol. 2006 Jul;46(7):747-57 [16809800.001]
  • [Cites] Anticancer Drugs. 2007 Mar;18(3):277-81 [17264759.001]
  • [Cites] Curr Opin Oncol. 2007 Jul;19(4):328-35 [17545795.001]
  • [Cites] Curr Med Res Opin. 2007 Sep;23(9):2283-95 [17697451.001]
  • [Cites] J Pediatr Hematol Oncol. 2000 May-Jun;22(3):227-41 [10864054.001]
  • [Cites] J Clin Oncol. 2000 Jul;18(13):2522-8 [10893282.001]
  • [Cites] J Clin Oncol. 2002 Feb 1;20(3):727-31 [11821454.001]
  • [Cites] Ann Oncol. 2003 Jan;14(1):29-35 [12488289.001]
  • [Cites] Curr Hematol Rep. 2002 Nov;1(2):95-102 [12901130.001]
  • [Cites] Pharmacotherapy. 2003 Aug;23(8 Pt 2):9S-14S [12921217.001]
  • [Cites] J Pharm Sci. 2004 May;93(5):1367-73 [15067712.001]
  • [Cites] Curr Pharm Des. 2004;10(11):1235-44 [15078138.001]
  • [Cites] J Clin Oncol. 2004 Aug 15;22(16):3350-6 [15310780.001]
  • [Cites] J Clin Oncol. 1996 Feb;14(2):362-72 [8636745.001]
  • [Cites] Cancer. 1996 Aug 15;78(4):901-11 [8756388.001]
  • [Cites] J Clin Oncol. 2005 Feb 20;23(6):1178-84 [15718314.001]
  • [Cites] Transfusion. 2006 Feb;46(2):180-5 [16441592.001]
  • (PMID = 19920107.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / / NIH0010072919; United States / NCRR NIH HHS / RR / UL1 RR025014; United States / Intramural NIH HHS / / Z01 SC006880-30; United States / NCRR NIH HHS / RR / I ULI RR025014-01
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 3A58010674 / pegfilgrastim; PVI5M0M1GW / Filgrastim
  • [Other-IDs] NLM/ NIHMS148339; NLM/ PMC2787766
  •  go-up   go-down


41. Raynov J, Danon S, Valerianova Z: Control of acute emesis in repeated courses of moderately emetogenic chemotherapy. J BUON; 2002 Jan-Mar;7(1):57-60

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Control of acute emesis in repeated courses of moderately emetogenic chemotherapy.
  • PURPOSE: Cyclophosphamide (CY)-containing chemotherapy is usually characterized as moderately emetogenic.
  • The aim of this study was to evaluate the efficacy of different antiemetics in the control of acute emesis in repeated cycles of moderately emetogenic chemotherapy.
  • PATIENTS AND METHODS: A total of 101 patients with breast cancer (41, 40.6%), Hodgkin's disease (46, 45.5%) and non-Hodgkin's lymphoma (14, 13.9%) were studied.
  • These patients received standard protocols of CY-based (>/=750 mg/m(2)) moderately emetogenic chemotherapy.
  • Intravenous (i.v.) bolus metoclopramide (MCL), ondansetron (OND) and their combinations with corticosteroids (CS) were administered to the patients.
  • The MCL-alone group of patients was used as control group.
  • Emesis was evaluated during the first 3 courses of chemotherapy according to the internationally accepted criteria.
  • RESULTS: During the first course of chemotherapy no differences in the efficacy between the control group and the other groups were noted (p >0.05).
  • On the contrary, during the next 2 courses the efficacy of MCL progressively decreased and OND, OND plus CS and MCL plus CS showed significantly higher efficacy compared with MCL alone (p <0.05).
  • Excluding MCL alone, the other antiemetics showed similar efficacy in the 2nd and 3rd course of chemotherapy (p >0.05).
  • CONCLUSION: The combination of MCL plus CS showed similar efficacy compared with OND and OND plus CS, and is cost-effective.
  • The control of acute emesis in the first course and the patients' age are significant factors, influencing the efficacy of the antiemetic therapy in repeated courses of moderately emetogenic chemotherapy.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17577262.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  •  go-up   go-down


42. Josting A, Reiser M, Wickramanayake PD, Rueffer U, Draube A, Söhngen D, Tesch H, Wolf J, Diehl V, Engert A: Dexa-BEAM: an effective regimen for cytoreduction prior to high-dose chemotherapy with autologous stem cell support for patients with relapsed/refractory mantle-cell lymphoma. Leuk Lymphoma; 2000 Mar;37(1-2):185-7
Hazardous Substances Data Bank. DEXAMETHASONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dexa-BEAM: an effective regimen for cytoreduction prior to high-dose chemotherapy with autologous stem cell support for patients with relapsed/refractory mantle-cell lymphoma.
  • Mantle-cell lymphoma (MCL) is not a curable disease using conventional chemotherapy.
  • Patients with MCL have the shortest median time to progression and the shortest median survival of all lymphoma subtypes after first-line treatment.
  • In the present study we determined the efficacy of maximal cytoreductive therapy with up to four cycles of Dexa-BEAM (dexamethasone, carmustine [BCNU], etoposide, cytarabine, and melphalan) followed by high-dose chemotherapy (HDCT) and autologous hematopoietic stem cell support (ASCT) for patients with advanced relapsed or refractory MCL.
  • Nine consecutive patients with relapsed or refractory MCL were included.
  • Six of 8 patients responding to Dexa-BEAM received high-dose chemotherapy HDCT (BEAM) and autologous hematopoietic stem cell transplantation (ASCT).
  • With a median follow up of 24 months six patients are alive.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Lymphoma, Mantle-Cell / therapy. Salvage Therapy
  • [MeSH-minor] Adult. Carmustine / administration & dosage. Cytarabine / administration & dosage. Dexamethasone / administration & dosage. Etoposide / administration & dosage. Female. Humans. Male. Melphalan / administration & dosage. Middle Aged. Neoplasm Recurrence, Local / therapy. Remission Induction. Survival Analysis. Transplantation, Autologous

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. MELPHALAN .
  • Hazardous Substances Data Bank. Carmustine .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10721785.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] SWITZERLAND
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; Q41OR9510P / Melphalan; U68WG3173Y / Carmustine; Dexa-BEAM protocol
  •  go-up   go-down


43. Giordano G, Ferrucci PF, Nicci C, Grafone T, Tambaro R, Papini S, Farina G, Piano S, Zappacosta B, Storti S: Medium adsorbance fraction of reticulocyte and myeloperoxidase index may individuate a patient subset with a low risk of chemotherapy-related neutropenia. Oncol Rep; 2009 Jan;21(1):193-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Medium adsorbance fraction of reticulocyte and myeloperoxidase index may individuate a patient subset with a low risk of chemotherapy-related neutropenia.
  • In neoplastic patients chemotherapy frequently involves severe myeloid suppression.
  • Sometimes myeloid suppression is the main cause of therapy recycling delay with severe and prolonged neutropenia, anaemia and thrombocytopenia.
  • Our study aimed to verify whether there is a correlation between reticulocyte fractions, reticulocyte indices, myeloperoxidase index (MPXI) and post-chemotherapy myelopoietic function and severe post-chemotherapy neutropenia.
  • The patients were treated with chemotherapy (CT).
  • After CT, 60 patients had neutropenia (ANC <500/mcl) for a median of 7 days (range 3-21).
  • We assigned patients with an MPXI-positive value and medium adsorbance fraction of reticulocyte (MFR) >10.7% a score of 1, and a score of 0 was assigned to the remaining patients.
  • Patients with a score of 1 showed a lower number of neutropenic events (only 9 out of 36 patients) than those with a score of 0 (51 out of 76 patients), p<0.0001.
  • MPXI and MFR may be used in the assessment of myelopoiesis before CT administration, independently of the type of tumor, CT regimen and number of CT cycle, with the aim of identifying a patient subset with a lower risk of developing neutropenia post-CT.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Myelopoiesis / drug effects. Neutropenia / diagnosis. Peroxidase / drug effects. Reticulocytes / drug effects

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19082461.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 1.11.1.7 / Peroxidase
  •  go-up   go-down


44. Winquist E, Kirchner TS, Segal R, Chin J, Lukka H, Genitourinary Cancer Disease Site Group, Cancer Care Ontario Program in Evidence-based Care Practice Guidelines Initiative: Neoadjuvant chemotherapy for transitional cell carcinoma of the bladder: a systematic review and meta-analysis. J Urol; 2004 Feb;171(2 Pt 1):561-9
MedlinePlus Health Information. consumer health - Bladder Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neoadjuvant chemotherapy for transitional cell carcinoma of the bladder: a systematic review and meta-analysis.
  • PURPOSE: Despite local therapy most patients with muscle invasive transitional cell carcinoma (TCC) of the bladder die of systemic relapse, indicating a need for effective adjunctive systemic treatment.
  • We determined whether neoadjuvant chemotherapy improved overall survival.
  • MATERIALS AND METHODS: A systematic review and meta-analysis were performed of all known randomized controlled trials (RCTs) of neoadjuvant chemotherapy for stages II and III TCC conducted between 1984 and 2002.
  • Eight trials used cisplatin based combination chemotherapy and the pooled HR was 0.87 (95% CI 0.78 to 0.96, p = 0.006), consistent with an absolute overall survival benefit of 6.5% (95% CI 2 to 11%) from 50% to 56.5%.
  • Mortality due to combination chemotherapy was 1.1%.
  • CONCLUSIONS Neoadjuvant cisplatin based chemotherapy improves overall survival in muscle invasive TCC.
  • The size of the effect is modest and combination chemotherapy can be administered safely without adverse outcomes resulting in delayed local therapy.
  • An optimal chemotherapy regimen was not identified and newer regimens have not been tested in RCTs in this setting.
  • Further efforts to identify the patients most likely to benefit from neoadjuvant therapy are necessary to optimize its use.
  • [MeSH-major] Carcinoma, Transitional Cell / drug therapy. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Chemotherapy, Adjuvant. Humans. Randomized Controlled Trials as Topic. Survival Rate

  • Genetic Alliance. consumer health - Transitional cell carcinoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14713760.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 66
  •  go-up   go-down


45. Chen W, Bai L, Wang X, Xu S, Belinsky SA, Lin Y: Acquired activation of the Akt/cyclooxygenase-2/Mcl-1 pathway renders lung cancer cells resistant to apoptosis. Mol Pharmacol; 2010 Mar;77(3):416-23
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acquired activation of the Akt/cyclooxygenase-2/Mcl-1 pathway renders lung cancer cells resistant to apoptosis.
  • Acquired apoptosis resistance plays an important role in acquired chemoresistance in cancer cells during chemotherapy.
  • Our previous observations demonstrated that acquired tumor necrosis factor-related apoptosis-inducing ligand resistance in lung cancer cells was associated with Akt-mediated stabilization of cellular FLICE-like inhibitory protein (c-FLIP) and Mcl-1.
  • In this report, we determined that these cells also have acquired resistance to apoptosis induced by chemotherapeutics such as cisplatin and doxorubicin (Adriamycin), which was detected in vitro in cell cultures and in vivo in xenografted tumors.
  • COX-2 seems to be a crucial mediator in acquired apoptosis resistance because suppressing COX-2 activity with a chemical inhibitor or reducing COX-2 protein expression level with COX-2 small interfering RNA dramatically alleviated resistance to therapeutic-induced apoptosis.
  • Inhibiting Akt markedly suppressed COX-2 expression, suggesting COX-2 is a downstream effector of this cell survival kinase-mediated apoptosis resistance.
  • Furthermore, the expression of Mcl-1 but not c-FLIP was significantly reduced when COX-2 was suppressed, and knockdown of Mcl-1 substantially sensitized the cells to apoptosis.
  • Our results establish a novel pathway that consists of Akt, COX-2, and Mcl-1 for acquired apoptosis resistance, which could be a molecular target for circumventing acquired chemoresistance in lung cancer.

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell Biol. 2000 Sep;20(18):6638-45 [10958661.001]
  • [Cites] PLoS One. 2009;4(8):e6651 [19684859.001]
  • [Cites] J Pharmacol Exp Ther. 2003 Mar;304(3):959-67 [12604670.001]
  • [Cites] J Biol Chem. 2004 Feb 6;279(6):3949-55 [14607840.001]
  • [Cites] Biochim Biophys Acta. 2004 Mar 11;1697(1-2):3-16 [15023346.001]
  • [Cites] Nat Med. 2004 Apr;10(4):411-5 [14991050.001]
  • [Cites] MedGenMed. 2004;6(1):6 [15208519.001]
  • [Cites] Clin Cancer Res. 2004 Jun 15;10(12 Pt 2):4266s-4269s [15217972.001]
  • [Cites] Cancer Res. 1996 Jun 1;56(11):2573-83 [8653700.001]
  • [Cites] Cancer Res. 1998 Sep 1;58(17):3761-4 [9731479.001]
  • [Cites] Nature. 1999 Sep 2;401(6748):82-5 [10485710.001]
  • [Cites] Cytokine Growth Factor Rev. 2005 Feb;16(1):55-76 [15733832.001]
  • [Cites] Oncogene. 2006 Jan 5;25(1):43-50 [16278684.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):1089-95 [16424045.001]
  • [Cites] Anticancer Agents Med Chem. 2006 May;6(3):187-208 [16712448.001]
  • [Cites] Cancer Res. 2006 Jul 15;66(14):7059-66 [16849551.001]
  • [Cites] Oncogene. 2006 Nov 30;25(56):7333-5 [16785986.001]
  • [Cites] Crit Rev Oncol Hematol. 2008 Jun;66(3):208-17 [18304833.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Apr 13;355(3):807-12 [17316570.001]
  • [Cites] Mol Pharmacol. 2007 May;71(5):1381-8 [17296806.001]
  • [Cites] Carcinogenesis. 2007 Oct;28(10):2114-21 [17548900.001]
  • [Cites] Mol Pharmacol. 2007 Nov;72(5):1269-79 [17684158.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2008 Apr;294(4):L778-86 [18245266.001]
  • [Cites] Mol Cancer Ther. 2008 May;7(5):1156-63 [18483303.001]
  • [Cites] Mol Cancer. 2008;7:38 [18485224.001]
  • [Cites] Cytokine Growth Factor Rev. 2008 Jun-Aug;19(3-4):325-31 [18495520.001]
  • [Cites] Gastroenterology. 2008 Oct;135(4):1322-32 [18722373.001]
  • [Cites] Acta Pharmacol Sin. 2008 Nov;29(11):1275-88 [18954521.001]
  • [Cites] Oncogene. 2008 Oct 27;27(50):6419-33 [18955970.001]
  • [Cites] Int J Cancer. 2009 Feb 1;124(3):511-5 [19003982.001]
  • [Cites] Lung Cancer. 2009 Jan;63(1):72-6 [18499296.001]
  • [Cites] J Cell Mol Med. 2008 Dec;12(6B):2566-85 [19210756.001]
  • [Cites] Carcinogenesis. 2009 Mar;30(3):377-86 [19136477.001]
  • [Cites] Clin Cancer Res. 2009 Mar 15;15(6):2158-65 [19276291.001]
  • [Cites] Cancer Invest. 2009 May;27(4):391-6 [19266367.001]
  • [Cites] Curr Cancer Drug Targets. 2009 May;9(3):307-19 [19442051.001]
  • [Cites] Cancer Res. 2009 Jun 1;69(11):4894-903 [19487300.001]
  • [Cites] Mol Cancer Ther. 2009 Jun;8(6):1636-45 [19509265.001]
  • [Cites] J Biol Chem. 2009 Aug 14;284(33):21777-81 [19473994.001]
  • [Cites] J Biol Chem. 2001 Dec 28;276(52):48997-9002 [11585835.001]
  • (PMID = 19933775.001).
  • [ISSN] 1521-0111
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R03 CA125796; United States / NCI NIH HHS / CA / R03-CA125796
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Proto-Oncogene Proteins c-bcl-2; 80168379AG / Doxorubicin; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC2835422
  •  go-up   go-down


46. Tannock IF, Lee CM, Tunggal JK, Cowan DS, Egorin MJ: Limited penetration of anticancer drugs through tumor tissue: a potential cause of resistance of solid tumors to chemotherapy. Clin Cancer Res; 2002 Mar;8(3):878-84
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Limited penetration of anticancer drugs through tumor tissue: a potential cause of resistance of solid tumors to chemotherapy.
  • PURPOSE: Potential causes of drug resistance in solid tumors include genetically determined factors expressed in individual cells and those related to the solid tumor environment.
  • Important among the latter is the requirement for drugs to penetrate into tumor tissue and to achieve a lethal concentration in all of the tumor cells.
  • The present study was designed to characterize further the multicellular layer (MCL) method for studying drug penetration through tumor tissue and to provide information about tissue penetration for drugs used commonly in the treatment of human cancer.
  • EXPERIMENTAL DESIGN: EMT-6 mouse mammary and MGH-U1 human bladder cancer cells were grown on collagen-coated semiporous Teflon membranes to form MCLs approximately 200 microm thick.
  • The penetration of drugs through the MCL was evaluated by using radiolabeled drugs or analytical methods.
  • RESULTS: The MCL developed an extracellular matrix containing both laminin and collagen, although there were some differences in expression of extracellular matrix proteins.
  • Electron microscopy showed rare desmosomes in both MCL and tumors.
  • The penetration of cisplatin, etoposide, gemcitabine, paclitaxel, and vinblastine through tissue in the MCL was slow compared with penetration through the Teflon support membrane alone.
  • CONCLUSIONS: Our results suggest limited ability of anticancer drugs to reach tumor cells that are distant from blood vessels.
  • The limited penetration of anticancer drugs through tumor tissue may be an important cause of clinical resistance of solid tumors to chemotherapy.
  • [MeSH-major] Antineoplastic Agents / pharmacokinetics. Deoxycytidine / analogs & derivatives. Drug Resistance, Neoplasm. Mammary Neoplasms, Experimental / metabolism. Membranes, Artificial. Urinary Bladder Neoplasms / metabolism

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. TAXOL .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. VINBLASTINE .
  • Hazardous Substances Data Bank. TEFLON .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11895922.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Membranes, Artificial; 0W860991D6 / Deoxycytidine; 5V9KLZ54CY / Vinblastine; 6PLQ3CP4P3 / Etoposide; 9002-84-0 / Polytetrafluoroethylene; B76N6SBZ8R / gemcitabine; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


47. Ito A, Fujioka M, Yoshida T, Wakamatsu K, Ito S, Yamashita T, Jimbow K, Honda H: 4-S-Cysteaminylphenol-loaded magnetite cationic liposomes for combination therapy of hyperthermia with chemotherapy against malignant melanoma. Cancer Sci; 2007 Mar;98(3):424-30
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 4-S-Cysteaminylphenol-loaded magnetite cationic liposomes for combination therapy of hyperthermia with chemotherapy against malignant melanoma.
  • Previously, in order to improve the adsorption of magnetite nanoparticles to target cell surfaces, and generate heat in an alternating magnetic field (AMF) for cancer hyperthermia, we produced hyperthermia using magnetite cationic liposomes (MCL) that have a positive charge at the liposomal surface.
  • In the present study, we constructed 4-S-CAP-loaded MCL (4-S-CAP/MCL), which act as a novel modality, combining melanoma-specific chemotherapy by 4-S-CAP with intracellular hyperthermia mediated by MCL.
  • The 4-S-CAP/MCL exerted 4-S-CAP-mediated anticancer effects on B16 melanoma cells in vitro and in vivo.
  • Moreover, after intratumoral injection of 4-S-CAP/MCL in vivo, the melanoma nodules were heated to 45 degrees C under an AMF.
  • Significantly higher therapeutic effects were observed in mice treated with the combination therapy mediated by 4-S-CAP/MCL plus AMF irradiation compared with mice treated with 4-S-CAP/MCL alone (without AMF) or mice treated with hyperthermia alone (MCL + AMF irradiation).
  • These results suggest that this novel therapeutic tool is applicable to the treatment of malignant melanoma.
  • [MeSH-major] Cysteamine / analogs & derivatives. Hyperthermia, Induced. Liposomes / metabolism. Melanoma, Experimental / therapy
  • [MeSH-minor] Animals. Cations. Combined Modality Therapy. Magnetics. Mice. Nanoparticles. Neoplasm Transplantation. Tumor Cells, Cultured

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYSTEAMINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17270032.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cations; 0 / Liposomes; 5UX2SD1KE2 / Cysteamine; 91281-34-4 / 4-S-cysteaminylphenol
  •  go-up   go-down


48. Sourbier C, Valera-Romero V, Giubellino A, Yang Y, Sudarshan S, Neckers L, Linehan WM: Increasing reactive oxygen species as a therapeutic approach to treat hereditary leiomyomatosis and renal cell carcinoma. Cell Cycle; 2010 Oct 15;9(20):4183-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Increasing reactive oxygen species as a therapeutic approach to treat hereditary leiomyomatosis and renal cell carcinoma.
  • Hereditary leiomyomatosis renal cell carcinoma (HLRCC)-associated renal tumors are aggressive and tend to metastasize early.
  • There are currently no effective forms of therapy for patients with advanced HLRCC-associated kidney cancer.
  • We have previously shown that HLRCC cells express a high level of reactive oxygen species (ROS).
  • In the present study we investigated the cytotoxic effects of increasing ROS level using bortezomib in combination with cisplatin on HLRCC cells in vitro and in an in vivo xenograft model.
  • The cytotoxic effect of several ROS inducers on FH-deficient cells was assessed by synthetic lethality.
  • ROS inducers had a pronounced impact on the viability of FH-deficient cells.
  • Bortezomib induced apoptosis in vitro in HLRCC cells and inhibited HLRCC tumour growth in vivo.
  • Bortezomib-associated cytotoxicity was highly correlated with cellular ROS level: combining bortezomib with other ROS inducers enhanced cytotoxicity, while combining bortezomib with a ROS scavenger inhibited its cytotoxic effect.
  • Finally, HLRCC murine xenografts were treated with bortezomib and cisplatin, another ROS inducer.
  • This regimen induced HLRCC tumour regression in vivo.
  • These findings suggest that increasing ROS level in HLRCC above a certain threshold can induce HLRCC-tumor cell death.
  • Increasing tumor ROS with bortezomib in combination with cisplatin represents a novel targeted therapeutic approach to treat advanced HLRCC-associated renal tumors.

  • Genetic Alliance. consumer health - Renal cell carcinoma.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hum Mol Genet. 2001 May 15;10(11):1221-8 [11371515.001]
  • [Cites] J Cell Mol Med. 2009 Sep;13(9A):2800-21 [19602054.001]
  • [Cites] Leukemia. 2003 Oct;17(10):2036-45 [14513055.001]
  • [Cites] Curr Opin Cell Biol. 2003 Dec;15(6):725-31 [14644197.001]
  • [Cites] Nature. 2004 Feb 26;427(6977):853-8 [14985765.001]
  • [Cites] Clin Cancer Res. 2004 Jun 1;10(11):3839-52 [15173093.001]
  • [Cites] J Clin Lab Anal. 1995;9(6):424-30 [8587013.001]
  • [Cites] Braz J Med Biol Res. 2005 Jul;38(7):995-1014 [16007271.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11658-66 [16357177.001]
  • [Cites] Int J Biochem Cell Biol. 2007;39(1):44-84 [16978905.001]
  • [Cites] J Urol. 2007 Jun;177(6):2074-9; discussion 2079-80 [17509289.001]
  • [Cites] Joint Bone Spine. 2007 Jul;74(4):324-9 [17590367.001]
  • [Cites] Exp Cell Res. 2008 Feb 1;314(3):651-67 [18166172.001]
  • [Cites] J Cancer Res Clin Oncol. 2008 Mar;134(3):323-30 [17701215.001]
  • [Cites] Science. 2008 May 2;320(5876):661-4 [18388260.001]
  • [Cites] Ter Arkh. 2008;80(10):53-5 [19105416.001]
  • [Cites] Mol Cancer Ther. 2009 Mar;8(3):626-35 [19276158.001]
  • [Cites] Biochim Biophys Acta. 2009 Apr;1795(2):83-91 [19121370.001]
  • [Cites] Anticancer Res. 2009 Mar;29(3):817-21 [19414314.001]
  • [Cites] Hepatogastroenterology. 2009 Mar-Apr;56(90):343-7 [19579595.001]
  • [Cites] Mol Cell Biol. 2009 Aug;29(15):4080-90 [19470762.001]
  • [Cites] Chem Biol Interact. 2009 Sep 14;181(1):115-23 [19464278.001]
  • [Cites] Infect Disord Drug Targets. 2009 Aug;9(4):445-52 [19689385.001]
  • [Cites] Apoptosis. 2009 Dec;14(12):1451-8 [19466552.001]
  • [Cites] Cancer Genet Cytogenet. 2010 Jan 1;196(1):45-55 [19963135.001]
  • [Cites] Anticancer Drugs. 2010 Feb;21(2):140-50 [20010425.001]
  • [Cites] Nat Genet. 2002 Apr;30(4):406-10 [11865300.001]
  • (PMID = 20953139.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Pyrazines; 0 / Reactive Oxygen Species; 69G8BD63PP / Bortezomib; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC3055201
  •  go-up   go-down


49. Gill S, Ritchie D: Therapeutic options in mantle cell lymphoma. Leuk Lymphoma; 2008 Mar;49(3):398-409
Genetic Alliance. consumer health - Mantle cell lymphoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic options in mantle cell lymphoma.
  • Mantle cell lymphoma (MCL) is an aggressive lymphoma requiring intensive chemotherapy +/- autologous stem cell transplantation (SCT) to achieve optimal rates of progression-free survival.
  • Here we review the treatment options for patients with newly-diagnosed or relapsed MCL and discuss recent advances in management, including the role of autologous and allogeneic SCT.
  • [MeSH-major] Lymphoma, Mantle-Cell / therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Humans. MEDLINE. Radioimmunotherapy / methods. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18297516.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 74
  •  go-up   go-down


50. Kahl B: Chemotherapy combinations with monoclonal antibodies in non-Hodgkin's lymphoma. Semin Hematol; 2008 Apr;45(2):90-4
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotherapy combinations with monoclonal antibodies in non-Hodgkin's lymphoma.
  • Although the use of monoclonal antibodies as single agents has had a tremendous impact on the care of patients with non-Hodgkin's lymphoma (NHL), the greatest benefit has been generated by the addition of monoclonal antibodies to conventional cytotoxic chemotherapy.
  • The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy (R-CHOP regimen) improves the response rate, progression-free survival (PFS), and overall survival (OS) in diffuse large B-cell lymphoma (DLBCL).
  • Adding rituximab to CHOP chemotherapy improves response rates and PFS in mantle cell lymphoma (MCL).
  • Finally, the addition of rituximab to a variety of chemotherapy regimens improves the response rates, PFS, and OS in follicular lymphoma (FL).
  • Several other (epratuzumab, bevacizumab, alemtuzumab) monoclonal antibody-chemotherapy combinations are currently under study in NHL.
  • This review will summarize the data supporting the addition of rituximab to chemotherapy in NHL and discuss preliminary data regarding the use of other monoclonal antibodies in combination with chemotherapy.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10209-13 [10954754.001]
  • [Cites] J Clin Oncol. 2005 Aug 1;23(22):5044-51 [15955901.001]
  • [Cites] N Engl J Med. 2002 Jan 24;346(4):235-42 [11807147.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4279-84 [12576316.001]
  • [Cites] J Clin Oncol. 2005 Aug 1;23(22):5027-33 [15955905.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3725-32 [16123223.001]
  • [Cites] Lancet Oncol. 2006 May;7(5):379-91 [16648042.001]
  • [Cites] J Clin Oncol. 2006 Jul 1;24(19):3121-7 [16754935.001]
  • [Cites] Leuk Lymphoma. 2006 Jun;47(6):998-1005 [16840188.001]
  • [Cites] J Clin Oncol. 2006 Aug 20;24(24):3880-6 [16864854.001]
  • [Cites] Mol Immunol. 2007 Feb;44(6):1331-41 [16814387.001]
  • [Cites] Clin Cancer Res. 2006 Dec 1;12(23):7174-9 [17145843.001]
  • [Cites] Cancer. 2006 Dec 15;107(12):2826-32 [17099879.001]
  • [Cites] Leuk Lymphoma. 2007 Jun;48(6):1102-9 [17577773.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2316-23 [17581918.001]
  • [Cites] J Clin Oncol. 2003 Aug 15;21(16):3051-9 [12837807.001]
  • [Cites] Clin Cancer Res. 2003 Sep 1;9(10 Pt 2):3982S-90S [14506197.001]
  • [Cites] Leuk Lymphoma. 2003 Dec;44(12):2089-93 [14959852.001]
  • [Cites] Clin Cancer Res. 2004 Aug 15;10(16):5327-34 [15328168.001]
  • [Cites] Cancer Res. 1997 Oct 15;57(20):4593-9 [9377574.001]
  • [Cites] Clin Cancer Res. 1997 May;3(5):647-51 [9815732.001]
  • [Cites] Toxicol Pathol. 1999 Jan-Feb;27(1):78-86 [10367678.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1984-92 [15668467.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4117-26 [15867204.001]
  • [Cites] Clin Cancer Res. 2001 Mar;7(3):709-23 [11297268.001]
  • (PMID = 18381103.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA014520; None / None / / P30 CA014520-36; United States / NCI NIH HHS / CA / P30 CA014520-36
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 2S9ZZM9Q9V / Bevacizumab; 3A189DH42V / alemtuzumab; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 28
  • [Other-IDs] NLM/ NIHMS213237; NLM/ PMC2919066
  •  go-up   go-down


51. Garcia M, Romaguera JE, Inamdar KV, Rassidakis GZ, Medeiros LJ: Proliferation predicts failure-free survival in mantle cell lymphoma patients treated with rituximab plus hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone alternating with rituximab plus high-dose methotrexate and cytarabine. Cancer; 2009 Mar 1;115(5):1041-8
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proliferation predicts failure-free survival in mantle cell lymphoma patients treated with rituximab plus hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone alternating with rituximab plus high-dose methotrexate and cytarabine.
  • BACKGROUND: It has been demonstrated that the tumor proliferation index has prognostic significance in patients with mantle cell lymphoma (MCL).
  • Patients in most of studies, however, have been treated with relatively traditional chemotherapy regimens.
  • At the authors' institution, patients with MCL received an aggressive chemotherapy regimen: rituximab plus hyperfractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone alternating with rituximab plus high-dose methotrexate and cytarabine (R-hyper-CVAD).
  • METHODS: The authors assessed the proliferation rate of MCL using immunohistochemistry and an antibody specific for Ki-67 in 71 untreated patients who subsequently received R-hyper-CVAD.
  • The study group included 59 patients who had classic MCL and 12 patients who had the blastoid variant of MCL.
  • RESULTS: For the entire study group and for the group of patients with classic MCL, a proliferation index of >20% Ki-67-positive cells was correlated significantly with shorter failure-free survival.
  • CONCLUSIONS: The current results indicated that the proliferation index in patients with MCL predicted prognosis in those who uniformly received the R-hyper-CVAD chemotherapy regimen.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Mantle-Cell / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal. Antibodies, Monoclonal, Murine-Derived. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Dexamethasone / administration & dosage. Disease-Free Survival. Doxorubicin / administration & dosage. Drug Administration Schedule. Female. Humans. Ki-67 Antigen / metabolism. Male. Methotrexate / administration & dosage. Middle Aged. Prognosis. Rituximab. Survival Analysis. Vincristine / administration & dosage

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2009 American Cancer Society.
  • (PMID = 19170236.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Ki-67 Antigen; 04079A1RDZ / Cytarabine; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


52. Till BG, Gooley TA, Crawford N, Gopal AK, Maloney DG, Petersdorf SH, Pagel JM, Holmberg L, Bensinger W, Press OW: Effect of remission status and induction chemotherapy regimen on outcome of autologous stem cell transplantation for mantle cell lymphoma. Leuk Lymphoma; 2008 Jun;49(6):1062-73
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of remission status and induction chemotherapy regimen on outcome of autologous stem cell transplantation for mantle cell lymphoma.
  • We analysed the outcomes of autologous stem cell transplantation (ASCT) following high-dose therapy with respect to remission status at the time of transplantation and induction regimen used in 56 consecutive patients with mantle cell lymphoma (MCL).
  • Twenty-one patients received induction chemotherapy with HyperCVAD with or without rituximab (+/-R) followed by ASCT in first complete or partial remission (CR1/PR1), 15 received CHOP (+/-R) followed by ASCT in CR1/PR1 and 20 received ASCT following disease progression.
  • The hazard of mortality among patients transplanted with relapsed/refractory disease was 6.09 times that of patients transplanted in CR1/PR1 (P = 0.006).
  • These results suggest that ASCT in CR1/PR1 leads to improved survival outcomes for patients with MCL compared to ASCT with relapsed/refractory disease, and a HyperCVAD (+/-R) induction regimen may be associated with an improved PFS among patients transplanted in CR1/PR1.

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 1999 Apr;17(4):1244 [10561185.001]
  • [Cites] J Clin Oncol. 2000 Feb;18(4):773-9 [10673518.001]
  • [Cites] Biol Blood Marrow Transplant. 2000;6(6):640-5 [11128815.001]
  • [Cites] J Clin Oncol. 2002 Mar 1;20(5):1288-94 [11870171.001]
  • [Cites] Hematol J. 2000;1(2):87-94 [11920175.001]
  • [Cites] Blood. 2002 May 1;99(9):3158-62 [11964278.001]
  • [Cites] Leuk Lymphoma. 2002 Jun;43(6):1229-37 [12152990.001]
  • [Cites] Br J Haematol. 2003 Mar;120(5):793-800 [12614212.001]
  • [Cites] Blood. 2003 Jul 15;102(2):749-55 [12663455.001]
  • [Cites] Eur J Haematol. 2003 Aug;71(2):73-80 [12890145.001]
  • [Cites] Cancer. 2003 Dec 15;98(12):2630-5 [14669282.001]
  • [Cites] Ann Oncol. 2004 Feb;15(2):283-90 [14760123.001]
  • [Cites] Haematologica. 2004 Oct;89(10):1275-6 [15477221.001]
  • [Cites] Ann Oncol. 1995 Mar;6(3):257-62 [7612491.001]
  • [Cites] Leukemia. 1996 Dec;10(12):1975-9 [8946940.001]
  • [Cites] Ann Oncol. 1997 Jul;8(7):701-4 [9296227.001]
  • [Cites] J Clin Oncol. 1998 Jan;16(1):13-8 [9440717.001]
  • [Cites] Cancer. 1998 Feb 1;82(3):567-75 [9452276.001]
  • [Cites] Eur J Cancer. 1998 Feb;34(3):329-36 [9640217.001]
  • [Cites] J Clin Oncol. 1998 Aug;16(8):2780-95 [9704731.001]
  • [Cites] Biol Blood Marrow Transplant. 2005 Jan;11(1):39-46 [15625543.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1984-92 [15668467.001]
  • [Cites] Ann Oncol. 2005 Apr;16(4):618-24 [15781489.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2677-84 [15591112.001]
  • [Cites] Cancer. 2005 Oct 1;104(7):1434-41 [16104036.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):7013-23 [16145068.001]
  • [Cites] Haematologica. 2005 Nov;90(11):1580-2 [16266909.001]
  • [Cites] Haematologica. 2006 Mar;91(3):425-6 [16531272.001]
  • [Cites] Cancer. 2006 Sep 1;107(5):1014-22 [16878325.001]
  • [Cites] Ann Hematol. 2007 Feb;86(2):101-5 [17089127.001]
  • [CommentIn] Leuk Lymphoma. 2008 Jun;49(6):1017-8 [18452075.001]
  • (PMID = 18452065.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA044991-21; United States / NCI NIH HHS / CA / K23 CA085479; United States / NCI NIH HHS / CA / P01 CA44991; United States / NCI NIH HHS / CA / P01 CA044991; United States / NCI NIH HHS / CA / K23CA85479; United States / NCI NIH HHS / CA / K23 CA085479-06; United States / NCI NIH HHS / CA / CA085479-06; United States / NCI NIH HHS / CA / CA044991-21
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone
  • [Other-IDs] NLM/ NIHMS147578; NLM/ PMC2769072
  •  go-up   go-down


53. Hegde GV, Munger CM, Emanuel K, Joshi AD, Greiner TC, Weisenburger DD, Vose JM, Joshi SS: Targeting of sonic hedgehog-GLI signaling: a potential strategy to improve therapy for mantle cell lymphoma. Mol Cancer Ther; 2008 Jun;7(6):1450-60
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting of sonic hedgehog-GLI signaling: a potential strategy to improve therapy for mantle cell lymphoma.
  • Mantle cell lymphoma (MCL) has one of the worst clinical outcomes among the B-cell lymphomas, with a median survival of only 3 to 4 years.
  • Therefore, a better understanding of the underlying mechanisms that regulate MCL proliferation/survival is needed to develop an effective therapy.
  • Because sonic hedgehog (Shh)-GLI signaling has been shown to be important in the proliferation and survival of several cancers, and no such information is available for MCL, this study was undertaken.
  • Our results show that the molecules associated with Shh-GLI signaling, such as PTCH and SMO receptors, and GLI1 and GLI2 target transcription factors were expressed in the human MCL cell lines and primary MCL cells from patients.
  • Perturbation of this signaling in the presence of exogenous Shh/cyclopamine significantly (P < 0.001) influenced the proliferation of JVM2 MCL cells.
  • Furthermore, down-regulation of GLI transcription factors using antisense oligonucleotides not only resulted in significantly (P < 0.001) decreased proliferation of the MCL cells but also significantly (P < 0.05) increased their susceptibility to chemotherapeutic drug, doxorubicin.
  • Also, down-regulation of GLI decreased cyclin D1 and BCL2 transcript levels, which suggests that these key molecules might be regulated by GLI in MCL.
  • Thus, our results indicate a significant role for Shh-GLI signaling in the proliferation of MCL, and molecular targeting of GLI is a potential therapeutic approach to improve the treatment for MCL.
  • [MeSH-major] Hedgehog Proteins / metabolism. Lymphoma, Mantle-Cell / therapy. Signal Transduction. Transcription Factors / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D1 / genetics. Cyclin D1 / metabolism. Down-Regulation / drug effects. Doxorubicin / pharmacology. Gene Expression Regulation, Neoplastic / genetics. Humans. Models, Biological. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18524848.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR016469
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GLI1 protein, human; 0 / Hedgehog Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Transcription Factors; 136601-57-5 / Cyclin D1; 80168379AG / Doxorubicin
  •  go-up   go-down


54. Suh KS, Goy A: Bortezomib in mantle cell lymphoma. Future Oncol; 2008 Apr;4(2):149-68
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bortezomib in mantle cell lymphoma.
  • Mantle cell lymphoma (MCL) represents 6% of non-Hodgkin lymphomas, but is one of the most active fields of clinical investigation.
  • Unfortunately, there is still no standard or curative therapy in MCL.
  • Front-line therapy appears to benefit from intensification either through high-dose therapy with stem cell transplant consolidation or dose-intense chemotherapy with hyperfractionated cyclophosphamide, vincristine, adriamycin/doxorubicin and dexamethasone/rituximab.
  • Most patients still relapse and a multitude of novel agents are currently being tested in this setting, including proteasome inhibitors with bortezomib (the first of its class and the first US FDA-approved drug for MCL), mTOR inhibitors, Bcl-2 inhibitors, antiangiogenesis agents and histone deacetylase inhibitors among others.
  • An obvious effort is needed to enroll patients on clinical trials, the design of which might benefit from pharmacogenomics and a better understanding of MCL biology and its diversity.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Lymphoma, Mantle-Cell / drug therapy. Pyrazines / therapeutic use
  • [MeSH-minor] Aged. Bortezomib. Clinical Trials as Topic. Female. Humans. Male. Middle Aged. Protease Inhibitors / pharmacology. Protease Inhibitors / therapeutic use. Recurrence. Treatment Outcome

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18407730.001).
  • [ISSN] 1744-8301
  • [Journal-full-title] Future oncology (London, England)
  • [ISO-abbreviation] Future Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  • [Number-of-references] 112
  •  go-up   go-down


55. Lepelletier Y, Camara-Clayette V, Jin H, Hermant A, Coulon S, Dussiot M, Arcos-Fajardo M, Baude C, Canionni D, Delarue R, Brousse N, Benaroch P, Benhamou M, Ribrag V, Monteiro RC, Moura IC, Hermine O: Prevention of mantle lymphoma tumor establishment by routing transferrin receptor toward lysosomal compartments. Cancer Res; 2007 Feb 1;67(3):1145-54
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Mantle cell lymphoma (MCL) is one of the most frequent of the newly recognized non-Hodgkin's lymphomas.
  • The major problem of MCL therapy is the occurrence of relapse and subsequent resistance to chemotherapy and immunotherapy in virtually all cases.
  • Here, we show that one injection of anti-human transferrin receptor (TfR) monoclonal antibody A24 totally prevented xenografted MCL tumor establishment in nude mice.
  • In vitro, A24 induced up to 85% reduction of MCL cell proliferation (IC(50) = 3.75 nmol/L) independently of antibody aggregation, complement-dependent or antibody-dependent cell-mediated cytotoxicity.
  • A24 induced MCL cell apoptosis through caspase-3 and caspase-9 activation, either alone or synergistically with chemotherapeutic agents.
  • Therefore, A24-based therapies alone or in association with classic chemotherapies could provide a new alternative strategy against MCL, particularly in relapsing cases.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Immunization, Passive / methods. Lymphoma, Mantle-Cell / prevention & control. Lysosomes / metabolism. Receptors, Transferrin / metabolism
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Endocytosis / drug effects. Female. Humans. Lymph Nodes / metabolism. Lymph Nodes / pathology. Mice. Mice, Nude. Xenograft Model Antitumor Assays

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17283149.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Receptors, Transferrin
  •  go-up   go-down


56. Gianni AM, Magni M, Martelli M, Di Nicola M, Carlo-Stella C, Pilotti S, Rambaldi A, Cortelazzo S, Patti C, Parvis G, Benedetti F, Capria S, Corradini P, Tarella C, Barbui T: Long-term remission in mantle cell lymphoma following high-dose sequential chemotherapy and in vivo rituximab-purged stem cell autografting (R-HDS regimen). Blood; 2003 Jul 15;102(2):749-55
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term remission in mantle cell lymphoma following high-dose sequential chemotherapy and in vivo rituximab-purged stem cell autografting (R-HDS regimen).
  • Mantle cell lymphoma (MCL) is rarely cured with standard-dose chemotherapy.
  • From January 1997 to February 2000, 28 previously untreated advanced-stage MCL patients younger than 61 years of age were treated at 9 Italian hematologic departments with 3 cycles of standard-dose debulking chemotherapy followed by a high-dose rituximab-supplemented sequence (R-HDS) including intravenous administration of high-dose cyclophosphamide, high-dose cytarabine, high-dose melphalan, and high-dose mitoxantrone plus melphalan.
  • These results compare with the 42% OS rate and the 18% EFS rate observed in 35 age-matched historic controls treated with standard-dose chemotherapy at the participating centers.
  • The use of rituximab in combination with high-dose chemotherapy represents a very effective in vivo purging method.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow Purging / methods. Lymphoma, Mantle-Cell / therapy. Peripheral Blood Stem Cell Transplantation
  • [MeSH-minor] Adult. Antibodies, Monoclonal, Murine-Derived. Bone Marrow / pathology. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Disease-Free Survival. Female. Follow-Up Studies. Hematopoietic Stem Cell Mobilization. Humans. Leukapheresis. Male. Melphalan / administration & dosage. Middle Aged. Mitoxantrone / administration & dosage. Neoplasm, Residual. Polymerase Chain Reaction. Remission Induction. Retrospective Studies. Rituximab. Survival Rate. Transplantation, Autologous. Treatment Outcome

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. MELPHALAN .
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12663455.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 04079A1RDZ / Cytarabine; 4F4X42SYQ6 / Rituximab; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; Q41OR9510P / Melphalan
  •  go-up   go-down


57. Wang M, Han XH, Zhang L, Yang J, Qian JF, Shi YK, Kwak LW, Romaguera J, Yi Q: Bortezomib is synergistic with rituximab and cyclophosphamide in inducing apoptosis of mantle cell lymphoma cells in vitro and in vivo. Leukemia; 2008 Jan;22(1):179-85
Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bortezomib is synergistic with rituximab and cyclophosphamide in inducing apoptosis of mantle cell lymphoma cells in vitro and in vivo.
  • Mantle cell lymphoma (MCL) is an aggressive B-cell lymphoma with poor clinical outcome.
  • Although front therapy induces a high rate of complete remission (CR), relapse is inevitable and new regimens are much needed for relapsed MCL.
  • The proteasome inhibitor bortezomib (BTZ) induces apoptosis and sensitizes MCL cells to chemotherapy in relapsed MCL, but CR rates are low, with a short duration of response and severe toxicity.
  • Increasing doses of BTZ with a fixed dose of RTX and CTX (BRC regimen) resulted in markedly synergistic growth inhibition of MCL cells.
  • BRC significantly enhanced apoptosis in MCL cell lines and primary tumor cells compared with single-agent treatment.
  • Furthermore, western blotting analysis indicated that BRC induces apoptosis earlier via activation and cleavage of caspases-8, -9 and -3, and poly (ADP-ribose) polymerase, than single-agent treatment.
  • In vivo studies showed that BRC eradicated subcutaneous tumors in MCL-bearing SCID mice and significantly prolonged the long-term event-free survival in 70% of the mice.
  • Hence, our study demonstrates that cytoreductive chemotherapy with both BTZ and anti-CD20 antibody may offer a better therapeutic modality for relapsed MCL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Lymphoma, Mantle-Cell / pathology
  • [MeSH-minor] Animals. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Blotting, Western. Boronic Acids / administration & dosage. Bortezomib. Caspases / metabolism. Cell Proliferation. Cyclophosphamide / administration & dosage. Drug Synergism. Immunophenotyping. In Vitro Techniques. Male. Mice. Mice, SCID. Poly(ADP-ribose) Polymerases / metabolism. Pyrazines / administration & dosage. Rituximab. Survival Rate. Transplantation, Heterologous

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17898787.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Boronic Acids; 0 / Pyrazines; 4F4X42SYQ6 / Rituximab; 69G8BD63PP / Bortezomib; 8N3DW7272P / Cyclophosphamide; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspases
  •  go-up   go-down


58. Medina DJ, Sheay W, Osman M, Goodell L, Martin J, Rabson AB, Strair RK: Adenovirus infection and cytotoxicity of primary mantle cell lymphoma cells. Exp Hematol; 2005 Nov;33(11):1337-47
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adenovirus infection and cytotoxicity of primary mantle cell lymphoma cells.
  • Mantle cell lymphoma (MCL) is a distinct form of non-Hodgkin's lymphoma (NHL) derived from CD5+ B cells.
  • MCL cells overexpress cyclin D1 as a consequence of translocation of the gene into the immunoglobulin heavy-chain gene locus.
  • MCL is an aggressive form of NHL with frequent relapses after standard-dose chemotherapy.
  • In this context, a variety of novel therapies for patients with MCL have been investigated.
  • In this study, we use an expanded panel of attenuated adenoviruses to study adenovirus-mediated cytotoxicity of MCL cells.
  • 1) adenovirus infection of MCL cells despite the absence of receptor/coreceptor molecules known to be important for adenovirus infection of other cells types;.
  • 2) cytotoxicity of MCL cells after infection with specific adenovirus mutants;.
  • 3) a high degree of cytotoxicity after infection of some patient samples with viruses lacking the E1B 19k "antiapoptotic" gene; and 4) cytotoxicity after infection with viruses containing mutations in E1A pRb or p300 binding.
  • 1) the development of adenoviruses as cytotoxic agents for MCL and 2) analyses of key regulatory pathways operative in MCL cells.
  • [MeSH-major] Adenoviridae / pathogenicity. Adenoviridae Infections. Biological Therapy / methods. Lymphoma, Mantle-Cell / therapy
  • [MeSH-minor] Adenovirus E1A Proteins / genetics. Adenovirus E1B Proteins / deficiency. Adenovirus E1B Proteins / genetics. Cell Death. Humans. Mutation. Vaccines, Attenuated / pharmacology. Virulence / genetics


59. Hauck P, Chao BH, Litz J, Krystal GW: Alterations in the Noxa/Mcl-1 axis determine sensitivity of small cell lung cancer to the BH3 mimetic ABT-737. Mol Cancer Ther; 2009 Apr;8(4):883-92
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alterations in the Noxa/Mcl-1 axis determine sensitivity of small cell lung cancer to the BH3 mimetic ABT-737.
  • To understand the molecular basis for variable sensitivity to the BH3 mimetic drug ABT-737, the abundance of Bcl-2 family members was assayed in a panel of small cell lung cancer cell lines whose sensitivity varied over a 2-log range.
  • Elevated Noxa and Bcl-2 levels directly correlated with sensitivity to ABT-737, whereas Mcl-1 levels were similar in all cell lines tested regardless of sensitivity.
  • Transgenically enforced expression of Noxa but not Bcl-2 resulted in increased sensitivity to ABT-737 in multiple cell lines.
  • This increase was especially pronounced in the H209 cell line in which expression of Noxa resulted in a proportionate decline in Mcl-1 expression.
  • Although overexpression of Noxa enhanced sensitivity of the H526 and H82 cell lines to ABT-737, it did not result in altered Mcl-1 levels.
  • Similarly, small interfering RNA-mediated knockdown of Noxa expression in the H146 cell line, which increased resistance to ABT-737, did not result in altered Mcl-1 levels.
  • Therefore, three of four cell lines studied failed to show Noxa-mediated regulation of Mcl-1 expression.
  • However, despite failure to regulate Mcl-1 levels, Noxa blocked binding of Bim to Mcl-1 following its release from Bcl-2 by ABT-737.
  • Finally, we observed that a 24-hour incubation of the H526 and WBA cell lines with ABT-737 resulted in increased Noxa expression, suggesting that Noxa may play a direct role in ABT-737-mediated apoptosis.
  • These results indicate that Noxa expression is the critical determinant of ABT-737 sensitivity and loss of Noxa-mediated regulation of Mcl-1 expression may be an important feature of small cell lung cancer biology.
  • [MeSH-major] Apoptosis / drug effects. Biphenyl Compounds / pharmacology. Lung Neoplasms / drug therapy. Nitrophenols / pharmacology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Small Cell Lung Carcinoma / drug therapy. Sulfonamides / pharmacology
  • [MeSH-minor] Apoptosis Regulatory Proteins / metabolism. Blotting, Western. Cell Proliferation / drug effects. Drug Resistance, Neoplasm. Humans. Immunoprecipitation. Membrane Proteins / metabolism. Molecular Mimicry. Myeloid Cell Leukemia Sequence 1 Protein. Peptide Fragments. Piperazines / pharmacology. Proto-Oncogene Proteins / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19372561.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABT-737; 0 / Apoptosis Regulatory Proteins; 0 / Bax protein (53-86); 0 / Bcl-2-like protein 11; 0 / Biphenyl Compounds; 0 / Membrane Proteins; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Nitrophenols; 0 / PMAIP1 protein, human; 0 / Peptide Fragments; 0 / Piperazines; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Sulfonamides
  •  go-up   go-down


60. Romaguera JE, Khouri IF, Kantarjian HM, Hagemeister FB, Rodriguez MA, McLaughlin P, Sarris AH, Younes A, Rodriguez J, Cabanillas F: Untreated aggressive mantle cell lymphoma: results with intensive chemotherapy without stem cell transplant in elderly patients. Leuk Lymphoma; 2000 Sep;39(1-2):77-85
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Untreated aggressive mantle cell lymphoma: results with intensive chemotherapy without stem cell transplant in elderly patients.
  • Aggressive mantle cell lymphoma has a poor prognosis with current therapy and occurs frequently in an elderly population which cannot receive stem cell transplantation.
  • Newer aggressive therapies are needed.
  • In this study, 25 consecutive previously untreated patients 65 years or older with MCL were enrolled in two sequential phase II trials.
  • With a median follow-up of 17 months, the median FFS for the entire group is 15 months.
  • Treatment-related death occurred in 2 patients.
  • In conclusion, GI involvement by MCL is common in this age group.
  • Hyper-CVAD alternating with M-A with adjustment of the cytarabine is an active regimen in this elderly group of patients with untreated MCL and the toxicity is manageable.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Mantle-Cell / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Cyclophosphamide / administration & dosage. Cyclophosphamide / toxicity. Dexamethasone / administration & dosage. Dexamethasone / toxicity. Disease-Free Survival. Doxorubicin / administration & dosage. Doxorubicin / toxicity. Female. Gastrointestinal Neoplasms / complications. Gastrointestinal Neoplasms / drug therapy. Hematopoietic Stem Cell Transplantation. Humans. Infection / chemically induced. Male. Neutropenia / chemically induced. Remission Induction. Survival Rate. Thrombocytopenia / chemically induced. Treatment Outcome. Vincristine / administration & dosage. Vincristine / toxicity

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10975386.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] SWITZERLAND
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; CVAD protocol
  •  go-up   go-down


61. Haritunians T, Mori A, O'Kelly J, Luong QT, Giles FJ, Koeffler HP: Antiproliferative activity of RAD001 (everolimus) as a single agent and combined with other agents in mantle cell lymphoma. Leukemia; 2007 Feb;21(2):333-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiproliferative activity of RAD001 (everolimus) as a single agent and combined with other agents in mantle cell lymphoma.
  • Mantle cell lymphoma (MCL) is an aggressive form of B-cell non-Hodgkin's lymphoma, with a mean survival of only 3-5 years and suboptimal therapeutic options.
  • MCL is characterized by a balanced translocation t(11;14)(q13;q32), resulting in overexpression of cyclin D1, a G(1) cyclin regulated by the PI3K/Akt/mammalian target of rapamycin (mTOR) signaling pathway.
  • As improved therapy for MCL is required and the mTOR pathway may be involved in its pathophysiology, the antiproliferative effects of RAD001 (everolimus), an mTOR inhibitor, against three MCL cell lines were investigated.
  • As a single agent, RAD001 inhibited proliferation in MCL cell lines (Jeko1, SP49 and NCEB1) approximately 40-65% compared to diluent control cells.
  • This was associated with G(1) cell-cycle arrest and reduced phosphorylation of the mTOR downstream target, 4E-BP1.
  • Furthermore, combination drug studies revealed predominantly synergistic cytotoxicity with RAD001 and several secondary agents, including doxorubicin, vincristine or rituximab (components of the standard MCL regimen), as well as paclitaxel, vorinostat and bortezomib.
  • These data indicate that single agent RAD001 is effective in inhibiting growth of MCL cells in vitro and combination studies with secondary agents further demonstrate synergistic cytotoxicity.
  • Thus, these findings support future clinical studies of RAD001 in the treatment of MCL.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Lymphoma, Mantle-Cell / pathology. Sirolimus / analogs & derivatives
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Cell Division / drug effects. Cell Line, Tumor. Dimethyl Sulfoxide / pharmacology. Everolimus. Humans


62. Corradini P, Ladetto M, Zallio F, Astolfi M, Rizzo E, Sametti S, Cuttica A, Rosato R, Farina L, Boccadoro M, Benedetti F, Pileri A, Tarella C: Long-term follow-up of indolent lymphoma patients treated with high-dose sequential chemotherapy and autografting: evidence that durable molecular and clinical remission frequently can be attained only in follicular subtypes. J Clin Oncol; 2004 Apr 15;22(8):1460-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term follow-up of indolent lymphoma patients treated with high-dose sequential chemotherapy and autografting: evidence that durable molecular and clinical remission frequently can be attained only in follicular subtypes.
  • PURPOSE: To evaluate the prognostic relevance of molecular monitoring of minimal residual disease in indolent lymphomas receiving high-dose sequential chemotherapy and autografting.
  • PATIENTS, MATERIALS, AND METHODS: A polymerase chain reaction- (PCR-)based strategy was used to evaluate the presence of residual tumor cells in a panel of 70 indolent lymphoma patients: 40 with follicular (FCL), 14 with small lymphocytic (SLL), and 16 with mantle-cell (MCL) lymphomas.
  • They were treated either with first-line (n = 61) or second-line (n = 9) therapy with an intensified high-dose chemotherapy program followed by peripheral-blood progenitor cells autografting.
  • The Bcl-1, Bcl-2, and immunoglobulin gene rearrangements were used as lymphoma-specific markers.
  • Overall, a molecular marker was obtained from the diagnostic tissue in 60 of 70 patients (86%).
  • Results The collection of PCR-negative cells and the achievement of posttransplantation molecular remission (MR) were common in patients with FCL subtype (54% and 70%, respectively), whereas they were not frequent among SLL and MCL (25% and 12.5%, respectively) patients.
  • With a median molecular follow-up of 75 months, an 88% incidence of relapse was observed among patients never attaining MR.
  • CONCLUSION: Our results indicate that among indolent lymphomas, FCL and non-FCL subtypes show a significantly different behavior in terms of MR achievement, and MR after intensive chemotherapy and autografting is predictive for a prolonged disease-free survival, whereas persistent PCR positivity is associated with a high risk of relapse.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Lymphoma, Non-Hodgkin / therapy
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Lymphoma, Follicular / therapy. Lymphoma, Mantle-Cell / therapy. Male. Middle Aged. Molecular Diagnostic Techniques. Neoplasm, Residual / therapy. Polymerase Chain Reaction. Transplantation, Autologous

  • Genetic Alliance. consumer health - Follicular Lymphoma.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15084619.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


63. Mollinedo F, de la Iglesia-Vicente J, Gajate C, Estella-Hermoso de Mendoza A, Villa-Pulgarin JA, de Frias M, Roué G, Gil J, Colomer D, Campanero MA, Blanco-Prieto MJ: In vitro and In vivo selective antitumor activity of Edelfosine against mantle cell lymphoma and chronic lymphocytic leukemia involving lipid rafts. Clin Cancer Res; 2010 Apr 1;16(7):2046-54
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro and In vivo selective antitumor activity of Edelfosine against mantle cell lymphoma and chronic lymphocytic leukemia involving lipid rafts.
  • PURPOSE: Mantle cell lymphoma (MCL) and chronic lymphocytic leukemia (CLL) remain B-cell malignancies with limited therapeutic options.
  • The present study investigates the in vitro and in vivo effect of the phospholipid ether edelfosine (1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine) in MCL and CLL.
  • EXPERIMENTAL DESIGN: Several cell lines, patient-derived tumor cells, and xenografts in severe combined immunodeficient mice were used to examine the anti-MCL and anti-CLL activity of edelfosine.
  • Furthermore, we analyzed the mechanism of action and drug biodistribution of edelfosine in MCL and CLL tumor-bearing severe combined immunodeficient mice.
  • RESULTS: Here, we have found that the phospholipid ether edelfosine was the most potent alkyl-lysophospholipid analogue in killing MCL and CLL cells, including patient-derived primary cells, while sparing normal resting lymphocytes.
  • Alkyl-lysophospholipid analogues ranked edelfosine > perifosine >> erucylphosphocholine > or = miltefosine in their capacity to elicit apoptosis in MCL and CLL cells.
  • Edelfosine induced coclustering of Fas/CD95 death receptor and rafts in MCL and CLL cells.
  • Edelfosine was taken up by malignant cells, whereas normal resting lymphocytes hardly incorporated the drug.
  • Raft disruption by cholesterol depletion inhibited drug uptake, Fas/CD95 clustering, and edelfosine-induced apoptosis.
  • Edelfosine oral administration showed a potent in vivo anticancer activity in MCL and CLL xenograft mouse models, and the drug accumulated dramatically and preferentially in the tumor.
  • CONCLUSIONS: Our data indicate that edelfosine accumulates and kills MCL and CLL cells in a rather selective way, and set coclustering of Fas/CD95 and lipid rafts as a new framework in MCL and CLL therapy.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Mantle-Cell / drug therapy. Membrane Microdomains / drug effects. Phospholipid Ethers / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Humans. Mice. Mice, Inbred C57BL. Mice, SCID. Substrate Specificity / drug effects. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 AACR.
  • (PMID = 20233887.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Phospholipid Ethers; 1Y6SNA8L5S / edelfosine
  •  go-up   go-down


64. Brugger W, Hirsch J, Grünebach F, Repp R, Brossart P, Vogel W, Kopp HG, Manz MG, Bitzer M, Schlimok G, Kaufmann M, Ganser A, Fehnle K, Gramatzki M, Kanz L: Rituximab consolidation after high-dose chemotherapy and autologous blood stem cell transplantation in follicular and mantle cell lymphoma: a prospective, multicenter phase II study. Ann Oncol; 2004 Nov;15(11):1691-8
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rituximab consolidation after high-dose chemotherapy and autologous blood stem cell transplantation in follicular and mantle cell lymphoma: a prospective, multicenter phase II study.
  • BACKGROUND: Patients with follicular (FL) or mantle cell lymphoma (MCL) are incurable with conventional therapy.
  • We investigated the safety and efficacy of rituximab consolidation after autologous stem cell transplantation (ASCT) in order to prevent relapse by clearance of minimal residual disease (MRD).
  • METHODS: Rituximab was given approximately 8 weeks after CD34+ cell enriched ASCT at 375 mg/m2, weekly for 4 weeks.
  • Thirty patients (20 FL, 10 MCL) were evaluable after rituximab consolidation, and 27 of these were assessable for MRD detection.
  • Four patients (two FL, two MCL) relapsed, and one additional MCL patient died unexpectedly in complete remission.
  • CONCLUSIONS: One single course of rituximab consolidation given after ASCT is safe, may help to eliminate MRD and may translate into improved EFS in both FL and MCL patients.

  • Genetic Alliance. consumer health - Follicular Lymphoma.
  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15520073.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  •  go-up   go-down


65. Castillo R, Mascarenhas J, Telford W, Chadburn A, Friedman SM, Schattner EJ: Proliferative response of mantle cell lymphoma cells stimulated by CD40 ligation and IL-4. Leukemia; 2000 Feb;14(2):292-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proliferative response of mantle cell lymphoma cells stimulated by CD40 ligation and IL-4.
  • Mantle cell lymphoma (MCL) is a tumor of intermediate-size, IgM+, IgD+ B cells derived from the mantle zone of the germinal center.
  • Little is known about its specific immunologic features or responsiveness to T cell-derived signals.
  • In this work, we evaluated the proliferation and cell cycle properties of freshly isolated MCL cells after CD40 ligation, in the absence and presence of interleukin 4 (IL-4).
  • In each MCL case examined, there was a marked growth-enhancing effect of these two stimuli characterized by improved viability, augmented expression of Ki-67, and induction of the proliferating cell nuclear antigen (PCNA).
  • Cyclin D1 was expressed throughout the cell cycle in MCL cells induced to enter S phase.
  • From these investigations, we conclude that the biology of MCL B lymphocytes is affected by CD154 (CD40 ligand) and IL-4, two signals usually provided by CD4+ T cells.
  • The capacity to manipulate the activation and cell cycle state of MCL cells by these specific immunological stimuli may be exploited to confer susceptibility to chemotherapy agents and develop novel therapies in this disease.
  • [MeSH-major] Antigens, CD40 / metabolism. B-Lymphocytes / metabolism. Interleukin-4 / metabolism. Lymphoma, Mantle-Cell / metabolism
  • [MeSH-minor] Cell Division. Cyclin D1 / metabolism. Flow Cytometry. Gene Expression Regulation, Neoplastic. Humans. Immunophenotyping. Ki-67 Antigen / metabolism. Proliferating Cell Nuclear Antigen / metabolism. Protein Binding. S Phase. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10673747.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA71589
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Ki-67 Antigen; 0 / Proliferating Cell Nuclear Antigen; 136601-57-5 / Cyclin D1; 207137-56-2 / Interleukin-4
  •  go-up   go-down


66. Roué G, López-Guerra M, Milpied P, Pérez-Galán P, Villamor N, Montserrat E, Campo E, Colomer D: Bendamustine is effective in p53-deficient B-cell neoplasms and requires oxidative stress and caspase-independent signaling. Clin Cancer Res; 2008 Nov 1;14(21):6907-15
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bendamustine is effective in p53-deficient B-cell neoplasms and requires oxidative stress and caspase-independent signaling.
  • PURPOSE: Chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL) are two incurable B-cell lymphoid neoplasms characterized by distinct clinical presentation and evolution.
  • Bendamustine hydrochloride is a multifunctional, alkylating agent with a purine-like ring system that exhibits activity in multiple cancer models, including CLL and MCL, but whose mechanism is only partially described.
  • Our aim was to analyze the apoptotic pathways activated by bendamustine in CLL and MCL together with the relevance of p53 mutation in determining the response to this drug.
  • EXPERIMENTAL DESIGN: Thirteen CLL/MCL cell lines and primary tumor cells from 8 MCL and 25 CLL patients were cultured for up to 24 h with bendamustine followed by cytotoxic assays, flow cytometry, immunofluorescence, and Western blot analysis of p53 response pathway and apoptosis-related factors.
  • RESULTS: Bendamustine displayed cytotoxic activity on most CLL and MCL primary cells and cell lines irrespective of ZAP-70 expression and p53 status.
  • Bendamustine was found to act synergistically with nucleoside analogues in both CLL and MCL, this combination being effective in p53 mutated cases resistant to standard chemotherapy.
  • CONCLUSIONS: Our findings support the use of bendamustine as a therapeutic agent, alone or in combination, for CLL and MCL with p53 alterations and describe the molecular basis of its activity in these entities.
  • [MeSH-major] Antineoplastic Agents, Alkylating / therapeutic use. Genes, p53. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Mantle-Cell / drug therapy. Mutation. Nitrogen Mustard Compounds / therapeutic use. Oxidative Stress
  • [MeSH-minor] Aged. Aged, 80 and over. Apoptosis / drug effects. Bendamustine Hydrochloride. Caspases / metabolism. Female. Humans. Male. Middle Aged. Signal Transduction. Tumor Cells, Cultured

  • Hazardous Substances Data Bank. Bendamustine .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18980985.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Nitrogen Mustard Compounds; 981Y8SX18M / Bendamustine Hydrochloride; EC 3.4.22.- / Caspases
  •  go-up   go-down


67. Boullanger N, Renou P, Dugay J, Boyer J, de Yberlucea LR, Combe M, Coulon MA: [Palpable mantel cell lymphoma in the breast]. Presse Med; 2001 Feb 03;30(4):163-5
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Palpable mantel cell lymphoma in the breast].
  • BACKGROUND: Extranodal involvement is not unusual in mantle cell lymphoma (MCL) which accounts for 6% of non-Hodgkin's lymphomas.
  • Blood immunoflow cytometry analysis, occurrence of rapidly growing tumors involving the two breasts and eyelids and cytogenetic and molecular features led to the diagnosis of MCL.
  • Such localizations are exceptional in MCL and are signs of aggressive disease.
  • Before extra-nodal involvement, MCL may simulate banal CLL.
  • Therefore, systematic immunohistochemistry and if necessary molecular analysis are useful for early diagnosis of MCL.
  • Conventional chemotherapy cannot provide cure of MCL and median survival is 48 months.
  • For this reason, high-dose chemotherapy with stem cell graft has to be discussed in young patients.
  • MCL is currently characterized by Bcl1 rearrangement, t(11-14) translocation and cyclin D1 overexpression among small B-cell lymphomas in recent REAL- and WHO-classifications.
  • [MeSH-major] Breast Neoplasms / pathology. Eyelid Neoplasms / pathology. Lymphoma, Mantle-Cell / pathology
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Female. Hematopoietic Stem Cell Transplantation. Humans. Immunohistochemistry. Prognosis

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11229304.001).
  • [ISSN] 0755-4982
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


68. Le Gouill S: [Mantle cell lymphoma: an overview from diagnosis to future therapies]. Rev Med Interne; 2010 Sep;31(9):615-20
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Mantle cell lymphoma: an overview from diagnosis to future therapies].
  • [Transliterated title] Le lymphome à cellules du manteau : du diagnostic aux perspectives thérapeutiques.
  • Mantle cell lymphoma (MCL) is a rare non-Hodgkin lymphoma (NHL) entity.
  • The translocation between chromosomes 11 and 14 is the cytogenetics hallmark of MCL.
  • This translocation leads to the dysregulation of the CCDN1 gene, and overexpression of cyclin D1 which promotes cell cycling.
  • Despite a classical phenotype (CD19+, CD20+, CD5+, CCND1+, CD10-, CD23-, Bcl-2+, Ig at the membrane, mainly IgM), MCL is not a homogeneous disease and several cytological, phenotypic, cytogenetic and clinical variants have been described.
  • MCL represents 5 % of NHLs with its incidence constantly increasing over the last years.
  • Intensive strategies including high-dose chemotherapy, followed by autologous stem cell transplantation have significantly improved the outcome of MCL patients.
  • At present, induction chemotherapy followed by high-dose chemotherapy and autologous stem cell transplantation is the standard regimen in younger patients.
  • However, most of MCL patients will experience relapse.
  • Future innovative therapies that are being presently investigated in prospective trials include transduction pathways inhibitors, proteasome inhibitors, pro-apoptotic molecules, immunotherapy and/or radiolabeled immunotherapy, and will likely open a new era for targeted therapies in MCL.

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010. Published by Elsevier SAS.
  • (PMID = 20488592.001).
  • [ISSN] 1768-3122
  • [Journal-full-title] La Revue de medecine interne
  • [ISO-abbreviation] Rev Med Interne
  • [Language] FRE
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  •  go-up   go-down


69. Leshchenko VV, Kuo PY, Shaknovich R, Yang DT, Gellen T, Petrich A, Yu Y, Remache Y, Weniger MA, Rafiq S, Suh KS, Goy A, Wilson W, Verma A, Braunschweig I, Muthusamy N, Kahl BS, Byrd JC, Wiestner A, Melnick A, Parekh S: Genomewide DNA methylation analysis reveals novel targets for drug development in mantle cell lymphoma. Blood; 2010 Aug 19;116(7):1025-34
SciCrunch. ArrayExpress: Data: Microarray .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genomewide DNA methylation analysis reveals novel targets for drug development in mantle cell lymphoma.
  • Mantle cell lymphoma (MCL) is a mostly incurable malignancy arising from naive B cells (NBCs) in the mantle zone of lymph nodes.
  • We analyzed genomewide methylation in MCL patients with the HELP (HpaII tiny fragment Enrichment by Ligation-mediated PCR) assay and found significant aberrancy in promoter methylation patterns compared with normal NBCs.
  • Using biologic and statistical criteria, we further identified 4 hypermethylated genes CDKN2B, MLF-1, PCDH8, and HOXD8 and 4 hypomethylated genes CD37, HDAC1, NOTCH1, and CDK5 when aberrant methylation was associated with inverse changes in mRNA levels.
  • Immunohistochemical analysis of an independent cohort of MCL patient samples confirmed CD37 surface expression in 93% of patients, validating its selection as a target for MCL therapy.
  • Treatment of MCL cell lines with a small modular immunopharmaceutical (CD37-SMIP) resulted in significant loss of viability in cell lines with intense surface CD37 expression.
  • Treatment of MCL cell lines with the DNA methyltransferase inhibitor decitabine resulted in reversal of aberrant hypermethylation and synergized with the histone deacetylase inhibitor suberoylanilide hydroxamic acid in induction of the hypermethylated genes and anti-MCL cytotoxicity.
  • Our data show prominent and aberrant promoter methylation in MCL and suggest that differentially methylated genes can be targeted for therapeutic benefit in MCL.

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2001 Feb 15;61(4):1629-36 [11245476.001]
  • [Cites] Mol Cell Biol. 2000 Aug;20(15):5363-9 [10891477.001]
  • [Cites] Adv Enzyme Regul. 1984;22:27-55 [6382953.001]
  • [Cites] J Immunol. 1986 Nov 1;137(9):3013-8 [3489782.001]
  • [Cites] J Immunol. 1988 Feb 1;140(3):905-14 [3257508.001]
  • [Cites] J Clin Oncol. 1989 Aug;7(8):1027-38 [2666588.001]
  • [Cites] J Clin Oncol. 1992 Nov;10(11):1696-711 [1403053.001]
  • [Cites] EMBO J. 1994 May 1;13(9):2124-30 [8187765.001]
  • [Cites] Genes Dev. 1997 Apr 1;11(7):847-62 [9106657.001]
  • [Cites] Nat Genet. 1999 Jan;21(1):103-7 [9916800.001]
  • [Cites] Oncogene. 2005 Apr 28;24(19):3091-9 [15735669.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1376-83 [15931266.001]
  • [Cites] Br J Haematol. 2005 Aug;130(4):516-26 [16098065.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6364-9 [16155021.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):15785-90 [16243968.001]
  • [Cites] Genes Chromosomes Cancer. 2006 Feb;45(2):203-10 [16258956.001]
  • [Cites] Genome Res. 2006 Aug;16(8):1046-55 [16809668.001]
  • [Cites] Biochim Biophys Acta. 2007 Jan;1775(1):138-62 [17045745.001]
  • [Cites] Cell. 2007 Feb 23;128(4):683-92 [17320506.001]
  • [Cites] Haematologica. 2007 Apr;92(4):460-8 [17488656.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2569-77 [17440052.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2667-73 [17606765.001]
  • [Cites] Nucleic Acids Res. 2007;35(18):e119 [17855397.001]
  • [Cites] Hum Pathol. 2007 Dec;38(12):1849-57 [17900658.001]
  • [Cites] Bioinformatics. 2008 May 1;24(9):1161-7 [18353789.001]
  • [Cites] EMBO J. 2008 May 7;27(9):1368-77 [18388863.001]
  • [Cites] Oncogene. 2008 Aug 7;27(34):4657-65 [18408767.001]
  • [Cites] Clin Cancer Res. 2008 Sep 1;14(17):5314-7 [18765521.001]
  • [Cites] Leuk Res. 2009 Mar;33(3):434-42 [18829110.001]
  • [Cites] Breast Cancer Res. 2009;11(1):R14 [19250546.001]
  • [Cites] Gastroenterology. 2009 Jun;136(7):2149-58 [19375421.001]
  • [Cites] J Cell Biochem. 2009 Jul 1;107(4):600-8 [19459166.001]
  • [Cites] Biochim Biophys Acta. 2009 Sep;1790(9):847-62 [19364478.001]
  • [Cites] Br J Haematol. 2008 Jun;142(2):149-65 [18410453.001]
  • [Cites] Cancer Cell. 2010 Jan 19;17(1):13-27 [20060365.001]
  • [Cites] Methods Mol Biol. 2010;632:191-201 [20217579.001]
  • [Cites] Blood. 2001 Mar 1;97(5):1172-9 [11222358.001]
  • [Cites] Cancer Res. 2002 Aug 1;62(15):4398-405 [12154046.001]
  • [Cites] Oncogene. 2002 Aug 12;21(35):5400-13 [12154403.001]
  • [Cites] Nat Med. 2002 Nov;8(11):1323-7 [12389040.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):185-97 [12620412.001]
  • [Cites] Science. 2003 Apr 18;300(5618):455 [12702868.001]
  • [Cites] Science. 2003 Apr 18;300(5618):489-92 [12702876.001]
  • [Cites] Leukemia. 2004 Feb;18(2):356-8 [14614518.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2505-13 [15226187.001]
  • [Cites] N Engl J Med. 1999 Nov 11;341(20):1520-9 [10559454.001]
  • (PMID = 20427703.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA95426; United States / NCI NIH HHS / CA / P01 CA813534; United States / NCI NIH HHS / CA / P01 CA095426; United States / NCI NIH HHS / CA / K12 CA132783; United States / NHLBI NIH HHS / HL / R01 HL082946; United States / NCI NIH HHS / CA / K12 CA132783-01; United States / NCI NIH HHS / CA / R01 CA104348
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / CD37 protein, human; 0 / Tetraspanins
  • [Other-IDs] NLM/ PMC2938124
  •  go-up   go-down


70. Rasmussen P, Sjö LD, Prause JU, Ralfkiaer E, Heegaard S: Mantle cell lymphoma in the orbital and adnexal region. Br J Ophthalmol; 2009 Aug;93(8):1047-51
MedlinePlus Health Information. consumer health - Eye Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mantle cell lymphoma in the orbital and adnexal region.
  • AIMS: To characterise clinicopathological features of mantle cell lymphoma (MCL) in the orbital and adnexal region.
  • METHODS: Data on lymphoid lesions were retrieved searching the Danish Ocular Lymphoma Database 1980-2005.
  • Specimens were collected from Danish pathological departments and re-evaluated with a panel of monoclonal antibodies.
  • For all patients with confirmed MCL the complete clinical files were collected and reviewed.
  • RESULTS: Twenty-one patients with MCL in the orbital and adnexal region were identified comprising 9% (21/230) of all lymphoma in the ocular region.
  • Orbital and adnexal region MCL as first presenting symptom comprised 67% of the patients.
  • Secondary MCL comprised 33% of the patients.
  • Patients receiving anti-CD20 (rituximab)-containing chemotherapy had a significantly better 5-year overall survival (OS) rate (83%) than patients in treatment regimes without rituximab (5-year OS rate, 8%).
  • CONCLUSIONS: Orbital and adnexal region MCL presents in elderly males.
  • There is a very high proportion of systemic involvement in general with MCL of the orbital and adnexal region.
  • Most patients presented with stage IV disease and had multiple relapses and short survival time.
  • Treatment with rituximab-containing chemotherapy improved survival significantly compared with combination chemotherapy without rituximab.
  • [MeSH-major] Eye Neoplasms / pathology. Lymphoma, Mantle-Cell / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Neoplasm Staging. Orbital Neoplasms / pathology. Orbital Neoplasms / therapy. Prognosis. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Genetic Alliance. consumer health - Orbital lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19429588.001).
  • [ISSN] 1468-2079
  • [Journal-full-title] The British journal of ophthalmology
  • [ISO-abbreviation] Br J Ophthalmol
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


71. Hipp S, Ringshausen I, Oelsner M, Bogner C, Peschel C, Decker T: Inhibition of the mammalian target of rapamycin and the induction of cell cycle arrest in mantle cell lymphoma cells. Haematologica; 2005 Oct;90(10):1433-4
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of the mammalian target of rapamycin and the induction of cell cycle arrest in mantle cell lymphoma cells.
  • The mTOR inhibitor, rapamycin, inhibited proliferation in three mantle cell lymphoma (MCL) cell lines and reduced cyclin D3 expression while cyclin D1 levels remained unchanged.
  • This finding was confirmed in cells from a MCL patient.
  • [MeSH-major] Cell Cycle / drug effects. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / pathology. Protein Kinases. Sirolimus / administration & dosage
  • [MeSH-minor] Cell Line, Tumor. Drug Delivery Systems / methods. Humans. TOR Serine-Threonine Kinases

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16219581.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comparative Study; Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
  •  go-up   go-down


72. Shieh JJ, Liu KT, Huang SW, Chen YJ, Hsieh TY: Modification of alternative splicing of Mcl-1 pre-mRNA using antisense morpholino oligonucleotides induces apoptosis in basal cell carcinoma cells. J Invest Dermatol; 2009 Oct;129(10):2497-506
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modification of alternative splicing of Mcl-1 pre-mRNA using antisense morpholino oligonucleotides induces apoptosis in basal cell carcinoma cells.
  • Myeloid cell leukemia-1 (Mcl-1, Mcl-1L) is an anti-apoptotic protein of the Bcl-2 family that acts as a critical molecule in apoptosis control.
  • Mcl-1 pre-mRNA can undergo alternative splicing to yield the short isoform, Mcl-1S, which resembles BH3-only pro-apoptotic proteins and induces apoptosis.
  • Overexpression of Mcl-1 may play a role in various human tumors, and Mcl-1 may serve as a target in cancer therapy.
  • In this study, we found an imbalance between the expression levels of Mcl-1L and Mcl-1S in the skin basal cell carcinoma (BCC) cell line when compared with primary keratinocytes.
  • We showed that overexpression of Mcl-1S induces apoptosis in BCC cells.
  • Finally, we showed that Mcl-1 antisense morpholino oligonucleotides (AMOs) can specifically target Mcl-1 pre-mRNA and shift the splicing pattern from Mcl-1L to Mcl-1S mRNA and protein.
  • This shift increases the level of pro-apoptotic Mcl-1S and reduces the level of anti-apoptotic Mcl-1L, which induces apoptosis in BCC cells and AGS cells, a human gastric adenocarcinoma epithelial cell line.
  • Thus, this report provides a strategy for cancer therapy in which AMOs change the alternative splicing pattern of Mcl-1 pre-mRNA and thereby induce apoptosis.
  • [MeSH-major] Alternative Splicing / drug effects. Apoptosis / drug effects. Carcinoma, Basal Cell / pathology. Oligonucleotides, Antisense / pharmacology. Proto-Oncogene Proteins c-bcl-2 / genetics. RNA, Messenger / genetics. Skin Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Cell Line, Tumor. Humans. Keratinocytes / metabolism. Keratinocytes / pathology. Myeloid Cell Leukemia Sequence 1 Protein. Stomach Neoplasms / metabolism. Stomach Neoplasms / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19369967.001).
  • [ISSN] 1523-1747
  • [Journal-full-title] The Journal of investigative dermatology
  • [ISO-abbreviation] J. Invest. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger
  •  go-up   go-down


73. Rao R, Nalluri S, Fiskus W, Savoie A, Buckley KM, Ha K, Balusu R, Joshi A, Coothankandaswamy V, Tao J, Sotomayor E, Atadja P, Bhalla KN: Role of CAAT/enhancer binding protein homologous protein in panobinostat-mediated potentiation of bortezomib-induced lethal endoplasmic reticulum stress in mantle cell lymphoma cells. Clin Cancer Res; 2010 Oct 1;16(19):4742-54
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of CAAT/enhancer binding protein homologous protein in panobinostat-mediated potentiation of bortezomib-induced lethal endoplasmic reticulum stress in mantle cell lymphoma cells.
  • PURPOSE: Bortezomib induces unfolded protein response (UPR) and endoplasmic reticulum stress, as well as exhibits clinical activity in patients with relapsed and refractory mantle cell lymphoma (MCL).
  • Here, we determined the molecular basis of the improved in vitro and in vivo activity of the combination of the pan-histone deacetylase inhibitor panobinostat and bortezomib against human, cultured, and primary MCL cells.
  • EXPERIMENTAL DESIGN: Immunoblot analyses, reverse transcription-PCR, and immunofluorescent and electron microscopy were used to determine the effects of panobinostat on bortezomib-induced aggresome formation and endoplasmic reticulum stress in MCL cells.
  • RESULTS: Treatment with panobinostat induced heat shock protein 90 acetylation; depleted the levels of heat shock protein 90 client proteins, cyclin-dependent kinase 4, c-RAF, and AKT; and abrogated bortezomib-induced aggresome formation in MCL cells.
  • Conversely, knockdown of CHOP attenuated panobinostat-induced cell death of MCL cells.
  • Compared with each agent alone, cotreatment with panobinostat increased bortezomib-induced expression of CHOP and NOXA, as well as increased bortezomib-induced UPR and apoptosis of cultured and primary MCL cells.
  • Cotreatment with panobinostat also increased bortezomib-mediated in vivo tumor growth inhibition and improved survival of mice bearing human Z138C MCL cell xenograft.
  • CONCLUSION: These findings suggest that increased UPR and induction of CHOP are involved in enhanced anti-MCL activity of the combination of panobinostat and bortezomib.
  • [MeSH-major] Boronic Acids / pharmacology. Endoplasmic Reticulum / drug effects. Hydroxamic Acids / pharmacology. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / pathology. Pyrazines / pharmacology. Stress, Physiological / drug effects. Transcription Factor CHOP / metabolism
  • [MeSH-minor] Acetylation / drug effects. Animals. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Blotting, Western. Bortezomib. Cell Line, Tumor. Cell Proliferation / drug effects. Fluorescent Antibody Technique. HSP90 Heat-Shock Proteins / antagonists & inhibitors. HSP90 Heat-Shock Proteins / metabolism. Humans. Indoles. Mice. Microscopy, Confocal. Protein Folding / drug effects. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Xenograft Model Antitumor Assays

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] ©2010 AACR.
  • [Cites] N Engl J Med. 2009 Oct 15;361(16):1570-83 [19828534.001]
  • [Cites] Cancer Biol Ther. 2009 Jul;8(13):1273-80 [19440035.001]
  • [Cites] Cancer Sci. 2010 Jan;101(1):196-200 [19817748.001]
  • [Cites] J Cell Biol. 2001 May 28;153(5):1011-22 [11381086.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):300-7 [11460154.001]
  • [Cites] Eur J Cancer. 2002 Feb;38(3):401-8 [11818206.001]
  • [Cites] EMBO J. 2003 Mar 3;22(5):1180-7 [12606582.001]
  • [Cites] Cell. 2003 Dec 12;115(6):727-38 [14675537.001]
  • [Cites] J Cell Biol. 1998 Dec 28;143(7):1883-98 [9864362.001]
  • [Cites] Genes Dev. 2004 Dec 15;18(24):3066-77 [15601821.001]
  • [Cites] J Clin Invest. 2005 Feb;115(2):268-81 [15690081.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8567-72 [15937109.001]
  • [Cites] J Biol Chem. 2005 Jul 22;280(29):26729-34 [15937340.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11510-9 [16357160.001]
  • [Cites] Blood. 2006 Jan 1;107(1):257-64 [16166592.001]
  • [Cites] Nat Rev Cancer. 2006 Jan;6(1):38-51 [16397526.001]
  • [Cites] EMBO Rep. 2006 Sep;7(9):880-5 [16953201.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3441-9 [16728695.001]
  • [Cites] Blood. 2007 Jan 1;109(1):31-9 [16960145.001]
  • [Cites] Cancer Cell. 2007 Apr;11(4):349-60 [17418411.001]
  • [Cites] Nat Rev Cancer. 2007 Oct;7(10):750-62 [17891190.001]
  • [Cites] Science. 2007 Nov 9;318(5852):944-9 [17991856.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2007;:270-6 [18024640.001]
  • [Cites] Cell Cycle. 2008 Jan 1;7(1):7-10 [18196966.001]
  • [Cites] Clin Cancer Res. 2008 Jan 15;14(2):549-58 [18223231.001]
  • [Cites] Biochem J. 2008 Mar 15;410(3):439-53 [18290764.001]
  • [Cites] Curr Opin Hematol. 2008 Jul;15(4):415-21 [18536582.001]
  • [Cites] Cancer Res. 2008 Jun 15;68(12):4833-42 [18559531.001]
  • [Cites] Blood. 2008 Oct 1;112(7):2917-26 [18641367.001]
  • [Cites] Blood. 2008 Oct 1;112(7):2896-905 [18660379.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Jul;8(7):519-29 [17565364.001]
  • [Cites] Cell. 2007 Jun 29;129(7):1337-49 [17604722.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1631-8 [17502456.001]
  • [Cites] Genes Dev. 2007 Sep 1;21(17):2172-81 [17785525.001]
  • [Cites] Blood. 2007 Oct 1;110(7):2641-9 [17525289.001]
  • [Cites] Hematol Oncol Clin North Am. 2008 Oct;22(5):953-63, ix [18954745.001]
  • [Cites] Drug Resist Updat. 2008 Aug-Oct;11(4-5):164-79 [18818117.001]
  • [Cites] Mol Cell Biol. 2008 Dec;28(23):6989-7000 [18794359.001]
  • [Cites] Cancer Biol Ther. 2008 Oct;7(10):1648-62 [18787411.001]
  • [Cites] PLoS One. 2009;4(1):e4170 [19137072.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Feb 17;106(7):2200-5 [19164757.001]
  • [Cites] Br J Haematol. 2009 Apr;145(1):34-9 [19220284.001]
  • [Cites] Semin Hematol. 2009 Apr;46(2):166-75 [19389500.001]
  • [Cites] Clin Cancer Res. 2009 Aug 15;15(16):5250-7 [19671864.001]
  • [Cites] Leukemia. 2009 Dec;23(12):2222-32 [19741729.001]
  • (PMID = 20647473.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA129962
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / HSP90 Heat-Shock Proteins; 0 / Hydroxamic Acids; 0 / Indoles; 0 / PMAIP1 protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 147336-12-7 / Transcription Factor CHOP; 69G8BD63PP / Bortezomib; 9647FM7Y3Z / panobinostat
  • [Other-IDs] NLM/ NIHMS222886; NLM/ PMC2948590
  •  go-up   go-down


74. Doschak MR, LaMothe JM, Cooper DM, Hallgrimsson B, Hanley DA, Bray RC, Zernicke RF: Bisphosphonates reduce bone mineral loss at ligament entheses after joint injury. Osteoarthritis Cartilage; 2005 Sep;13(9):790-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bisphosphonates reduce bone mineral loss at ligament entheses after joint injury.
  • OBJECTIVE: To examine the effects of anterior cruciate ligament (ACL) insufficiency, and subsequent bisphosphonate (BP) antiresorptive therapy, on the bone mineral interface at the enthesis of remaining ligamentous restraints.
  • METHODS: We measured bone mineral geometry (and subsequent adaptation) at the medial collateral ligament (MCL) origin, using micro-computed tomography (muCT).
  • Groups of normal control, 6 and 14 wk anterior cruciate ligament transected (ACLX), and 6 wk ACLX-BP (risedronate) dosed rabbits were evaluated.
  • Samples were then processed histologically, and the results of mineral adaptation and progression of osteoarthritis (OA) compared to joint laxity values obtained from previous biomechanical testing of the MCL-complex.
  • RESULTS: muCT defined the MCL origin as a symmetrical, metaphyseal depression that contained soft-tissue elements, including fibrocartilage and ligament--as seen in subsequent histological sections.
  • In contrast, the insertions from ACLX animals lost significant bone mineral, with an MCL-insertion volume 1.2 times that of normal controls at 6 wk ACLX, which further increased to 2.3 times that of normal controls at 14 wk ACLX.
  • Significant differences were also measured between 6 and 14 wk ACLX and age-matched normal controls in volume of cortical bone containing the MCL insertion.
  • However, there were no significant differences in the percentage of cortical bone to underlying trabecular bone at the MCL insertion.
  • When comparing muCT mineral adaptation at the MCL-enthesis with historical MCL-complex laxity data, the values for laxity after ACLX increased proportionately as bone mineral at the insertion was lost, and subsequent use of the BP risedronate reduced both mineral loss and MCL-complex laxity.
  • CONCLUSION: Compared to the untreated ACLX condition, administering bisphosphonate immediately after loss of the ACL conserved bone mineral at the MCL enthesis, suggesting the potential to therapeutically influence joint-complex laxity and OA progression.

  • MedlinePlus Health Information. consumer health - Minerals.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16153550.001).
  • [ISSN] 1063-4584
  • [Journal-full-title] Osteoarthritis and cartilage
  • [ISO-abbreviation] Osteoarthr. Cartil.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Diphosphonates; 0 / Minerals
  •  go-up   go-down


75. Ripperger T, von Neuhoff N, Kamphues K, Emura M, Lehmann U, Tauscher M, Schraders M, Groenen P, Skawran B, Rudolph C, Callet-Bauchu E, van Krieken JH, Schlegelberger B, Steinemann D: Promoter methylation of PARG1, a novel candidate tumor suppressor gene in mantle-cell lymphomas. Haematologica; 2007 Apr;92(4):460-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Promoter methylation of PARG1, a novel candidate tumor suppressor gene in mantle-cell lymphomas.
  • BACKGROUND AND OBJECTIVES: Mantle cell lymphoma (MCL), a mature B-cell neoplasm, is genetically characterized by the translocation t(11;14)(q13;q32).
  • The identification of inactivated tumor suppressor genes contributing to the development of MCL may lead to further elucidation of the biology of this disease and help to identify novel targets for therapy.
  • DESIGN AND METHODS: Whole genome microarray-based gene expression profiling on treated versus untreated MCL cell lines was used to identify genes induced by 5-aza-2'-deoxycytidine.
  • The degree of promoter methylation and transcriptional silencing of selected genes was then proven in MCL cell lines and primary cases by methylation-specific polymerase chain reaction (PCR) techniques, real-time PCR and gene expression profiling.
  • RESULTS: After 5-aza-2'-deoxycytidine treatment, we identified more than 1000 upregulated genes, 16 of which were upregulated > or =3-fold.
  • Most of them were not known to be silenced by methylation in MCL.
  • A low expression of ING1, RUNX3 and BNIP3L was observed in three of the five the MCL cell lines.
  • In addition, the expression of PARG1, which is located in the frequently deleted region 1p22.1, was substantially reduced and displayed at least partial promoter methylation in all investigated MCL cell lines as well as in 31 primary MCL cases.
  • INTERPRETATION AND CONCLUSIONS: In summary, we identified interesting novel candidate genes that probably contribute to the progression of MCL and suggest that PARG1 is a strong candidate tumor suppressor gene in MCL.
  • [MeSH-major] DNA Methylation. DNA, Neoplasm / chemistry. GTPase-Activating Proteins / genetics. Genes, Tumor Suppressor. Lymphoma, Mantle-Cell / genetics. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Cell Line, Tumor / drug effects. Cell Line, Tumor / metabolism. Chromosomes, Human, Pair 1 / genetics. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, Pair 14 / ultrastructure. Disease Progression. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / drug effects. Gene Silencing / drug effects. Humans. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Oligonucleotide Array Sequence Analysis. Polymerase Chain Reaction / methods. Transcription, Genetic / drug effects. Translocation, Genetic

  • Hazardous Substances Data Bank. AZACITIDINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17488656.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / ARHGAP29 protein, human; 0 / DNA, Neoplasm; 0 / GTPase-Activating Proteins; 0 / Neoplasm Proteins; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
  •  go-up   go-down


76. Richardson SJ, Eve HE, Copplestone JA, Dyer MJ, Rule SA: Activity of thalidomide and lenalidomide in mantle cell lymphoma. Acta Haematol; 2010;123(1):21-9
Hazardous Substances Data Bank. THALIDOMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activity of thalidomide and lenalidomide in mantle cell lymphoma.
  • Thalidomide and lenalidomide are immunomodulatory drugs that show promise in mantle cell lymphoma (MCL).
  • In this study, their potential mechanisms of action against MCL cells were investigated, both alone and in combination with rituximab.
  • Thalidomide, lenalidomide and rituximab have no direct effect on MCL cell viability.
  • However, both immunomodulatory drugs indirectly affect viability by enhancing peripheral blood mononuclear cell-mediated cytotoxicity, with lenalidomide inducing significantly higher levels of toxicity than thalidomide.
  • Rituximab induces both complement-dependent and antibody-dependent cellular cytotoxicity (ADCC) against MCL cells.
  • Preliminary in vivo findings in MCL patients treated with thalidomide support a role for natural killer cells in the efficacy of these drugs.
  • In conclusion, our data support a role for immunomodulatory drugs in the treatment of MCL.
  • [MeSH-major] Immunologic Factors / pharmacology. Lymphoma, Mantle-Cell / drug therapy. Thalidomide / analogs & derivatives. Thalidomide / pharmacology
  • [MeSH-minor] Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Antibody-Dependent Cell Cytotoxicity / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Complement System Proteins / metabolism. Cytotoxicity, Immunologic / drug effects. Drug Synergism. Humans. In Vitro Techniques. Leukocytes, Mononuclear / drug effects. Leukocytes, Mononuclear / immunology. Rituximab

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2009 S. Karger AG, Basel.
  • (PMID = 19907157.001).
  • [ISSN] 1421-9662
  • [Journal-full-title] Acta haematologica
  • [ISO-abbreviation] Acta Haematol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670597
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Immunologic Factors; 4F4X42SYQ6 / Rituximab; 4Z8R6ORS6L / Thalidomide; 9007-36-7 / Complement System Proteins; F0P408N6V4 / lenalidomide
  •  go-up   go-down


77. O'Connor OA, Moskowitz C, Portlock C, Hamlin P, Straus D, Dumitrescu O, Sarasohn D, Gonen M, Butos J, Neylon E, Hamelers R, Mac-Gregor Cortelli B, Blumel S, Zelenetz AD, Gordon L, Wright JJ, Vose J, Cooper B, Winter J: Patients with chemotherapy-refractory mantle cell lymphoma experience high response rates and identical progression-free survivals compared with patients with relapsed disease following treatment with single agent bortezomib: results of a multicentre Phase 2 clinical trial. Br J Haematol; 2009 Apr;145(1):34-9
Hazardous Substances Data Bank. BORTEZOMIB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patients with chemotherapy-refractory mantle cell lymphoma experience high response rates and identical progression-free survivals compared with patients with relapsed disease following treatment with single agent bortezomib: results of a multicentre Phase 2 clinical trial.
  • The recent approval of bortezomib for the treatment of mantle cell lymphoma (MCL) by the US Food and Drug Administration is based on the results of the multicentre PINNACLE study with supportive data from a number of single and multicentre Phase 2 studies.
  • This multicentre Phase 2 study enrolled 40 patients with heavily pretreated MCL.
  • Responding patients experienced a PFS from bortezomib that was similar to their line of prior therapy (7.8 months vs. 8.4 months, respectively).
  • The data showed similar responses in relapsed and refractory patients as well as remission durations similar to prior therapy, suggesting that there may be little cross-resistance with other conventional cytotoxic agents.
  • Importantly, these data suggest that MCL patients with refractory or poorly responsive disease may still derive meaningful clinical benefit from treatment with bortezomib.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Boronic Acids / therapeutic use. Lymphoma, Mantle-Cell / drug therapy. Neoplasm Recurrence, Local / drug therapy. Protease Inhibitors / administration & dosage. Pyrazines / therapeutic use
  • [MeSH-minor] Bortezomib. Disease-Free Survival. Drug Administration Schedule. Drug Resistance, Multiple. Female. Humans. Male. Remission Induction

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19220284.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K23 CA109613; United States / NCI NIH HHS / CA / U01 CA 69913
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  •  go-up   go-down


78. Williams ME, Dreyling M, Winter J, Muneer S, Leonard JP: Management of mantle cell lymphoma: key challenges and next steps. Clin Lymphoma Myeloma Leuk; 2010 Oct;10(5):336-46
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of mantle cell lymphoma: key challenges and next steps.
  • Mantle cell lymphoma (MCL) is regarded as an aggressive lymphoid malignancy that exhibits varied clinical behavior and prognoses, reflecting the biologic heterogeneity of the disease.
  • In most cases, patients with MCL achieve a shorter median survival compared with more common B-cell lymphomas, such as follicular lymphoma, and are less likely to achieve a durable response with chemotherapy.
  • Currently, there is no defined standard of care for patients with MCL.
  • Rituximab-containing immunochemotherapy strategies are commonly used, but the addition of rituximab to conventional induction chemotherapy has produced suboptimal responses that are relatively short-lived and have not resulted in a survival advantage.
  • Further intensification of the chemotherapy component, including autologous stem cell transplantation, has increased response and survival rates but has not proven to be curative while being associated with higher toxicity.
  • Clearly, there is a need for developing novel agents and strategies that will improve clinical outcomes for patients with MCL.
  • Targeted therapies and new cytotoxic agents are showing great promise and may have a role in maintenance and/or initial therapy.
  • This summary highlights current challenges in the management of MCL, and outlines expert perspectives, key questions, and future directions.
  • For the third consecutive year, a panel of global experts in MCL assembled to deliberate on topical issues in MCL including advances in pathobiology, strategies for risk-adapted therapy, front-line treatment options, consolidation approaches, and novel therapeutic strategies.
  • It must be emphasized that this synopsis is not meant to serve as an exhaustive review of MCL biology and management, but is a distillation of the expert discussions, highlighting key questions and future directions identified.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Mantle-Cell / drug therapy
  • [MeSH-minor] Aged. Female. Humans. Male. Molecular Targeted Therapy / methods

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21030346.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  •  go-up   go-down


79. Zhou Y, Zhang L, Romaguera J, Delasalle K, Han X, Du X, Kwak L, Yi Q, Wang M: Immunotherapy in mantle cell lymphoma: anti-CD20-based therapy and beyond. Am J Hematol; 2008 Feb;83(2):144-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunotherapy in mantle cell lymphoma: anti-CD20-based therapy and beyond.
  • Mantle cell lymphoma (MCL), an aggressive non-Hodgkin's lymphoma characterized by t(11; 14)(q13;.
  • Recent advances in biology, genetics, and immunology have supported the development of immunotherapy in MCL.
  • Rituximab monotherapy in MCL has limited activity.
  • It is more effective when used in combination with chemotherapy such as R-CHOP, R-hyperCVAD/MTX-Ara-C, or R-FCM as front-line or salvage therapy for mantle cell lymphoma.
  • Although most results have suggested that combining autologous stem cell transplantation with Rituximab may lead to durable remission, the sample size was not sufficient to declare survival benefit.
  • Anti-CD20 radioimmunoconjugates (RICs) (90)Yttrium-ibritumomab tiuxetan and (131)Iodine-tositumomab have been used in mantle cell lymphoma even when patients are relatively resistant to Rituximab-based therapy.
  • Allogeneic stem cell transplantation is a treatment modality in advanced or relapsed MCL, particularly using reduced-intensity conditioning.
  • MCL may have high response rates and sustained remissions after donor lymphocyte infusion.
  • Dendritic cells (DCs) fused with MCL cells for immunostimulation have preliminarily shown anti-lymphoma effects as well.
  • Idiotype vaccination in MCL patients following Rituximab-containing chemotherapy induced tumor-specific T-cell immunity in the absence of B cells.
  • A Phase I/II study is ongoing to determine the maximum tolerated dose (MTD) and the efficacy of lenalidomide in combination with Rituximab for relapsed/refractory MCL.
  • This review summarizes the latest and exciting advances in MCL.
  • [MeSH-major] Antigens, CD20 / immunology. Immunotherapy / methods. Lymphoma, Mantle-Cell / therapy
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antigens, CD / immunology. Antineoplastic Agents / therapeutic use. Cancer Vaccines / therapeutic use. Dendritic Cells / immunology. Graft vs Tumor Effect. Humans. Rituximab


80. Ritchie DS, Seymour JF, Grigg AP, Roberts AW, Hoyt R, Thompson S, Szer J, Prince HM: The hyper-CVAD-rituximab chemotherapy programme followed by high-dose busulfan, melphalan and autologous stem cell transplantation produces excellent event-free survival in patients with previously untreated mantle cell lymphoma. Ann Hematol; 2007 Feb;86(2):101-5
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The hyper-CVAD-rituximab chemotherapy programme followed by high-dose busulfan, melphalan and autologous stem cell transplantation produces excellent event-free survival in patients with previously untreated mantle cell lymphoma.
  • This regimen, when used as initial therapy for patients under 65 years of age with previously untreated mantle cell lymphoma (MCL), results in remission rates of > 85% with a median event-free survival (EFS) of > 50 months, but with a pattern of continuous relapse out to 60 months.
  • We performed a study of hyper-CVAD + R, followed by consolidative peripheral blood progenitor cells autograft [autologous stem cell transplant (AuSCT)] with high-dose busulfan and melphalan (Bu/Mel) conditioning, in patients with responsive disease.
  • Thirteen patients with a median age of 54 (range = 33-61) were treated.
  • Complete remission (CR) was achieved in 12 patients (92%) after hyper-CVAD + R and 12 completed AuSCT after Bu/Mel conditioning.
  • With a median follow-up from diagnosis of 36 months (range = 16-53 months), the observed 36 months overall survival and EFS are both 92% for the whole cohort.
  • These data confirm the excellent CR rates achieved by the use of hyper-CVAD + R in patients with MCL and suggest that consolidation with Bu/Mel and AuSCT may improve durable disease control when compared to published outcomes of hyper-CVAD + R alone.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Busulfan / therapeutic use. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / pathology. Melphalan / therapeutic use. Stem Cell Transplantation
  • [MeSH-minor] Adult. Antibodies, Monoclonal, Murine-Derived. Cyclophosphamide / therapeutic use. Dexamethasone / therapeutic use. Disease-Free Survival. Doxorubicin / therapeutic use. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Rituximab. Survival Rate. Time Factors. Transplantation, Homologous. Vincristine / therapeutic use

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. MELPHALAN .
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. BUSULFAN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17089127.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; G1LN9045DK / Busulfan; Q41OR9510P / Melphalan; CVAD protocol
  •  go-up   go-down


81. Romaguera JE: Mantle cell lymphoma: Frontline and salvage therapy. Curr Hematol Malig Rep; 2008 Oct;3(4):204-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mantle cell lymphoma: Frontline and salvage therapy.
  • Mantle cell lymphoma (MCL) is a therapeutic challenge because of its lower cure rate when compared with other lymphomas such as diffuse large cell lymphoma.
  • The current emphasis in the treatment of newly diagnosed MCL has been on intensifying chemotherapy, but there is no consensus on the need to consolidate with autologous stem cell transplantation.
  • Newer strategies include the use of models to aid in tailoring therapy.
  • Likewise, autologous stem cell consolidation does not cure relapsed disease.
  • Because of its known graft-versus-lymphoma effect, allogeneic stem cell transplantation offers a potentially curative option for relapsed MCL.
  • New insights into resistance pathways and new drugs created to inhibit them offer great promise in the treatment of newly diagnosed and previously treated MCL.
  • [MeSH-major] Lymphoma, Mantle-Cell / therapy. Salvage Therapy
  • [MeSH-minor] Clinical Trials as Topic. Drug Therapy, Combination. Humans. Neoplasm, Residual. Recurrence. Stem Cell Transplantation. Transplantation, Autologous. Transplantation, Homologous

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2003 Jul 15;102(2):749-55 [12663455.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):546-53 [10080598.001]
  • [Cites] Leuk Lymphoma. 2007 Nov;48(11):2172-8 [17990179.001]
  • [Cites] Ann Oncol. 2005 Apr;16(4):618-24 [15781489.001]
  • [Cites] Blood. 2008 Feb 15;111(4):2385-7 [18077791.001]
  • [Cites] Histopathology. 2000 Jan;36(1):69-86 [10632755.001]
  • [Cites] Leuk Lymphoma. 2001 Sep-Oct;42(5):1015-22 [11697618.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2271-8 [16332971.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1984-92 [15668467.001]
  • [Cites] Blood. 2006 Dec 15;108(13):4003-8 [16946304.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2677-84 [15591112.001]
  • [Cites] Blood. 2002 May 1;99(9):3158-62 [11964278.001]
  • [Cites] Nat Rev Cancer. 2007 Oct;7(10):750-62 [17891190.001]
  • [Cites] J Clin Oncol. 1998 Feb;16(2):579-83 [9469344.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2269-71 [15166030.001]
  • [Cites] Ann Oncol. 2006 Sep;17 (9):1418-23 [16766582.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):185-97 [12620412.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):705-11 [15598978.001]
  • [Cites] Cancer. 2003 Dec 15;98(12):2630-5 [14669282.001]
  • [Cites] J Natl Cancer Inst. 2007 May 2;99(9):706-14 [17470738.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):7013-23 [16145068.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3383-9 [15908650.001]
  • [Cites] Clin Lymphoma Myeloma. 2007 Dec;8 Suppl 2:S57-62 [18284717.001]
  • [Cites] Haematologica. 2006 Mar;91(3):425-6 [16531272.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4407-12 [14645431.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3064-71 [15284112.001]
  • [Cites] Br J Haematol. 2005 Oct;131(1):29-38 [16173960.001]
  • [Cites] Leukemia. 2002 Apr;16(4):587-93 [11960337.001]
  • [Cites] Br J Haematol. 2003 Mar;120(5):793-800 [12614212.001]
  • [Cites] Blood. 2008 Jan 15;111(2):558-65 [17962512.001]
  • [Cites] J Clin Oncol. 2000 Feb;18(4):773-9 [10673518.001]
  • [Cites] J Clin Oncol. 2006 Oct 20;24(30):4867-74 [17001068.001]
  • [Cites] Leuk Lymphoma. 2007 Jun;48(6):1092-101 [17577772.001]
  • [Cites] Leukemia. 1997 Apr;11 Suppl 2:S60-4 [9178843.001]
  • (PMID = 20425467.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


82. Rolland D, Raharijaona M, Barbarat A, Houlgatte R, Thieblemont C: Inhibition of GST-pi nuclear transfer increases mantle cell lymphoma sensitivity to cisplatin, cytarabine, gemcitabine, bortezomib and doxorubicin. Anticancer Res; 2010 Oct;30(10):3951-7
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of GST-pi nuclear transfer increases mantle cell lymphoma sensitivity to cisplatin, cytarabine, gemcitabine, bortezomib and doxorubicin.
  • PURPOSE: Mantle cell lymphoma (MCL) is a chemoresistant lymphoma overexpressing the class pi glutathione-S-transferase (GST-pi).
  • The nuclear localisation of GST-pi is induced by chemotherapy and is correlated to cell resistance.
  • In this study, the effect of the Agaricus bisporus lectin (ABL), a GST-pi nuclear transfer inhibitor, on the chemosensitivity of MCL cells was investigated.
  • METHODS: The proliferation of three MCL cell lines was evaluated in the presence of doxorubicin (DOX), cisplatin (CDDP), cytarabine (Ara-C), gemcitabine (GEM) or bortezomib with or without ABL pre-treatment.
  • RESULTS: The cytotoxic activities of CDDP, Ara-C, GEM and bortezomib were increased in all cell lines.
  • The DOX cytotoxic activity was enhanced in two of three cell lines.
  • The inhibition of GST-pi nuclear transfer led to the potentialisation of all drug combinations.
  • CONCLUSION: The inhibition of the nuclear transfer of GST-pi increases the MCL sensitivity to DOX, CDDP, Ara-C, GEM and bortezomib, alone or in combination.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Glutathione S-Transferase pi / antagonists & inhibitors. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / enzymology
  • [MeSH-minor] Active Transport, Cell Nucleus / drug effects. Boronic Acids / administration & dosage. Boronic Acids / pharmacology. Bortezomib. Cell Growth Processes / drug effects. Cell Line, Tumor. Cisplatin / administration & dosage. Cisplatin / pharmacology. Cytarabine / administration & dosage. Cytarabine / pharmacology. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Doxorubicin / administration & dosage. Doxorubicin / pharmacology. Drug Screening Assays, Antitumor. Humans. Lectins / administration & dosage. Lectins / pharmacology. Pyrazines / administration & dosage. Pyrazines / pharmacology

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21036708.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Agaricus lectins; 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Lectins; 0 / Pyrazines; 04079A1RDZ / Cytarabine; 0W860991D6 / Deoxycytidine; 69G8BD63PP / Bortezomib; 80168379AG / Doxorubicin; B76N6SBZ8R / gemcitabine; EC 2.5.1.18 / GSTP1 protein, human; EC 2.5.1.18 / Glutathione S-Transferase pi; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


83. Goy A, Feldman T: Expanding therapeutic options in mantle cell lymphoma. Clin Lymphoma Myeloma; 2007 Aug;7 Suppl 5:S184-91
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expanding therapeutic options in mantle cell lymphoma.
  • Mantle cell lymphoma (MCL) still carries a poor prognosis.
  • Chemoimmunotherapy (combination with rituximab) is the routine first-line therapy, although data strongly suggest a benefit from intensification through high-dose therapy with stem cell transplantation consolidation or dose-intense chemotherapy with HyperCVAD (fractionated cyclophosphamide/vincristine/doxorubicin/dexamethasone)/rituximab.
  • Unfortunately, most patients still experience relapse, and a multitude of novel agents are currently being tested in this setting, including proteasome inhibitors with bortezomib (the first of its class and first Food and Drug Administration-approved drug in MCL), mammalian target of rapamycin inhibitors, Bcl-2 inhibitors, and antiangiogenesis agents, among others.
  • Because of the relative rarity of the disease-MCL represents 6% of non-Hodgkin lymphoma-an obvious effort is needed to enroll patients on clinical trials.
  • Not surprisingly, as in other non-Hodgkin lymphomas, MCL appears more and more as a heterogeneous disease, which might impact future clinical trial design through pharmacogenomics and hopefully help us develop smaller "molecular" relevant trials.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Mantle-Cell / drug therapy
  • [MeSH-minor] Animals. Combined Modality Therapy. Humans. Radioimmunotherapy

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17877843.001).
  • [ISSN] 1557-9190
  • [Journal-full-title] Clinical lymphoma & myeloma
  • [ISO-abbreviation] Clin Lymphoma Myeloma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 90
  •  go-up   go-down


84. Ford RJ, Shen L, Lin-Lee YC, Pham LV, Multani A, Zhou HJ, Tamayo AT, Zhang C, Hawthorn L, Cowell JK, Ambrus JL Jr: Development of a murine model for blastoid variant mantle-cell lymphoma. Blood; 2007 Jun 1;109(11):4899-906
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development of a murine model for blastoid variant mantle-cell lymphoma.
  • Blastoid-variant mantle-cell lymphoma (MCL-BV), unlike most B-cell non-Hodgkin lymphomas (NHL-Bs), is refractory to conventional chemotherapy and associated with a very poor prognosis.
  • Development of new therapies has been hampered by the lack of valid animal models.
  • We have developed a novel murine model of MCL-BV by crossing interleukin 14alpha (IL-14alpha) transgenic mice with c-Myc transgenic mice (double transgenic [DTG]).
  • IL-14alpha is a B-cell growth factor that is expressed in a number of high-grade lymphomas, including MCL-BV.
  • Ninety-five percent of IL-14alpha transgenic mice develop CD5(+) large B-cell lymphomas by 18 months of age.
  • Sixty percent of c-Myc transgenic mice develop pre-B-cell lymphomas by 12 months of age.
  • The tumor is found in the blood, bone marrow, liver, spleen, lymph nodes, gastrointestinal tract, and lungs and rarely in the brain, similar to the involvement seen in human MCL-BV.
  • Immunoglobulin gene rearrangements document the monoclonality of the tumor.
  • Cyclin D1 is highly expressed in these tumors, as it is in MCL-BV.
  • DTG represents a novel model for MCL-BV that should reveal important insights into the pathogenesis of the lymphoma and contribute to the development of new forms of therapy.

  • COS Scholar Universe. author profiles.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Haematol. 2004 Feb;124(3):289-98 [14717775.001]
  • [Cites] Leuk Lymphoma. 2004 Jan;45(1):49-54 [15061196.001]
  • [Cites] J Immunol. 2004 Jun 1;172(11):6684-91 [15153484.001]
  • [Cites] Oncogene. 2004 Aug 23;23(38):6524-34 [15322522.001]
  • [Cites] Blood. 2004 Oct 15;104(8):2505-13 [15226187.001]
  • [Cites] Blood. 1975 Aug;46(2):219-34 [1139039.001]
  • [Cites] J Clin Invest. 1985 Feb;75(2):732-9 [2982918.001]
  • [Cites] Nature. 1985 Dec 12-18;318(6046):533-8 [3906410.001]
  • [Cites] Nature. 1988 Sep 29;335(6189):440-2 [3262202.001]
  • [Cites] Cell. 1989 Apr 7;57(1):79-88 [2649247.001]
  • [Cites] EMBO J. 1989 Mar;8(3):749-55 [2785918.001]
  • [Cites] Oncogene Res. 1989;4(4):253-8 [2549487.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Apr 15;166(2):101-11 [16631465.001]
  • [Cites] Leukemia. 2006 May;20(5):891-3 [16525491.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4540-8 [16497967.001]
  • [Cites] Nature. 2006 May 25;441(7092):431-6 [16724054.001]
  • [Cites] N Engl J Med. 2006 Jun 8;354(23):2419-30 [16760442.001]
  • [Cites] J Immunol. 2006 Oct 15;177(8):5676-86 [17015757.001]
  • [Cites] Leukemia. 1999 Dec;13(12):2087-93 [10602433.001]
  • [Cites] J Immunol. 2000 Feb 15;164(4):2200-6 [10657675.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2773-8 [10706620.001]
  • [Cites] Lab Invest. 2000 Apr;80(4):557-73 [10780672.001]
  • [Cites] J Exp Med. 2000 Oct 16;192(8):1183-90 [11034608.001]
  • [Cites] J Clin Invest. 2001 Feb;107(3):241-6 [11160144.001]
  • [Cites] Curr Opin Hematol. 2002 Jan;9(1):56-62 [11753079.001]
  • [Cites] CA Cancer J Clin. 2002 Jan-Feb;52(1):23-47 [11814064.001]
  • [Cites] Leuk Lymphoma. 2002 Aug;43(8):1563-71 [12400598.001]
  • [Cites] Br J Haematol. 2003 Feb;120(3):434-41 [12580957.001]
  • [Cites] Annu Rev Immunol. 2003;21:841-94 [12615894.001]
  • [Cites] Nat Immunol. 2003 May;4(5):410-5 [12719730.001]
  • [Cites] Hum Pathol. 2003 Apr;34(4):330-5 [12733111.001]
  • [Cites] Cancer Genet Cytogenet. 2003 May;143(1):32-8 [12742154.001]
  • [Cites] Mol Cell Biol. 2003 Jun;23(12):4283-94 [12773570.001]
  • [Cites] J Immunol. 2003 Jul 1;171(1):88-95 [12816986.001]
  • [Cites] Am J Clin Pathol. 1999 Apr;111(4):495-500 [10191769.001]
  • [Cites] Semin Hematol. 1999 Apr;36(2):171-7 [10319386.001]
  • [Cites] J Clin Invest. 1989 Nov;84(5):1595-608 [2681271.001]
  • [Cites] J Immunol. 1990 Dec 15;145(12):3949-55 [2258603.001]
  • [Cites] Hematol Oncol Clin North Am. 1991 Oct;5(5):871-89 [1938759.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jul 1;90(13):6330-4 [8327514.001]
  • [Cites] EMBO J. 1994 May 1;13(9):2124-30 [8187765.001]
  • [Cites] EMBO J. 1994 Aug 1;13(15):3487-95 [8062825.001]
  • [Cites] Blood. 1995 Jul 1;86(1):283-93 [7795235.001]
  • [Cites] Cell. 1996 Oct 4;87(1):13-20 [8858144.001]
  • [Cites] Nat Genet. 1996 Nov;14(3):312-5 [8896561.001]
  • [Cites] Mol Cell Biol. 1997 Mar;17(3):1324-35 [9032259.001]
  • [Cites] Leuk Lymphoma. 1997 Aug;26(5-6):539-50 [9389361.001]
  • [Cites] Clin Immunol Immunopathol. 1998 Apr;87(1):42-9 [9576009.001]
  • [Cites] Growth Factors. 2006 Mar;24(1):13-9 [16393691.001]
  • [Cites] Br J Haematol. 2006 Feb;132(3):303-16 [16409295.001]
  • [Cites] Haematologica. 2006 Jan;91(1):11-6 [16434365.001]
  • [Cites] Haematologica. 2006 Jan;91(1):40-7 [16434369.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2352-7 [16461462.001]
  • [Cites] Oncogene. 2006 Feb 16;25(7):998-1007 [16247460.001]
  • [Cites] Hematol Oncol. 2006 Mar;24(1):22-7 [16402392.001]
  • [Cites] Cell Death Differ. 2006 May;13(5):759-72 [16410803.001]
  • [Cites] J Biol Chem. 1999 Jul 30;274(31):22033-40 [10419529.001]
  • [Cites] Curr Opin Hematol. 2004 Nov;11(6):411-8 [15548996.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):298-306 [15549091.001]
  • [Cites] Curr Hematol Rep. 2005 Jan;4(1):31-8 [15610657.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 15;102(11):4097-102 [15753301.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 22;102(12):4324-9 [15738393.001]
  • [Cites] J Pathol. 2005 Jun;206(2):123-34 [15880597.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4445-54 [15718413.001]
  • [Cites] Virchows Arch. 2005 May;446(5):475-82 [15856292.001]
  • [Cites] Mol Cell Biol. 2005 Jul;25(14):6225-34 [15988031.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jul 5;102(27):9613-8 [15983382.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Aug;6(8):635-45 [16064138.001]
  • [Cites] Curr Opin Oncol. 2005 Sep;17(5):425-31 [16093790.001]
  • [Cites] Med Oncol. 2005;22(4):327-41 [16260850.001]
  • [Cites] Leuk Lymphoma. 2006 Jan;47(1):121-7 [16321836.001]
  • [Cites] Leuk Lymphoma. 2006 Feb;47(2):195-205 [16321849.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4315-21 [16123218.001]
  • [Cites] Neoplasia. 2003 May-Jun;5(3):198-204 [12869303.001]
  • [Cites] Am J Clin Pathol. 2003 Nov;120(5):760-6 [14608904.001]
  • [Cites] Cancer Res. 2003 Dec 1;63(23):8226-32 [14678979.001]
  • (PMID = 17311992.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA 16672-26; United States / NCI NIH HHS / CA / R01 CA 100836
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulins; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptors, Interleukin; 0 / interleukin-14 receptor
  • [Other-IDs] NLM/ PMC1885517
  •  go-up   go-down


85. Terasawa T, Ohashi H, Utsumi M, Tsushita K, Kinoshita T, Nakamura S, Saito H: Case of Epstein-Barr virus-associated transformation of mantle cell lymphoma. Am J Hematol; 2003 Jul;73(3):194-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Case of Epstein-Barr virus-associated transformation of mantle cell lymphoma.
  • We report here a case of mantle cell lymphoma (MCL) in a patient who, following Epstein-Barr virus (EBV) infection, developed diffuse large B-cell lymphoma (DLBCL).
  • A 47-year-old woman was diagnosed as having MCL with clinical stage IIIA in July 1990.
  • After treatment with a third-generation chemotherapy without response, she was kept under observation for 8 years.
  • In January 1999, fever and night sweats appeared with laboratory evidence for EBV infection, and acute swelling of lymph nodes and hepatosplenomegaly developed in May 1999.
  • Sequence analysis of the complementarity-determining region (CDR)-III of the immunoglobulin heavy chain gene demonstrated clonal identity between the initial MCL and the subsequent DLBCL.
  • Immunohistochemistry revealed that cyclin D1, CD5, and CD20 were expressed in the MCL but lost in the DLBCL cells, and EBER-ISH confirmed that EBV infection was absent in the former but present in the latter.
  • All these results suggest that EBV infection may have been the molecular event that caused transformation of MCL cell(s) to DLBCL in this case.
  • This is, to the best of our knowledge, the first well-documented case of EBV-associated transformation of MCL.
  • [MeSH-major] Epstein-Barr Virus Infections / complications. Lymphoma, Mantle-Cell / virology
  • [MeSH-minor] Antigens, CD / blood. Antigens, CD / genetics. Base Sequence. DNA, Neoplasm / blood. DNA, Neoplasm / genetics. DNA, Neoplasm / isolation & purification. Female. Gene Rearrangement. Humans. In Situ Hybridization. Middle Aged. Molecular Sequence Data. Pseudogenes. Sequence Alignment. Sequence Homology, Nucleic Acid

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 12827658.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / DNA, Neoplasm
  •  go-up   go-down


86. Liu Q, Alinari L, Chen CS, Yan F, Dalton JT, Lapalombella R, Zhang X, Mani R, Lin T, Byrd JC, Baiocchi RA, Muthusamy N: FTY720 shows promising in vitro and in vivo preclinical activity by downmodulating Cyclin D1 and phospho-Akt in mantle cell lymphoma. Clin Cancer Res; 2010 Jun 15;16(12):3182-92
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FTY720 shows promising in vitro and in vivo preclinical activity by downmodulating Cyclin D1 and phospho-Akt in mantle cell lymphoma.
  • PURPOSE: Despite the progress that has been made in the treatment of mantle cell lymphoma (MCL), all patients invariably relapse with the currently available therapies.
  • Because of the absence of curative therapy for MCL, we explored FTY720 as a novel agent against MCL.
  • EXPERIMENTAL DESIGN: The cytotoxic effect of FTY720 in primary MCL tumor cells and cell lines were evaluated in vitro.
  • The effects of FTY720 on caspase activation, generation of reactive oxygen species, and modulation of Cyclin D1 and Akt, which are implied in the pathogenesis of MCL, were investigated.
  • The in vivo efficacy of FTY720 was evaluated in a Jeko-severe combined immunodeficient xenograft model of human MCL.
  • RESULTS: FTY720 mediated time- and dose-dependent cytotoxicity in primary MCL tumor cells and MCL cell lines in vitro.
  • FTY720-induced cytotoxicity occured independent of caspase activation but dependent on the generation of ROS in MCL.
  • In addition, FTY720 treatment resulted in the time-dependent downmodulation of Cyclin D1 and accumulation of cells in G(0)-G(1) and G(2)-M phases of the cell cycle with concomitant decrease in S-phase entry.
  • Furthermore, concentrations of FTY720 that induced cytotoxicity led to decreased phospho-Akt in primary MCL cells and cell lines.
  • Most importantly, the in vivo therapeutic activity of FTY720 was shown in severe combined immunodeficient mice engrafted with the Jeko MCL cell line.
  • CONCLUSIONS: These results provide the first evidence for a potential use of FTY720 in targeting key pathways that are operable in the pathogenesis of MCL and warrant further investigation of FTY720 in clinical trials to treat patients with MCL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cyclin D1 / metabolism. Lymphoma, Mantle-Cell / drug therapy. Propylene Glycols / therapeutic use. Proto-Oncogene Proteins c-akt / metabolism. Sphingosine / analogs & derivatives
  • [MeSH-minor] Animals. Apoptosis. Cell Cycle. Cell Line, Tumor. Female. Fingolimod Hydrochloride. Humans. Mice. Mice, SCID. Reactive Oxygen Species / metabolism. Xenograft Model Antitumor Assays

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2010 AACR.
  • [Cites] Mod Pathol. 2000 Feb;13(2):193-207 [10697278.001]
  • [Cites] Leukemia. 2008 Nov;22(11):2097-105 [18685613.001]
  • [Cites] Cell. 2000 Oct 13;103(2):185-8 [11057891.001]
  • [Cites] Jpn J Cancer Res. 2001 Jun;92(6):680-7 [11429058.001]
  • [Cites] Science. 2002 Apr 12;296(5566):346-9 [11923495.001]
  • [Cites] J Biol Chem. 2002 Apr 19;277(16):14040-7 [11842081.001]
  • [Cites] J Pathol. 2002 Jun;197(2):256-63 [12015751.001]
  • [Cites] Arch Pathol Lab Med. 2003 Apr;127(4):424-31 [12683869.001]
  • [Cites] J Biol Chem. 2003 Sep 5;278(36):33714-23 [12821677.001]
  • [Cites] Br J Haematol. 2004 Jan;124(2):130-40 [14687022.001]
  • [Cites] Leukemia. 2004 Nov;18(11):1883-90 [15356648.001]
  • [Cites] J Exp Med. 1993 Sep 1;178(3):1103-7 [8350049.001]
  • [Cites] Transplantation. 1996 Jan 27;61(2):200-5 [8600623.001]
  • [Cites] Transplant Proc. 1996 Jun;28(3):1375-6 [8658701.001]
  • [Cites] J Exp Med. 1996 Sep 1;184(3):1155-60 [9064332.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):4997-5002 [9560217.001]
  • [Cites] J Cell Biol. 1998 Jun 15;141(6):1423-32 [9628898.001]
  • [Cites] Leukemia. 1998 Oct;12(10):1630-7 [9766510.001]
  • [Cites] Transplantation. 2005 Jun 15;79(11):1553-60 [15940045.001]
  • [Cites] Curr Opin Oncol. 2005 Sep;17(5):425-31 [16093790.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7478-84 [16103102.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4315-21 [16123218.001]
  • [Cites] Cancer Res. 2008 Feb 15;68(4):1204-12 [18281497.001]
  • [Cites] Ann Oncol. 2006 May;17 Suppl 4:iv12-4 [16702178.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1668-76 [16645163.001]
  • [Cites] Br J Haematol. 2006 Oct;135(1):68-71 [16925576.001]
  • [Cites] Clin Lymphoma Myeloma. 2007 Aug;7 Suppl 5:S184-91 [17877843.001]
  • [Cites] Blood. 2008 Jan 1;111(1):275-84 [17761520.001]
  • [Cites] Pancreas. 2008 Apr;36(3):e10-5 [18362832.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3065-74 [18725988.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3051-64 [18725989.001]
  • [Cites] J Biol Chem. 2000 Mar 24;275(12):8271-4 [10722653.001]
  • (PMID = 20460491.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA140158
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Propylene Glycols; 0 / Reactive Oxygen Species; 136601-57-5 / Cyclin D1; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; G926EC510T / Fingolimod Hydrochloride; NGZ37HRE42 / Sphingosine
  • [Other-IDs] NLM/ NIHMS628790; NLM/ PMC4180653
  •  go-up   go-down


87. Alinari L, White VL, Earl CT, Ryan TP, Johnston JS, Dalton JT, Ferketich AK, Lai R, Lucas DM, Porcu P, Blum KA, Byrd JC, Baiocchi RA: Combination bortezomib and rituximab treatment affects multiple survival and death pathways to promote apoptosis in mantle cell lymphoma. MAbs; 2009 Jan-Feb;1(1):31-40
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combination bortezomib and rituximab treatment affects multiple survival and death pathways to promote apoptosis in mantle cell lymphoma.
  • Mantle cell lymphoma (MCL) is a distinct histologic subtype of B cell non-Hodgkins lymphoma (NHL) associated with an aggressive clinical course.
  • Inhibition of the ubiquitin-proteasome pathway modulates survival and proliferation signals in MCL and has shown clinical benefit in this disease.
  • This has provided rationale for exploring combination regimens with B-cell selective immunotherapies such as rituximab.
  • In this study, we examined the effects of combined treatment with bortezomib and rituximab on patient-derived MCL cell lines (Jeko, Mino, SP53) and tumor samples from patients with MCL where we validate reversible proteasome inhibition concurrent with cell cycle arrest and additive induction of apoptosis.
  • When MCL cells were exposed to single agent bortezomib or combination bortezomib/rituximab, caspase dependent and independent apoptosis was observed.
  • Single agent bortezomib or rituximab treatment of Mino and Jeko cell lines and patient samples resulted in decreased levels of nuclear NFkappaB complex(es) capable of binding p65 consensus oligonucleotides, and this decrease was enhanced by the combination.
  • On the basis of in vitro data demonstrating additive apoptosis and enhanced NFkappaB and phosphorylated Akt depletion in MCL with combination bortezomib plus rituximab, a phase II trial of bortezomib-rituximab in patients with relapsed/refractory MCL is underway.

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cancer Ther. 2003 Nov;2(11):1183-93 [14617792.001]
  • [Cites] Cancer Res. 2003 Dec 1;63(23):8226-32 [14678979.001]
  • [Cites] Clin Cancer Res. 2003 Dec 15;9(17):6316-25 [14695130.001]
  • [Cites] J Clin Oncol. 2004 Jun 1;22(11):2108-21 [15169797.001]
  • [Cites] Cancer Invest. 2004;22(2):304-11 [15199612.001]
  • [Cites] J Natl Cancer Inst. 2004 Oct 6;96(19):1447-57 [15467034.001]
  • [Cites] Oncogene. 2004 Oct 14;23(47):7863-73 [15378010.001]
  • [Cites] Blood. 1995 Feb 15;85(4):1075-82 [7849295.001]
  • [Cites] Science. 1995 Aug 4;269(5224):682-5 [7624798.001]
  • [Cites] J Clin Oncol. 1995 Nov;13(11):2819-26 [7595744.001]
  • [Cites] J Biol Chem. 1997 May 16;272(20):12893-6 [9148891.001]
  • [Cites] Blood. 1997 Jun 1;89(11):3909-18 [9166827.001]
  • [Cites] Mol Cell Biol. 1997 Jul;17(7):3629-39 [9199297.001]
  • [Cites] J Clin Invest. 1997 Dec 15;100(12):2961-9 [9399941.001]
  • [Cites] Cancer. 1998 Feb 1;82(3):567-75 [9452276.001]
  • [Cites] Blood. 1998 Mar 1;91(5):1644-52 [9473230.001]
  • [Cites] Br J Haematol. 1998 Sep;102(5):1323-6 [9753063.001]
  • [Cites] J Clin Oncol. 1998 Dec;16(12):3803-9 [9850025.001]
  • [Cites] Clin Cancer Res. 1999 Jan;5(1):119-27 [9918209.001]
  • [Cites] Mol Cell Biol. 1999 Apr;19(4):2690-8 [10082535.001]
  • [Cites] Blood. 1999 Apr 1;93(7):2360-8 [10090947.001]
  • [Cites] Semin Hematol. 1999 Apr;36(2):115-27 [10319380.001]
  • [Cites] Mol Cell Biol. 1999 Sep;19(9):5923-9 [10454539.001]
  • [Cites] J Clin Oncol. 2005 Jan 20;23(3):630-9 [15659509.001]
  • [Cites] Cancer Res. 2005 Jan 1;65(1):264-76 [15665303.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):705-11 [15598978.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2006;46:189-213 [16402903.001]
  • [Cites] Annu Rev Med. 2006;57:33-47 [16409135.001]
  • [Cites] Nat Clin Pract Oncol. 2006 Jul;3(7):374-87 [16826218.001]
  • [Cites] Blood. 2000 Jan 15;95(2):619-26 [10627471.001]
  • [Cites] J Clin Oncol. 2000 Jan;18(2):317-24 [10637245.001]
  • [Cites] J Immunol. 2000 Feb 15;164(4):2200-6 [10657675.001]
  • [Cites] Ann Oncol. 2000;11 Suppl 1:117-21 [10707792.001]
  • [Cites] Mol Cell Biol. 2000 Apr;20(7):2423-35 [10713166.001]
  • [Cites] Blood. 2001 Nov 1;98(9):2771-7 [11675350.001]
  • [Cites] Leuk Res. 2002 Sep;26(9):849-55 [12127561.001]
  • [Cites] J Clin Oncol. 2002 Nov 15;20(22):4420-7 [12431963.001]
  • [Cites] Arch Pathol Lab Med. 2003 Apr;127(4):424-31 [12683869.001]
  • [Cites] J Immunol. 2003 Jul 1;171(1):88-95 [12816986.001]
  • [Cites] Br J Haematol. 2003 Jul;122(2):260-8 [12846895.001]
  • [Cites] Leukemia. 2006 Aug;20(8):1341-52 [16810203.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1668-76 [16645163.001]
  • [Cites] Oncogene. 2007 May 28;26(25):3629-36 [17530016.001]
  • [Cites] Leukemia. 2008 Jan;22(1):179-85 [17898787.001]
  • [Cites] Clin Chem. 2000 May;46(5):673-83 [10794750.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):667-75 [15613697.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):676-84 [15613699.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1984-92 [15668467.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3255-62 [15613543.001]
  • [Cites] Int J Hematol. 2005 May;81(4):319-22 [15914363.001]
  • [Cites] J Clin Oncol. 2005 Sep 1;23(25):6107-16 [16135477.001]
  • [Cites] Blood. 2006 Jan 1;107(1):257-64 [16166592.001]
  • (PMID = 20046572.001).
  • [ISSN] 1942-0870
  • [Journal-full-title] mAbs
  • [ISO-abbreviation] MAbs
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA095426; United States / NCI NIH HHS / CA / P01 CA95426
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 4F4X42SYQ6 / Rituximab; 69G8BD63PP / Bortezomib
  • [Other-IDs] NLM/ PMC2715189
  • [Keywords] NOTNLM ; CD20 / apoptosis / mantle cell lymphoma / proteasome inhibition / survival and death pathways
  •  go-up   go-down


88. Ishibashi M, Yamamoto K, Kudo S, Chen KR: Mantle cell lymphoma with skin invasion characterized by the common variant in the subcutis and blastoid transformation in the overlying dermis. Am J Dermatopathol; 2010 Apr;32(2):180-2
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mantle cell lymphoma with skin invasion characterized by the common variant in the subcutis and blastoid transformation in the overlying dermis.
  • We report a case of common mantle cell lymphoma (MCL) with subcutis infiltration and transformation to blastoid MCL in the overlying dermis.
  • The patient was initially diagnosed as having chronic lymphocytic leukemia and treated with chemotherapy.
  • Eight months after the diagnosis of MCL with bone marrow involvement, subcutaneous nodules developed on the patient's left thigh and forearm.
  • A skin biopsy showed a massive infiltration of neoplastic lymphocytes throughout the dermis and subcutaneous tissue.
  • In the mid to lower dermis, the infiltrate was dense with a nodular growth pattern and was composed of atypical large lymphoblast-like cells with large nuclei, dispersed chromatin, and numerous mitoses.
  • In the subcutaneous tissue, there was a diffuse infiltration of neoplastic cells with common MCL cytologic features characterized by small- to medium-sized lymphoid cells.
  • Cells in the common and blastoid variants of MCL were immunohistochemically positive for CD20 and cyclin D1 but negative for CD5.
  • Neoplastic lymphocytes from the patient's bone marrow had the typical morphologic features and the immunophenotype of MCL (ie, CD5, CD20, cyclin D1, CD10, and CD23).
  • Other case reports in the medical literature indicate that an MCL with skin invasion tends to have a poor prognosis.
  • Our patient died 3 months after the appearance of skin invasion.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Dermis / pathology. Lymphoma, Mantle-Cell / diagnosis. Lymphoma, Mantle-Cell / pathology. Skin Neoplasms / diagnosis. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antigens, CD20 / metabolism. Biopsy. Cyclin D1 / metabolism. Fatal Outcome. Humans. Male. Prognosis. Skin / metabolism. Skin / pathology

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20010283.001).
  • [ISSN] 1533-0311
  • [Journal-full-title] The American Journal of dermatopathology
  • [ISO-abbreviation] Am J Dermatopathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD20; 136601-57-5 / Cyclin D1
  •  go-up   go-down


89. Pérez-Galán P, Roué G, Villamor N, Campo E, Colomer D: The BH3-mimetic GX15-070 synergizes with bortezomib in mantle cell lymphoma by enhancing Noxa-mediated activation of Bak. Blood; 2007 May 15;109(10):4441-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The BH3-mimetic GX15-070 synergizes with bortezomib in mantle cell lymphoma by enhancing Noxa-mediated activation of Bak.
  • Mantle cell lymphoma (MCL) is an aggressive B-cell lymphoma resistant to conventional chemotherapy.
  • The Bcl-2 pathway is deregulated in these tumors and may represent an interesting target for new therapeutic strategies.
  • The new small-molecule pan-Bcl-2 inhibitor GX15-070 mimics BH3-only proteins by binding to multiple antiapoptotic Bcl-2 members.
  • Here we show that GX15-070 induced apoptosis in vitro in MCL cell lines and primary cells from patients with MCL by releasing Bak from Mcl-1 and Bcl-X(L) at short incubation times and low micromolar doses.
  • GX15-070 was effective in cells bearing defective DNA damage-sensor genes or cell-cycle regulators, inducing Bax and Bak conformational changes, mitochondrial depolarization, phosphatidylserine exposure, and caspase-3 activation.
  • Furthermore, GX15-070 synergized with bortezomib, sensitizing MCL cells to low doses of this proteasome inhibitor, by neutralizing bortezomib-induced Mcl-1 accumulation and cooperating with Noxa to induce Bak displacement from this protein.
  • All these findings suggest that GX15-070 alone or in combination with bortezomib represents a new attractive therapeutic approach for MCL treatment.
  • [MeSH-major] Boronic Acids / pharmacology. Lymphoma, Mantle-Cell / drug therapy. Proto-Oncogene Proteins c-bcl-2 / metabolism. Pyrazines / pharmacology. Pyrroles / pharmacology. bcl-2 Homologous Antagonist-Killer Protein / metabolism
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Bortezomib. Drug Synergism. Gene Expression Regulation, Neoplastic. Humans. Molecular Mimicry. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Proteins / metabolism. Peptide Fragments / chemistry. Peptide Fragments / pharmacology. Protein Binding. Proto-Oncogene Proteins / chemistry. Proto-Oncogene Proteins / pharmacology. Tumor Cells, Cultured. bcl-X Protein / metabolism

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17227835.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BAK1 protein, human; 0 / BCL2L1 protein, human; 0 / Bax protein (53-86); 0 / Boronic Acids; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / PMAIP1 protein, human; 0 / Peptide Fragments; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / Pyrroles; 0 / bcl-2 Homologous Antagonist-Killer Protein; 0 / bcl-X Protein; 0 / obatoclax; 69G8BD63PP / Bortezomib
  •  go-up   go-down


90. Hisatake J, Kawakami K, Nakamaki T, Hino K, Tomoyasu S: [Primary subcutaneous mantle cell lymphoma treated successfully with THP-COP therapy]. Rinsho Ketsueki; 2002 May;43(5):384-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Primary subcutaneous mantle cell lymphoma treated successfully with THP-COP therapy].
  • A 73-year-old man noticed a subcutaneous tumor on the left upper palpebra from April 1998, but did not seek therapy for it.
  • Facial subcutaneous tumors appeared from November 1999, and multiple tumors appeared on the skin of the chest and both upper arms from January 2000.
  • The karyotype was t(11;14) (q13;q32), but bcl-1 gene rearrangement was not detected.
  • On the basis of these data, primary mantle cell lymphoma (MCL) of the subcutis was diagnosed.
  • The patient underwent eight courses of THP-COP therapy, and complete remission was achieved.
  • Primary subcutaneous B-cell lymphoma, especially MCL, is rare.
  • MCL is aggressive and difficult to cure; the median survival of patients is 3 to 5 years, and the 5-year survival is 30%.
  • However, the present patient showed a good response to chemotherapy, and complete remission has continued for 17 months since the MCL was first diagnosed.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Mantle-Cell / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Aged. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Doxorubicin / analogs & derivatives. Drug Administration Schedule. Humans. Male. Prednisolone / administration & dosage. Remission Induction. Vincristine / administration & dosage

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12096492.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; VEP-THP protocol
  •  go-up   go-down


91. Venkataraman G, Maududi T, Ozpuyan F, Bahar HI, Izban KF, Qin JZ, Alkan S: Induction of apoptosis and down regulation of cell cycle proteins in mantle cell lymphoma by flavopiridol treatment. Leuk Res; 2006 Nov;30(11):1377-84
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of apoptosis and down regulation of cell cycle proteins in mantle cell lymphoma by flavopiridol treatment.
  • Typical mantle cell lymphoma (MCL) is a distinct B-cell non-Hodgkin's lymphoma associated with over-expression of cyclin D1 related to translocation between the IgH and BCL-1 genes.
  • Due to the important functional interaction between cyclin D1 and cyclin dependent kinases, cyclin dependent kinase inhibitors such as flavopiridol are under consideration for treatment of patients with MCL.
  • The present study investigated the in vitro effects of flavopiridol on the MCL cell line (JeKo-1).
  • Flavopiridol at a dose of 10nmol/L induced apoptosis by 6h of treatment as noted by flow cytometric analysis, morphologic examination and Western blotting.
  • Furthermore, MCL cells exposed to flavopiridol showed down regulation of key cell cycle proteins acting at the restriction point control between the G1 and S phases.
  • The onset of flavopiridol-induced apoptosis also coincided with the down regulation of Mcl-1, anti-apoptotic protein.
  • Collectively, our data indicates that flavopiridol may have significant therapeutic potential in the context of MCL.
  • [MeSH-major] Apoptosis / drug effects. Cell Cycle Proteins / metabolism. Down-Regulation / drug effects. Flavonoids / pharmacology. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Mantle-Cell / metabolism. Piperidines / pharmacology
  • [MeSH-minor] Caspase 3 / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin D1 / metabolism. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Humans. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Proteins / metabolism. Poly(ADP-ribose) Polymerases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Retinoblastoma Protein / metabolism. Time Factors

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16624404.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Flavonoids; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Piperidines; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Retinoblastoma Protein; 136601-57-5 / Cyclin D1; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 45AD6X575G / alvocidib; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 3
  •  go-up   go-down


92. Czuczman MS, Leonard JP, Williams ME: Clinical roundtable monograph: Recent advances in the treatment of mantle cell lymphoma: a post-ASH 2009 discussion. Clin Adv Hematol Oncol; 2010 Apr;8(4 Suppl 8):1-14; quiz 2p following page 14
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical roundtable monograph: Recent advances in the treatment of mantle cell lymphoma: a post-ASH 2009 discussion.
  • Mantle cell lymphoma (MCL) is a rare subtype of non-Hodgkin lymphoma characterized by CD5 expression and a t(11;14) cytogenetic translocation that results in overexpression of the cyclin D1 gene.
  • Currently, there is no standard of care for the treatment of MCL, and patient prognosis is poor.
  • Traditional treatments for MCL rely on conventional chemotherapy agents, including cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).
  • The addition of the immunotherapeutic agent rituximab to this regimen (CHOP-R) has helped to improve patient response to treatment.
  • These treatments often provide good initial responses that are difficult to sustain.
  • In this clinical roundtable monograph, new strategies in the treatment of MCL are discussed.
  • Some of the drug classes examined here are proteasome inhibitors, inhibitors of the protein mammalian target of rapamycin (mTOR), the unique alkylating agent bendamustine, and immunomodulatory agents.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Immunologic Factors / therapeutic use. Lymphoma, Mantle-Cell / drug therapy. Nitrogen Mustard Compounds / therapeutic use. Protein Kinase Inhibitors / therapeutic use. TOR Serine-Threonine Kinases / antagonists & inhibitors
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived / therapeutic use. Antineoplastic Combined Chemotherapy Protocols. Bendamustine Hydrochloride. Cyclophosphamide. Doxorubicin. Humans. Prednisone. Rituximab. Vincristine


93. Pham LV, Tamayo AT, Li C, Bornmann W, Priebe W, Ford RJ: Degrasyn potentiates the antitumor effects of bortezomib in mantle cell lymphoma cells in vitro and in vivo: therapeutic implications. Mol Cancer Ther; 2010 Jul;9(7):2026-36
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Degrasyn potentiates the antitumor effects of bortezomib in mantle cell lymphoma cells in vitro and in vivo: therapeutic implications.
  • Mantle cell lymphoma (MCL) is an aggressive histotype of B-cell non-Hodgkin lymphoma that has increased in incidence over the past few decades and is incurable, usually poorly responsive to standard chemotherapy combinations, and associated with poor prognoses.
  • Discovering new therapeutic agents with low toxicity that produce better outcomes in patients with MCL is an ongoing challenge.
  • In the present study, we found that treatment of both typical and blastoid-variant MCL cells with degrasyn in combination with bortezomib resulted in synergistic growth inhibition and apoptosis induction in vitro.
  • The apoptosis in these cells was correlated with the downregulation of constitutive NF-kappaB and phosphorylated STAT3 activation, leading to the inhibition of c-Myc, cyclin D1, and bcl-2 protein expression and the upregulation of bax protein expression.
  • In vivo, degrasyn and bortezomib interacted to synergistically prevent tumor development and prolong survival durations in a xenotransplant severe combined immunodeficient mouse model of MCL.
  • These findings suggest that agents such as degrasyn that can pharmacologically target constitutively expressed NF-kappaB and STAT3 in MCL cells may be useful therapeutic agents for MCL when administered together with bortezomib.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Boronic Acids / pharmacology. Lymphoma, Mantle-Cell / drug therapy. Nitriles / pharmacology. Pyrazines / pharmacology. Pyridines / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Bortezomib. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Cells, Cultured. Cyanoacrylates. Cyclin D1 / genetics. Dose-Response Relationship, Drug. Drug Synergism. Female. Gene Expression Regulation, Leukemic / drug effects. Humans. Mice. Mice, SCID. NF-kappa B / metabolism. Phosphorylation. Proto-Oncogene Proteins c-myc / genetics. Reverse Transcriptase Polymerase Chain Reaction. STAT3 Transcription Factor / metabolism. Survival Analysis. Xenograft Model Antitumor Assays

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c)2010 AACR.
  • [Cites] Arch Pathol Lab Med. 2003 Apr;127(4):424-31 [12683869.001]
  • [Cites] Leuk Res. 2010 Jan;34(1):85-92 [19608275.001]
  • [Cites] Ann Oncol. 1996;7 Suppl 6:S35-9 [9010577.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3470-8 [17202319.001]
  • [Cites] Cancer Res. 2002 Sep 1;62(17):4996-5000 [12208752.001]
  • [Cites] Ann Oncol. 2009 Mar;20(3):520-5 [19074748.001]
  • [Cites] Clin Cancer Res. 2008 May 1;14(9):2756-62 [18451242.001]
  • [Cites] Br J Haematol. 2009 May;145(3):344-9 [19245430.001]
  • [Cites] Science. 1995 Mar 24;267(5205):1782-8 [7892601.001]
  • [Cites] Cancer Res. 2007 Apr 15;67(8):3912-8 [17440106.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):657-8 [15613690.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3175-84 [15070700.001]
  • [Cites] Blood Rev. 2009 Sep;23(5):205-16 [19362399.001]
  • [Cites] J Pathol. 2003 Jan;199(1):84-9 [12474230.001]
  • [Cites] J Clin Oncol. 2005 Aug 10;23(23):5347-56 [15983389.001]
  • [Cites] Ann Hematol. 2009 Sep;88(9):921-2 [19139889.001]
  • [Cites] Cancer Immunol Immunother. 2009 Jul;58(7):1023-32 [19002459.001]
  • [Cites] Leuk Lymphoma. 2008;49 Suppl 1:59-66 [18821434.001]
  • [Cites] Blood. 2004 Dec 1;104(12):3535-42 [15304387.001]
  • [Cites] Genes Dev. 2003 May 1;17(9):1101-14 [12695332.001]
  • [Cites] Cancer Cell. 2009 Apr 7;15(4):283-93 [19345327.001]
  • [Cites] Int J Cancer. 2008 Jul 1;123(1):56-65 [18386790.001]
  • [Cites] Leukemia. 2001 Nov;15(11):1785-91 [11681422.001]
  • [Cites] Ann Oncol. 1998;9 Suppl 5:S25-30 [9926234.001]
  • [Cites] Cancer Res. 2007 Dec 1;67(23):11291-9 [18056455.001]
  • [Cites] Leuk Res. 2006 Apr;30(4):497-501 [16203034.001]
  • [Cites] Clin Cancer Res. 2004 Jun 1;10(11):3839-52 [15173093.001]
  • [Cites] Int J Cancer. 2008 May 1;122(9):1987-98 [18172861.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4407-12 [14645431.001]
  • [Cites] Clin Cancer Res. 2008 Feb 1;14(3):788-96 [18245540.001]
  • [Cites] Cancer. 1998 Feb 1;82(3):567-75 [9452276.001]
  • [Cites] Cancer Res. 2007 Oct 15;67(20):9630-6 [17942891.001]
  • [Cites] Leuk Lymphoma. 2004 Jun;45(6):1255-60 [15360009.001]
  • [Cites] Hematol Oncol Clin North Am. 2008 Oct;22(5):953-63, ix [18954745.001]
  • [Cites] Immunity. 2002 Jan;16(1):37-50 [11825564.001]
  • [Cites] Clin Lymphoma Myeloma. 2006 Oct;7 Suppl 1:S24-32 [17101070.001]
  • [Cites] Anticancer Agents Med Chem. 2009 Nov;9(9):1024-38 [19663778.001]
  • [Cites] Blood. 2008 Apr 1;111(7):3701-13 [18160665.001]
  • [Cites] Clin Cancer Res. 2008 Sep 15;14(18):5759-68 [18794085.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4540-8 [16497967.001]
  • [Cites] J Clin Oncol. 2006 Oct 20;24(30):4867-74 [17001068.001]
  • [Cites] J Immunol. 2003 Jul 1;171(1):88-95 [12816986.001]
  • [Cites] Future Oncol. 2008 Apr;4(2):149-68 [18407730.001]
  • [Cites] Oncogene. 2007 Apr 12;26(17):2435-44 [17043651.001]
  • (PMID = 20606045.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA100836; United States / NCI NIH HHS / CA / CA-16672-26; United States / NCI NIH HHS / CA / CA-RO1-100836
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Cyanoacrylates; 0 / MYC protein, human; 0 / NF-kappa B; 0 / Nitriles; 0 / Proto-Oncogene Proteins c-myc; 0 / Pyrazines; 0 / Pyridines; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / degrasyn; 136601-57-5 / Cyclin D1; 69G8BD63PP / Bortezomib
  •  go-up   go-down


94. Witzig TE: Current treatment approaches for mantle-cell lymphoma. J Clin Oncol; 2005 Sep 10;23(26):6409-14
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current treatment approaches for mantle-cell lymphoma.
  • Mantle-cell lymphoma (MCL) is now recognized as a distinct clinicopathologic subtype of B-cell non-Hodgkin's lymphoma.
  • Patients with MCL are typically older adults with a male predominance and usually present with stage IV disease.
  • The cells are characterized as CD20+ CD5+ CD23- with a t(11;14)(q13;q32) and cyclin D1 overexpression on immunohistochemistry.
  • Response to chemotherapy usually results in a tumor response but unmaintained remissions are short and the median survival is 3 to 4 years.
  • The treatment approach to newly diagnosed patients with MCL depends on the patient's eligibility for stem cell transplantation (SCT).
  • Unfortunately none of these approaches can definitively cure patients with MCL, and new agents are needed.
  • Recent studies in patients with relapsed MCL have shown substantial antitumor activity of single-agent bortezomib, single-agent temsirolimus, and the combination of thalidomide and rituximab.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation / methods. Lymphoma, Mantle-Cell / mortality. Lymphoma, Mantle-Cell / therapy
  • [MeSH-minor] Combined Modality Therapy. Cyclophosphamide. Dose-Response Relationship, Drug. Doxorubicin. Drug Administration Schedule. Female. Humans. Male. Patient Selection. Prednisolone. Prognosis. Randomized Controlled Trials as Topic. Severity of Illness Index. Survival Analysis. Treatment Outcome. Vincristine

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16155027.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA25224; United States / NCI NIH HHS / CA / CA97274
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; VAP-cyclo protocol
  • [Number-of-references] 52
  •  go-up   go-down


95. Wang M, Zhang L, Han X, Yang J, Qian J, Hong S, Samaniego F, Romaguera J, Yi Q: Atiprimod inhibits the growth of mantle cell lymphoma in vitro and in vivo and induces apoptosis via activating the mitochondrial pathways. Blood; 2007 Jun 15;109(12):5455-62
antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Atiprimod inhibits the growth of mantle cell lymphoma in vitro and in vivo and induces apoptosis via activating the mitochondrial pathways.
  • This study was undertaken to evaluate the therapeutic efficacy of atiprimod on mantle cell lymphoma (MCL) and elucidate the mechanism by which it induces cell apoptosis.
  • Atiprimod inhibited the growth and induced apoptosis of MCL cell lines and freshly isolated primary tumor cells in vitro.
  • Atiprimod activated c-Jun N-terminal protein kinases (JNK) and up-regulated the level of Bax, Bad, and phosphorylated Bcl-2, resulting in release of apoptosis-inducing factor (AIF) and cytochrome c from mitochondria and activation and cleavage of caspase-9, caspase-3, and PARP.
  • However, AIF, but not activation of caspases or PARP, was responsible for apoptosis in MCL cells because an AIF inhibitor, but not pan-caspase or paspase-9 inhibitors, completely abrogated atiprimod-induced apoptosis.
  • Taken together, our results demonstrate that atiprimod displays a strong anti-MCL activity.
  • Cell apoptosis was induced mainly via activation of the AIF pathway.
  • These results support the use of atiprimod as a potential agent in MCL chemotherapy.
  • [MeSH-major] Apoptosis / drug effects. Cell Proliferation / drug effects. Lymphoma, Mantle-Cell / drug therapy. Mitochondria / drug effects. Spiro Compounds / pharmacology
  • [MeSH-minor] Animals. Apoptosis Regulatory Proteins / drug effects. Drug Evaluation, Preclinical. Mice. Mitochondrial Proteins / drug effects

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17317853.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Mitochondrial Proteins; 0 / Spiro Compounds; 123018-47-3 / azaspirane
  •  go-up   go-down


96. Hess G: Temsirolimus for the treatment of mantle cell lymphoma. Expert Rev Hematol; 2009 Dec;2(6):631-40
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Temsirolimus for the treatment of mantle cell lymphoma.
  • Although recent progress has been made in the treatment of mantle cell lymphoma (MCL) the majority of patients experience relapse and ultimately die of their disease.
  • The translocation t(11;14) is a prerequisite for the diagnosis of MCL and results in overexpression of cyclin D1.
  • Its protein translation is controlled by mTOR, a key element of the PI3K/Akt pathway, and mTOR constitutes an attractive therapeutic target.
  • Temsirolimus, a specific inhibitor of mTOR, has been evaluated in two Phase II trials in patients with relapsed MCL, and promising response rates up to 40% were found.
  • This adds temsirolimus to the therapeutic armamentarium for the treatment of MCL.
  • Further developments target combination therapy in MCL and other lymphoid neoplasms.
  • [MeSH-major] Antineoplastic Agents. Cyclin D1 / analysis. Cyclin D1 / metabolism. Intracellular Signaling Peptides and Proteins / metabolism. Lymphoma, Mantle-Cell. Sirolimus / analogs & derivatives. TOR Serine-Threonine Kinases / antagonists & inhibitors
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Clinical Trials as Topic. Disease-Free Survival. Drug Administration Schedule. Female. Humans. Male. Middle Aged. Remission Induction. Secondary Prevention


97. Calvopina M, Guevara AG, Armijos RX, Hashiguchi Y, Davidson RN, Cooper PJ: Itraconazole in the treatment of New World mucocutaneous leishmaniasis. Int J Dermatol; 2004 Sep;43(9):659-63
Hazardous Substances Data Bank. Itraconazole .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Itraconazole in the treatment of New World mucocutaneous leishmaniasis.
  • BACKGROUND: A well-tolerated oral drug is required for the treatment of mucocutaneous leishmaniasis (MCL).
  • Current parenteral treatment regimens with pentavalent antimonials are associated with marked toxicity and significant rates of relapse.
  • AIM: To evaluate the efficacy and tolerability of high-dose itraconazole for the treatment of MCL.
  • METHODS: An uncontrolled treatment study was performed in 13 Ecuadorian patients with MCL.
  • RESULTS: All 13 subjects responded to itraconazole during the first month of treatment, but by 12 months after treatment the complete resolution of MCL lesions was observed in only three (23%) subjects.
  • No adverse effects of treatment were reported.
  • Response to treatment was associated with a short evolution of the disease and mild to moderate disease severity.
  • CONCLUSION: Prolonged and high-dose treatment regimens with itraconazole are not effective for the treatment of the majority of patients with MCL.
  • [MeSH-major] Antiprotozoal Agents / therapeutic use. Itraconazole / therapeutic use. Leishmaniasis, Mucocutaneous / drug therapy
  • [MeSH-minor] Administration, Oral. Adult. Female. Humans. Male. Middle Aged. Treatment Outcome

  • Genetic Alliance. consumer health - Leishmaniasis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15357745.001).
  • [ISSN] 0011-9059
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiprotozoal Agents; 304NUG5GF4 / Itraconazole
  •  go-up   go-down


98. Murali S, Winton E, Waller EK, Heffner LT, Lonial S, Flowers C, Kaufman J, Arellano M, Lechowicz MJ, Mann KP, Khoury HJ, Langston AA: Long-term progression-free survival after early autologous transplantation for mantle-cell lymphoma. Bone Marrow Transplant; 2008 Oct;42(8):529-34
Hazardous Substances Data Bank. VINCRISTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term progression-free survival after early autologous transplantation for mantle-cell lymphoma.
  • Autologous hematopoietic progenitor SCT (HPCT) has been studied both as a consolidative and salvage maneuver in mantle-cell lymphoma (MCL), and may improve failure-free survival rates as well as overall survival.
  • We describe 21 patients with MCL who received autologous HPCT at Emory University Hospital as part of the primary treatment strategy.
  • Sixteen patients were in CR1 and five in PR1 at the time of HPCT.
  • The most commonly used induction chemotherapy was the hyper-CVAD (cyclophosphamide, vincristine, doxorubicin and dexamethasone) regimen with or without rituximab.
  • With a median follow-up of 54 months from HPCT, 5-year progression-free survival and overall survival are 73% and 76%, respectively.
  • Our retrospective analysis provides the longest follow-up to date for patients with MCL who received an autologous HPCT as part of primary treatment.
  • This lengthy follow-up helps define the natural course of MCL after autologous transplantation.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Lymphoma, Mantle-Cell / mortality. Lymphoma, Mantle-Cell / therapy
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cyclophosphamide / administration & dosage. Dexamethasone / administration & dosage. Disease-Free Survival. Doxorubicin / administration & dosage. Female. Follow-Up Studies. Humans. Male. Middle Aged. Recurrence. Salvage Therapy. Survival Rate. Transplantation, Autologous. Vincristine / administration & dosage

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Genetic Alliance. consumer health - Transplantation.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18622414.001).
  • [ISSN] 1476-5365
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; CVAD protocol
  •  go-up   go-down


99. O'Connor OA: Mantle cell lymphoma: identifying novel molecular targets in growth and survival pathways. Hematology Am Soc Hematol Educ Program; 2007;:270-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mantle cell lymphoma: identifying novel molecular targets in growth and survival pathways.
  • Mantle cell lymphoma (MCL) remains one of the more challenging sub-types of non-Hodgkin lymphoma.
  • This entity, which is only approximately 10 years old, is characterized by response to many different chemotherapy regimens, though the duration of those responses remains often times quite short.
  • Retreatment with second and third line combination regimens results in shorter and shorter durations of response, with the rapid emergence of a very drug-resistant phenotype.
  • Despite these often frustrating clinical features, there is now a lot of new hope in managing patients with MCL.
  • New insights into the molecular pathogenesis of MCL has revealed a plethora of new potential targets, while our continued efforts in novel targeted drug development has produced a host of agents that are already helping patients with this challenging disease.
  • The use of proteasome inhibitors, for example, represents one example of a new strategy that has offered new hope for patients, and new opportunities for the physician treating this disease.
  • In this review, we will put this biology into perspective, and describe how new revelations in MCL pathogenesis are leading to the identification of many exciting new drugs with promising activity.

  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18024640.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 136601-57-5 / Cyclin D1
  •  go-up   go-down


100. Forstpointner R, Unterhalt M, Dreyling M, Böck HP, Repp R, Wandt H, Pott C, Seymour JF, Metzner B, Hänel A, Lehmann T, Hartmann F, Einsele H, Hiddemann W, German Low Grade Lymphoma Study Group (GLSG): Maintenance therapy with rituximab leads to a significant prolongation of response duration after salvage therapy with a combination of rituximab, fludarabine, cyclophosphamide, and mitoxantrone (R-FCM) in patients with recurring and refractory follicular and mantle cell lymphomas: Results of a prospective randomized study of the German Low Grade Lymphoma Study Group (GLSG). Blood; 2006 Dec 15;108(13):4003-8
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Maintenance therapy with rituximab leads to a significant prolongation of response duration after salvage therapy with a combination of rituximab, fludarabine, cyclophosphamide, and mitoxantrone (R-FCM) in patients with recurring and refractory follicular and mantle cell lymphomas: Results of a prospective randomized study of the German Low Grade Lymphoma Study Group (GLSG).
  • In follicular lymphoma (FL) and mantle cell lymphoma (MCL) the monoclonal antibody rituximab (R) improves the prognosis when combined with chemotherapy.
  • The present study investigated R-maintenance after R-chemotherapy.
  • Patients with recurring or refractory FL and MCL were randomized to 4 courses of fludarabine, cyclophosphamide, and mitoxantrone (FCM) alone or combined with R (R-FCM).
  • Responding patients underwent a second randomization for R-maintenance comprising 2 further courses of 4-times-weekly doses of R after 3 and 9 months.
  • This beneficial effect was also observed when analyzing FL (P = .035) and MCL (P = .049) separately.
  • Hence, R-maintenance is effective after salvage with R-chemotherapy and significantly prolongs response duration in patients with recurring or refractory FL or MCL.
  • [MeSH-major] Lymphoma, Follicular / drug therapy. Lymphoma, Mantle-Cell / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols. Cyclophosphamide / administration & dosage. Disease-Free Survival. Female. Germany. Humans. Male. Middle Aged. Mitoxantrone / administration & dosage. Prospective Studies. Recurrence. Remission Induction. Rituximab. Salvage Therapy / methods. Survival Rate. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives






Advertisement