[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 47 of about 47
1. Zent CS, LaPlant BR, Johnston PB, Call TG, Habermann TM, Micallef IN, Witzig TE: The treatment of recurrent/refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL) with everolimus results in clinical responses and mobilization of CLL cells into the circulation. Cancer; 2010 May 1;116(9):2201-7
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] The treatment of recurrent/refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL) with everolimus results in clinical responses and mobilization of CLL cells into the circulation.
  • BACKGROUND: Patients with recurrent/refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL) often have chemotherapy-resistant disease, resulting in poor prognosis.
  • METHODS: This was a phase 2 study of oral single-agent everolimus (10 mg/day) for recurrent/refractory indolent lymphoid malignancies including CLL.
  • RESULTS: Four of 22 patients with CLL (18%; 95% confidence interval, 5%-40%) achieved a partial remission to therapy.
  • An unanticipated finding in this study was an increase in absolute lymphocyte count (ALC) associated with a decrease in lymphadenopathy in 8 (36%) patients.
  • Because CLL cells in lymphatic tissue and bone marrow can be more resistant to therapy than circulating CLL cells, the ability of everolimus to mobilize CLL cells into the circulation could be used in combination therapeutic regimens.

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. SIROLIMUS .
  • 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 American Cancer Society.
  • [Cites] J Clin Oncol. 1999 Apr;17(4):1244 [10561185.001]
  • [Cites] J Clin Invest. 2005 Mar;115(3):755-64 [15711642.001]
  • [Cites] Cancer. 2001 Sep 1;92(5):1325-30 [11571749.001]
  • [Cites] Blood. 2002 May 15;99(10):3554-61 [11986207.001]
  • [Cites] N Engl J Med. 2002 Aug 8;347(6):452-3 [12167696.001]
  • [Cites] Blood. 2003 Jan 1;101(1):278-85 [12393642.001]
  • [Cites] Cancer. 2004 Feb 15;100(4):657-66 [14770419.001]
  • [Cites] Blood. 2004 May 1;103(9):3278-81 [14726385.001]
  • [Cites] Br J Haematol. 1996 Apr;93(1):151-3 [8611450.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Leuk Lymphoma. 2005 Jan;46(1):11-9 [15621776.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4070-8 [15767647.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4079-88 [15767648.001]
  • [Cites] J Clin Oncol. 2005 Aug 10;23(23):5347-56 [15983389.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2005;:292-8 [16304394.001]
  • [Cites] Br J Cancer. 2006 Oct 23;95(8):955-60 [16953237.001]
  • [Cites] Blood. 2007 Jan 15;109(2):405-11 [17008537.001]
  • [Cites] Leuk Res. 2007 Jul;31(7):899-906 [17241660.001]
  • [Cites] Br J Haematol. 2007 Nov;139(4):600-4 [17979945.001]
  • [Cites] Cancer. 2008 Aug 1;113(3):508-14 [18543327.001]
  • [Cites] J Intern Med. 2008 Dec;264(6):549-62 [19017179.001]
  • [Cites] Leuk Lymphoma. 2008 Dec;49(12):2235-6 [19052968.001]
  • [Cites] Leuk Lymphoma. 2008 Dec;49(12):2333-43 [19052982.001]
  • [Cites] Ann Hematol. 2009 Mar;88(3):221-7 [18704419.001]
  • [Cites] Oncogene. 2000 Dec 27;19(56):6680-6 [11426655.001]
  • (PMID = 20166206.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA097274-04; United States / NCI NIH HHS / CA / P50 CA097274; United States / NCI NIH HHS / CA / CA97274; United States / NCI NIH HHS / CA / P50 CA097274-04
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 9HW64Q8G6G / Everolimus; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS189697; NLM/ PMC2861142
  •  go-up   go-down


2. Perkins JG, Flynn JM, Howard RS, Byrd JC: Frequency and type of serious infections in fludarabine-refractory B-cell chronic lymphocytic leukemia and small lymphocytic lymphoma: implications for clinical trials in this patient population. Cancer; 2002 Apr 1;94(7):2033-9
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] Frequency and type of serious infections in fludarabine-refractory B-cell chronic lymphocytic leukemia and small lymphocytic lymphoma: implications for clinical trials in this patient population.
  • BACKGROUND: Treatments for fludarabine-refractory chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) are limited.
  • Most new therapies being examined in fludarabine-refractory patients have shown a high frequency of serious infection.
  • Little data exist regarding the frequency of infections in this population treated with noninvestigational best supportive care therapies.
  • METHODS: The infectious courses of 27 patients with fludarabine-refractory CLL/SLL were retrospectively reviewed.
  • Fludarabine-refractoriness was defined as either relapse within six months of completion of or failure to respond to fludarabine treatment.
  • Infections were documented after patients met National Cancer Institute criteria for further treatment.
  • RESULTS: Patient characteristics included: median age 67 years (range, 40-83), median 3 chemotherapy treatments (range, 1-8), and hypogammaglobulinemia in 73% of patients.
  • Serious infections developed in 24 out of 27 patients (89%).
  • Most common sites for infection in decreasing frequency were: respiratory tract, urinary tract, blood/sepsis, and soft tissues.
  • CONCLUSIONS: The frequency of serious infections in patients with fludarabine-refractory CLL/SLL is high.
  • These findings are relevant to trials with new and highly effective agents for which the incidence of serious infections after treatment might otherwise appear to be prohibitively high.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Opportunistic Infections / complications. Vidarabine / therapeutic use

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • 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 2002 American Cancer Society.
  • (PMID = 11932906.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA 81534-02
  • [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 / Antineoplastic Agents; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  •  go-up   go-down


3. Schnaiter A, Stilgenbauer S: Refractory chronic lymphocytic leukemia--new therapeutic strategies. Oncotarget; 2010 Nov;1(7):472-82
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] Refractory chronic lymphocytic leukemia--new therapeutic strategies.
  • Treatment outcome of chronic lymphocytic leukemia (CLL) has considerably improved since the introduction of fludarabine (F) as part of the standard therapy.
  • For this subgroup the CD52 antibody alemtuzumab (A) presents a new treatment approach and has already been approved.
  • Importantly, the monoclonal CD20 antibody ofatumumab has now shown efficacy in F and A double-refractory CLL.
  • Further B-cell antigens are targeted by lumiliximab (CD23), TRU-016 (CD37) and blinatumomab (CD19).
  • Apart from monoclonal antibody therapies, a great number of small molecules are examined for the treatment of refractory and relapsed CLL.
  • Typical targets are regulators of the cell cycle and antiapoptotic molecules like the members of the Bcl-2 family.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Therapies, Investigational / methods
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Histone Deacetylase Inhibitors / therapeutic use. Humans. Immunotherapy / methods. Recurrence. Survival Analysis. Vidarabine / analogs & derivatives. Vidarabine / therapeutic use

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2009 Dec 10;27(35):6012-8 [19826119.001]
  • [Cites] Blood. 2000 Jul 15;96(2):393-7 [10887097.001]
  • [Cites] J Clin Oncol. 2009 Aug 20;27(24):3994-4001 [19597025.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2165-70 [11304768.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1326-31 [11520778.001]
  • [Cites] Blood. 2002 May 15;99(10):3554-61 [11986207.001]
  • [Cites] Cancer. 2003 Apr 1;97(7):1711-20 [12655528.001]
  • [Cites] Leuk Lymphoma. 2010 Jan;51(1):85-8 [20055660.001]
  • [Cites] Blood. 2010 Jan 21;115(3):489-95 [19843887.001]
  • [Cites] J Clin Oncol. 2010 Apr 1;28(10):1749-55 [20194866.001]
  • [Cites] Cancer. 2010 May 15;116(10):2360-5 [20225334.001]
  • [Cites] Lancet. 2010 Oct 2;376(9747):1164-74 [20888994.001]
  • [Cites] J Clin Oncol. 2010 Oct 10;28(29):4473-9 [20697090.001]
  • [Cites] Blood. 2011 Apr 28;117(17):4519-29 [21378274.001]
  • [Cites] Blood. 2003 May 1;101(9):3413-5 [12522009.001]
  • [Cites] Blood. 1995 Mar 15;85(6):1580-9 [7888675.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1165-71 [9694704.001]
  • [Cites] Blood. 1998 Nov 15;92(10):3804-16 [9808574.001]
  • [Cites] Blood. 2005 Feb 1;105(3):959-67 [15466934.001]
  • [Cites] Clin Cancer Res. 2005 Jun 1;11(11):4176-81 [15930354.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4070-8 [15767647.001]
  • [Cites] Leuk Res. 2005 Nov;29(11):1253-7 [15916806.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):7024-31 [16145065.001]
  • [Cites] J Clin Oncol. 2005 Oct 20;23(30):7697-702 [16186597.001]
  • [Cites] J Clin Oncol. 2006 Dec 1;24(34):5343-9 [17088571.001]
  • [Cites] Exp Hematol. 2006 Dec;34(12):1663-9 [17157163.001]
  • [Cites] J Clin Oncol. 2007 Mar 20;25(9):1114-20 [17296974.001]
  • [Cites] Lancet. 2007 Jul 21;370(9583):230-9 [17658394.001]
  • [Cites] Clin Cancer Res. 2007 Aug 1;13(15 Pt 1):4448-55 [17671129.001]
  • [Cites] Exp Hematol. 2007 Oct;35(10):1527-37 [17697742.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1094-100 [18003886.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3421-8 [18451170.001]
  • [Cites] Blood. 2008 Jun 1;111(11):5291-7 [18334676.001]
  • [Cites] Blood. 2008 Aug 15;112(4):975-80 [18411418.001]
  • [Cites] Blood. 2008 Aug 15;112(4):1443-52 [18550857.001]
  • [Cites] Eur J Haematol. 2008 Sep;81(3):170-6 [18510700.001]
  • [Cites] Br J Haematol. 2008 Dec;143(5):698-706 [19062342.001]
  • [Cites] Blood. 2009 Jan 1;113(1):149-53 [18836097.001]
  • [Cites] Blood. 2009 Jan 8;113(2):299-305 [18931344.001]
  • [Cites] Blood. 2009 Mar 19;113(12):2637-45 [18981292.001]
  • [Cites] Blood. 2009 Apr 30;113(18):4403-13 [19008458.001]
  • [Cites] N Engl J Med. 2000 Dec 14;343(24):1750-7 [11114313.001]
  • [CommentIn] Oncotarget. 2011 Oct;2(10):737-8 [22006556.001]
  • (PMID = 21317446.001).
  • [ISSN] 1949-2553
  • [Journal-full-title] Oncotarget
  • [ISO-abbreviation] Oncotarget
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Histone Deacetylase Inhibitors; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ PMC3248129
  •  go-up   go-down


Advertisement
4. Tsurumi S, Nakamura Y, Tadokoro J, Arai Y, Saito K, Furusawa S, Mitani K: [Small lymphocytic lymphoma during the course of pure red cell aplasia]. Rinsho Ketsueki; 2002 Nov;43(11):1020-2
Genetic Alliance. consumer health - Pure red cell aplasia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Small lymphocytic lymphoma during the course of pure red cell aplasia].
  • A 29-year-old woman was diagnosed as having pure red cell aplasia (PRCA) in 1983.
  • However, she relapsed in 1995 and her anemia became refractory to immunosuppressive therapy.
  • In 1998, she developed systemic lymph node enlargement and was diagnosed as having B-cell small lymphocytic lymphoma.
  • Combination chemotherapy resulted in regression of the lesion, but failed to improve the anemia.
  • In this patient's case, we can speculate that B cells producing autoantibodies against erythroid cells have undergone transformation, or alternatively that the immunosuppressive state caused by the PRCA therapy promoted generation of a neoplastic B cell clone.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / etiology. Red-Cell Aplasia, Pure / complications

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12508490.001).
  • [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
  •  go-up   go-down


5. Thieblemont C, Bouafia F, Hornez E, Dumontet C, Tartas S, Antal D, Lemieux B, Traullé C, Espinouse D, Salles G, Coiffier B: Maintenance therapy with a monthly injection of alemtuzumab prolongs response duration in patients with refractory B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma (B-CLL/SLL). Leuk Lymphoma; 2004 Apr;45(4):711-4
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] Maintenance therapy with a monthly injection of alemtuzumab prolongs response duration in patients with refractory B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma (B-CLL/SLL).
  • Alemtuzumab, the monoclonal anti-CD52 antibody, has clinical activity in B-cell and T-cell malignancies at the dose of 30 mg three times weekly for 9-12 weeks.
  • To prolong time to progression, we initialized a phase II study with an identical initial scheme until partial response, followed by a maintenance therapy lasting at least 4 months.
  • Eleven heavily pretreated patients (8 with B-chronic lymhocytic leukemia (B-CLL) and 3 with small lymphoctyic lymphoma (SLL)) have been treated with this maintenance regimen (MR patients) and were retrospectively compared to 5 patients (3 B-CLL and 2 SLL) treated with the standard regimen (SR patients).
  • Patients characteristics before treatment were identical in both groups.
  • After the treatment, 8 (73%) MR patients and all SR patients progressed with a median time at 12.2 months and 3 months respectively.
  • Survival time from alemtuzumab was significatively different (P < 0.005).
  • None of the patients died in the MR group with a median follow-up at 16 months.
  • In conclusion, maintenance alemtuzumab therapy seems to increase the time to progression and the survival, without adding hematological toxicities and infectious complications.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antibodies, Neoplasm / administration & dosage. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Antibodies, Monoclonal, Humanized. Disease-Free Survival. Drug Administration Schedule. Female. Hematologic Diseases / chemically induced. Humans. Male. Middle Aged. Opportunistic Infections / chemically induced. Remission Induction / methods. Salvage Therapy / methods. Survival Analysis


6. Barr PM, Fu P, Lazarus HM, Horvath N, Gerson SL, Koc ON, Bahlis NJ, Snell MR, Dowlati A, Cooper BW: Phase I trial of fludarabine, bortezomib and rituximab for relapsed and refractory indolent and mantle cell non-Hodgkin lymphoma. Br J Haematol; 2009 Oct;147(1):89-96
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of fludarabine, bortezomib and rituximab for relapsed and refractory indolent and mantle cell non-Hodgkin lymphoma.
  • Based on the hypothesis that bortezomib may potentiate fludarabine activity by inhibiting DNA repair, we designed a phase I trial using this combination with rituximab in patients with relapsed and refractory indolent and mantle cell non-Hodgkin lymphoma.
  • Non-Hodgkin lymphoma subtypes included 12 patients with follicular lymphoma, four with marginal zone lymphoma, three with lymphoplasmacytic lymphoma, three with mantle cell lymphoma and two with small lymphocytic/chronic lymphocytic leukaemia.
  • Clinical responses were observed in 11 patients, five of whom were refractory to their most recent treatment regimen.

  • Genetic Alliance. consumer health - Hodgkin lymphoma.
  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Genetic Alliance. consumer health - Non-Hodgkin Lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • [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] Chem Biol. 2001 Aug;8(8):739-58 [11514224.001]
  • [Cites] J Clin Oncol. 2002 Aug 1;20(15):3262-9 [12149300.001]
  • [Cites] Blood. 2003 Jan 1;101(1):6-14 [12393429.001]
  • [Cites] Blood. 2003 Feb 15;101(4):1530-4 [12393500.001]
  • [Cites] Blood. 2003 Mar 15;101(6):2377-80 [12424198.001]
  • [Cites] Br J Haematol. 2003 Jun;121(6):913-8 [12786803.001]
  • [Cites] N Engl J Med. 2003 Jun 26;348(26):2691-4; discussion 2691-4 [12826650.001]
  • [Cites] Haematologica. 2004 Mar;89(3):361-3 [15020279.001]
  • [Cites] Bone Marrow Transplant. 2004 May;33(9):921-3 [15034544.001]
  • [Cites] N Engl J Med. 1984 Dec 6;311(23):1471-5 [6548796.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Cancer Res. 1999 Jun 1;59(11):2615-22 [10363983.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):712-9 [15613695.001]
  • [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 Feb 1;23(4):694-704 [15681517.001]
  • [Cites] Eur J Haematol. 2005 May;74(5):407-17 [15813915.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3725-32 [16123223.001]
  • [Cites] J Clin Oncol. 2006 May 1;24(13):2105-12 [16606971.001]
  • [Cites] Clin Cancer Res. 2006 May 1;12(9):2902-11 [16675587.001]
  • [Cites] J Clin Oncol. 2006 Oct 20;24(30):4867-74 [17001068.001]
  • [Cites] Ann Oncol. 2007 Jan;18(1):116-21 [16971665.001]
  • [Cites] Ann Oncol. 2007 Feb;18(2):364-9 [17079695.001]
  • [Cites] J Biol Chem. 2007 Jun 15;282(24):17330-4 [17478428.001]
  • [Cites] Cancer Invest. 2007 Dec;25(8):766-75 [18058474.001]
  • [Cites] J Clin Oncol. 2008 Jan 10;26(2):204-10 [18182663.001]
  • [Cites] Leukemia. 2008 Jan;22(1):179-85 [17898787.001]
  • [Cites] Blood. 2008 May 1;111(9):4681-9 [18227347.001]
  • [Cites] Med Oncol. 2008;25(4):374-9 [18278570.001]
  • [Cites] J Clin Oncol. 2009 Feb 1;27(4):511-8 [19075279.001]
  • [Cites] J Peripher Nerv Syst. 2008 Dec;13(4):275-82 [19192067.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6069-76 [19380866.001]
  • [Cites] J Clin Oncol. 2009 Oct 20;27(30):5023-30 [19770386.001]
  • [CommentIn] Br J Haematol. 2010 Mar;148(5):810-2 [19919649.001]
  • (PMID = 19656151.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA043703-19; United States / NCI NIH HHS / CA / U01 CA062502-15; United States / NCI NIH HHS / CA / CA043703-19; United States / NCI NIH HHS / CA / U01 CA062502; United States / NCRR NIH HHS / RR / M01RR00080; United States / NCI NIH HHS / CA / P30 CA043703; United States / NCI NIH HHS / CA / CA62502; None / None / / U01 CA062502-15; United States / NCI NIH HHS / CA / P30 CA43703; United States / NCRR NIH HHS / RR / M01 RR000080
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Boronic Acids; 0 / Pyrazines; 4F4X42SYQ6 / Rituximab; 69G8BD63PP / Bortezomib; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ NIHMS174604; NLM/ PMC2827854
  •  go-up   go-down


7. Kahl BS, Bartlett NL, Leonard JP, Chen L, Ganjoo K, Williams ME, Czuczman MS, Robinson KS, Joyce R, van der Jagt RH, Cheson BD: Bendamustine is effective therapy in patients with rituximab-refractory, indolent B-cell non-Hodgkin lymphoma: results from a Multicenter Study. Cancer; 2010 Jan 1;116(1):106-14
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bendamustine is effective therapy in patients with rituximab-refractory, indolent B-cell non-Hodgkin lymphoma: results from a Multicenter Study.
  • In this multicenter study, the authors evaluated the efficacy and toxicity of single-agent bendamustine in patients with rituximab-refractory, indolent B-cell lymphoma.
  • Histologies included follicular (62%), small lymphocytic (21%), and marginal zone (16%) lymphomas.
  • Patients had received a median of 2 previous regimens (range, 0-6 previous regimens), and 36%were refractory to their most recent chemotherapy regimen.
  • Six deaths were considered to be possibly treatment related.
  • CONCLUSIONS: Single-agent bendamustine produced a high rate of objective responses with acceptable toxicity in patients with recurrent, rituximab-refractory indolent B-cell lymphoma.

  • Genetic Alliance. consumer health - Hodgkin lymphoma.
  • Genetic Alliance. consumer health - Indolent B cell lymphoma.
  • Genetic Alliance. consumer health - Non-Hodgkin Lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Bendamustine .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 American Cancer Society.
  • [Cites] J Clin Oncol. 2002 Aug 1;20(15):3262-9 [12149300.001]
  • [Cites] Anticancer Drugs. 2001 Oct;12(9):725-9 [11593053.001]
  • [Cites] J Clin Oncol. 2003 Mar 1;21(5):897-906 [12610191.001]
  • [Cites] Leuk Lymphoma. 2004 Sep;45(9):1821-7 [15223642.001]
  • [Cites] Anticancer Drugs. 1996 Jun;7(4):415-21 [8826610.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):712-9 [15613695.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1417-23 [15494430.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3383-9 [15908650.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4576-82 [15731177.001]
  • [Cites] Blood. 2005 Jun 15;105(12):4573-5 [15741224.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3725-32 [16123223.001]
  • [Cites] J Cancer Res Clin Oncol. 2006 Feb;132(2):105-12 [16088404.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2006;:368-74 [17124085.001]
  • [Cites] J Clin Oncol. 2007 May 20;25(15):1986-92 [17420513.001]
  • [Cites] Leuk Lymphoma. 2007 Jul;48(7):1299-306 [17613757.001]
  • [Cites] J Clin Oncol. 2007 Sep 20;25(27):4285-92 [17709799.001]
  • [Cites] Clin Cancer Res. 2008 Jan 1;14(1):309-17 [18172283.001]
  • [Cites] J Clin Oncol. 2008 Jan 10;26(2):204-10 [18182663.001]
  • [Cites] Clin Cancer Res. 2008 Mar 1;14(5):1550-60 [18316580.001]
  • [Cites] Clin Cancer Res. 2008 Mar 1;14(5):1561-70 [18316581.001]
  • [Cites] J Clin Oncol. 2008 Sep 20;26(27):4473-9 [18626004.001]
  • [Cites] J Clin Oncol. 1999 Apr;17(4):1244 [10561185.001]
  • [Cites] J Cancer Res Clin Oncol. 2002 Nov;128(11):603-9 [12458340.001]
  • (PMID = 19890959.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [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] Clinical Trial, Phase III; 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; 0 / Antineoplastic Agents; 0 / Nitrogen Mustard Compounds; 4F4X42SYQ6 / Rituximab; 981Y8SX18M / Bendamustine Hydrochloride
  • [Other-IDs] NLM/ NIHMS213240; NLM/ PMC2916680
  •  go-up   go-down


8. Woyach JA, Lin TS, Lucas MS, Heerema N, Moran ME, Cheney C, Lucas DM, Wei L, Caligiuri MA, Byrd JC: A phase I/II study of rituximab and etanercept in patients with chronic lymphocytic leukemia and small lymphocytic lymphoma. Leukemia; 2009 May;23(5):912-8
Hazardous Substances Data Bank. VIDARABINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I/II study of rituximab and etanercept in patients with chronic lymphocytic leukemia and small lymphocytic lymphoma.
  • Rituximab has modest activity in relapsed chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma but is associated with tumor necrosis factor-alpha (TNF-alpha) release that can cause CLL proliferation and inhibit apoptosis.
  • The 36 enrolled patients had a median of two prior treatments; 50% were fludarabine refractory and 22% had del(17p13.1).
  • Response was not affected by prior rituximab or fludarabine-refractory status, but no patients with del(17p13.1) responded.
  • Ten patients have had treatment-free intervals exceeding 12 months, including four who have remained untreated for 32, 43, 46 and 56 months.

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. Etanercept .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2007 Mar 1;25(7):799-804 [17283363.001]
  • [Cites] Haematologica. 2006 Jun;91(6 Suppl):ECR23 [16785126.001]
  • [Cites] Lancet. 2007 Jul 21;370(9583):230-9 [17658394.001]
  • [Cites] Best Pract Res Clin Haematol. 2007 Sep;20(3):455-68 [17707833.001]
  • [Cites] Blood. 2008 Jun 15;111(12):5446-56 [18216293.001]
  • [Cites] J Clin Oncol. 1999 Jun;17(6):1962-3 [10561242.001]
  • [Cites] Cancer Immunol Immunother. 2000 Mar;48(12):673-83 [10752475.001]
  • [Cites] Blood Cells Mol Dis. 2000 Apr;26(2):133-43 [10753604.001]
  • [Cites] Blood. 2000 May 15;95(10):3052-6 [10807768.001]
  • [Cites] Blood. 2000 Jun 15;95(12):3900-8 [10845926.001]
  • [Cites] Med Oncol. 2000 Aug;17(3):203-10 [10962531.001]
  • [Cites] N Engl J Med. 2000 Dec 14;343(24):1750-7 [11114313.001]
  • [Cites] N Engl J Med. 2000 Dec 28;343(26):1910-6 [11136261.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2153-64 [11304767.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2165-70 [11304768.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1326-31 [11520778.001]
  • [Cites] Blood. 2001 Oct 15;98(8):2319-25 [11588025.001]
  • [Cites] Blood. 2002 Feb 1;99(3):754-8 [11806974.001]
  • [Cites] Blood. 2002 May 15;99(10):3554-61 [11986207.001]
  • [Cites] Cancer Chemother Pharmacol. 2002 Sep;50(3):237-42 [12203106.001]
  • [Cites] Blood. 2003 Jan 1;101(1):6-14 [12393429.001]
  • [Cites] Cancer Res. 2003 Jan 1;63(1):36-8 [12517774.001]
  • [Cites] J Clin Oncol. 2003 Nov 1;21(21):3940-7 [12975461.001]
  • [Cites] Blood. 2004 Feb 15;103(4):1472-4 [14563637.001]
  • [Cites] Blood. 1975 Aug;46(2):219-34 [1139039.001]
  • [Cites] Control Clin Trials. 1989 Mar;10(1):1-10 [2702835.001]
  • [Cites] J Natl Cancer Inst. 1992 Sep 16;84(18):1422-7 [1512794.001]
  • [Cites] Eur J Cancer. 1994;30A(9):1259-63 [7999409.001]
  • [Cites] Blood. 1995 Jan 15;85(2):307-18 [7811987.001]
  • [Cites] J Immunol. 1995 Nov 15;155(10):5038-45 [7594512.001]
  • [Cites] Lancet. 1996 May 25;347(9013):1432-8 [8676625.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Immunol Cell Biol. 1997 Apr;75(2):127-35 [9107564.001]
  • [Cites] Blood. 1998 Jun 1;91(11):4342-9 [9596683.001]
  • [Cites] J Clin Oncol. 1998 Aug;16(8):2825-33 [9704735.001]
  • [Cites] Eur J Haematol. 1999 Feb;62(2):76-82 [10052709.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):791-5 [10071268.001]
  • [Cites] Blood. 2005 Jan 1;105(1):49-53 [15138165.001]
  • [Cites] J Clin Oncol. 2005 Jun 20;23(18):4070-8 [15767647.001]
  • [Cites] J Immunol Methods. 2005 Sep;304(1-2):88-99 [16109421.001]
  • [Cites] J Clin Oncol. 2006 Jan 20;24(3):437-43 [16344317.001]
  • [Cites] Blood. 2006 Feb 1;107(3):885-91 [16219797.001]
  • [Cites] Curr Opin Hematol. 2006 Jul;13(4):266-72 [16755224.001]
  • [Cites] J Clin Oncol. 2007 Mar 1;25(7):793-8 [17283364.001]
  • (PMID = 19225537.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA095426; United States / NCI NIH HHS / CA / P01 CA9542
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; 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; 0 / Immunoglobulin G; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; 4F4X42SYQ6 / Rituximab; FA2DM6879K / Vidarabine; OP401G7OJC / Etanercept; P2K93U8740 / fludarabine
  • [Other-IDs] NLM/ NIHMS79899; NLM/ PMC4099250
  •  go-up   go-down


9. Haas RL, Poortmans P, de Jong D, Verheij M, van der Hulst M, de Boer JP, Bartelink H: Effective palliation by low dose local radiotherapy for recurrent and/or chemotherapy refractory non-follicular lymphoma patients. Eur J Cancer; 2005 Aug;41(12):1724-30
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effective palliation by low dose local radiotherapy for recurrent and/or chemotherapy refractory non-follicular lymphoma patients.
  • In this work, we have studied the response rates and duration of response after low-dose (4 Gy) involved field radiotherapy (LD-IF-RT) in relapsed or chemotherapy refractory indolent and aggressive lymphoma patients.
  • 71 patients (177 symptomatic sites) received LD-IF-RT consisting of 39 males and 32 females with a median age of 69 years (range 43-93).
  • Patients included were those with small lymphocytic lymphoma/chronic lymphocytic leukaemia (n=23), marginal zone lymphoma, nodal type (n=18), mantle cell lymphoma (n=17), and diffuse large B-cell lymphoma (n=13).
  • A median of two prior chemotherapy regimens (range 0-10) preceded LD-IF-RT.
  • Median time since diagnosis was 31 months (range 1-216 months).
  • Time to (local) progression was calculated according to the Kaplan-Meier method.
  • The median time to progression (TP) was 12 months and the median time to local progression (TLP) was 22 months.
  • None of the factors studied (age, sex, lymphoma subtype, radiotherapy regimen, number of prior regimens or time since diagnosis, number of positive sites or largest lymphoma diameter) were found to relate to response.
  • At time of death 70% of patients were without in-field progression after LD-IF-RT.
  • It appears that LD-IF-RT is a valuable asset in the management of relapsed disease in both indolent and aggressive lymphoma and should be considered to palliate symptoms in patients with recurrent and/or chemotherapy refractory disease.
  • [MeSH-major] Lymphoma / radiotherapy. Palliative Care / methods
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Disease-Free Survival. Drug Resistance, Neoplasm. Humans. Male. Middle Aged. Prospective Studies. Radiotherapy / adverse effects. Recurrence. Treatment Outcome

  • Genetic Alliance. consumer health - Follicular Lymphoma.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • MedlinePlus Health Information. consumer health - Palliative Care.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16039113.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


10. Goy A, Younes A, McLaughlin P, Pro B, Romaguera JE, Hagemeister F, Fayad L, Dang NH, Samaniego F, Wang M, Broglio K, Samuels B, Gilles F, Sarris AH, Hart S, Trehu E, Schenkein D, Cabanillas F, Rodriguez AM: Phase II study of proteasome inhibitor bortezomib in relapsed or refractory B-cell non-Hodgkin's lymphoma. J Clin Oncol; 2005 Feb 1;23(4):667-75
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] Phase II study of proteasome inhibitor bortezomib in relapsed or refractory B-cell non-Hodgkin's lymphoma.
  • PURPOSE: Evaluate efficacy and toxicity of bortezomib in patients with relapsed or refractory B-cell non-Hodgkin's lymphoma.
  • PATIENTS AND METHODS: Patients were stratified, based on preclinical data, into arm A (mantle-cell lymphoma) or arm B (other B-cell lymphomas) without limitation in number of prior therapies.
  • RESULTS: Sixty patients with a median number of prior therapies of 3.5 (range, one to 12 therapies) were enrolled; 33 patients were in arm A and 27 were in arm B, including 12 diffuse large B-cell lymphomas, five follicular lymphomas (FL), three transformed FLs, four small lymphocytic lymphomas (SLL), two Waldenstrom's macroglobulinemias (WM), and one marginal zone lymphoma.
  • In arm A, 12 of 29 assessable patients responded (six complete responses [CR] and six partial responses [PR]) for an overall response rate (ORR) of 41% (95% CI, 24% to 61%), and a median time to progression not reached yet, with a median follow-up of 9.3 months (range, 1.7 to 24 months).
  • In arm B, four of 21 assessable patients responded (one SLL patient had a CR, one FL patient had a CR unconfirmed, one diffuse large B-cell lymphoma patient had a PR, and one WM patient had a PR) for an ORR of 19% (95% CI, 5% to 42%).
  • CONCLUSION: Bortezomib showed promising activity in relapsed mantle-cell lymphoma and encouraging results in other B-cell lymphomas.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Lymphoma, B-Cell / drug therapy. Protease Inhibitors / therapeutic use. Pyrazines / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Bortezomib. Female. Humans. Male. Middle Aged. Survival Rate. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Clin Oncol. 2005 Feb 1;23(4):657-8 [15613690.001]
  • (PMID = 15613697.001).
  • [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; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  •  go-up   go-down


11. Cheson BD, Friedberg JW, Kahl BS, Van der Jagt RH, Tremmel L: Bendamustine produces durable responses with an acceptable safety profile in patients with rituximab-refractory indolent non-Hodgkin lymphoma. Clin Lymphoma Myeloma Leuk; 2010 Dec;10(6):452-7
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bendamustine produces durable responses with an acceptable safety profile in patients with rituximab-refractory indolent non-Hodgkin lymphoma.
  • BACKGROUND: Although initially responsive to therapy, indolent non-Hodgkin lymphomas (NHLs) are generally incurable.
  • Therefore, active and tolerable treatments for patients with relapsed or refractory disease are needed.
  • Bendamustine, a mechlorethamine alkylator with novel mechanisms of action, is approved in the United States for rituximab-refractory indolent B-cell NHL.
  • RESULTS: The studies enrolled 161 patients with a median of 2 previous chemotherapy regimens.
  • Histologies included follicular (68%), small lymphocytic (20%), marginal zone (11%), and lymphoplasmacytic (1%) lymphoma.
  • Sixty patients (34.1%) were refractory to their last chemotherapy, 53 (30.1%) were alkylating agent refractory.
  • Among 127 patients previously treated with alkylators, ORR was 88% (28% CR/CRu) in responsive and 59% (12% CR/CRu) in refractory patients.
  • Second malignancies occurred in 9 patients (5.6%; 5 myelodysplastic syndromes, 2 acute myelogenous leukemia, 1 chronic myelomonocytic leukemia, and 1 squamous cell carcinoma).
  • CONCLUSION: Bendamustine induces durable responses with acceptable long-term safety in rituximab-refractory indolent NHL.
  • [MeSH-major] Antibodies, Monoclonal, Murine-Derived / therapeutic use. Drug Resistance, Neoplasm / drug effects. Lymphoma, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy. Nitrogen Mustard Compounds / therapeutic use
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Anemia / chemically induced. Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Alkylating / adverse effects. Antineoplastic Agents, Alkylating / therapeutic use. Bendamustine Hydrochloride. Female. Humans. Leukopenia / chemically induced. Male. Middle Aged. Multicenter Studies as Topic / statistics & numerical data. Nausea / chemically induced. Rituximab. Survival Analysis. Treatment Outcome

  • Genetic Alliance. consumer health - Hodgkin lymphoma.
  • Genetic Alliance. consumer health - Non-Hodgkin Lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Bendamustine .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21189660.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Nitrogen Mustard Compounds; 4F4X42SYQ6 / Rituximab; 981Y8SX18M / Bendamustine Hydrochloride
  •  go-up   go-down


12. Ganjoo KN, Robertson MJ, Fisher W, Jung SH, McClean J, Huh SY, Bufill J, Williams S, Cripe LD: A phase II study of single agent gemcitabine in relapsed or refractory follicular or small lymphocytic non-Hodgkin lymphomas: a Hoosier Oncology Group Study. Am J Clin Oncol; 2005 Apr;28(2):169-72
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of single agent gemcitabine in relapsed or refractory follicular or small lymphocytic non-Hodgkin lymphomas: a Hoosier Oncology Group Study.
  • This study assessed tumor response in patients with previously treated follicular or small lymphocytic non-Hodgkin lymphoma.
  • Gemcitabine was given as a single agent to patients with previously treated follicular or small lymphocytic lymphomas.
  • Thirteen patients were treated with 1 to 6 cycles of chemotherapy.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Follicular / drug therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15803012.001).
  • [ISSN] 1537-453X
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
  •  go-up   go-down


13. 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.
  • [Title] Update on a phase (ph) 2 study of bortezomib in patients (pts) with relapsed or refractory indolent or aggressive non-Hodgkin's lymphomas (NHL).
  • : 6581 Background: Proteasome inhibition disrupts many cell cycle checkpoints and pathways that lead to apoptosis.
  • Preclinical and ph 1 studies suggested the proteasome inhibitor bortezomib (VELCADE<sup>™</sup>, Vc) was active in lymphoma.
  • METHODS: The primary objective of this ph 2 study was to document the response rate (RR) and toxicity of Vc in pts with relapsed or refractory NHL.
  • 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).
  • 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


14. 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.
  • All patients with small lymphocytic lymphoma were found to have stable disease after 2 and 4 cycles respectively.
  • Six of nine evaluable patients with follicular lymphoma achieved a major response, with one patient obtaining a durable complete remission.
  • 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.
  • To date no patient with small lymphocytic lymphoma/CLL has responded (n=3).
  • 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


15. O'Connor OA, Portlock C, Moskowitz C, Straus D, Hamlin P, Stubblefield M, Dumetrescu O, Colevas AD, Grant B, Zelenetz A: A multicentre phase II clinical experience with the novel aza-epothilone Ixabepilone (BMS247550) in patients with relapsed or refractory indolent non-Hodgkin lymphoma and mantle cell lymphoma. Br J Haematol; 2008 Oct;143(2):201-9
Hazardous Substances Data Bank. Ixabepilone .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A multicentre phase II clinical experience with the novel aza-epothilone Ixabepilone (BMS247550) in patients with relapsed or refractory indolent non-Hodgkin lymphoma and mantle cell lymphoma.
  • The epothilones represent a novel group of microtubule stabilization agents that appear to retain activity even in chemotherapy-resistant cell lines and animal models.
  • Because of their ability to overcome chemotherapy resistance, we conducted a phase II study of Ixabepilone in patients with indolent non-Hodgkin lymphoma and mantle cell lymphoma (MCL).
  • Patients were required to have received < or =4 prior chemotherapy regimens, with an interval of at least one month since the last treatment, 3 months from prior rituximab, and 7 d from prior steroids, an absolute neutrophil count >1 x 10(9)/l and a platelet count >50 x 10(9)/l.
  • One patient with chemotherapy-refractory follicular lymphoma attained a complete remission that lasted approximately 8 months.
  • Three responses were also seen in refractory MCL and one in small lymphocytic lymphoma.
  • These data suggest that Ixabepilone has activity in chemotherapy-refractory lymphoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Epothilones / therapeutic use. Lymphoma, Mantle-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Drug Administration Schedule. Electromyography. Female. Humans. Lymphoma, Follicular / drug therapy. Male. Middle Aged. Motor Neurons. Neural Conduction. Recurrence. Remission Induction. Sensory Receptor Cells. Treatment Outcome

  • Genetic Alliance. consumer health - Hodgkin lymphoma.
  • Genetic Alliance. consumer health - Mantle cell lymphoma.
  • Genetic Alliance. consumer health - Non-Hodgkin Lymphoma.
  • 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 = 18691173.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30CA22435; United States / NCI NIH HHS / CA / U01 CA 69913
  • [Publication-type] Clinical Trial, Phase II; 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 / Epothilones; K27005NP0A / ixabepilone
  •  go-up   go-down


16. Montserrat E: Rituximab in chronic lymphocytic leukemia. Semin Oncol; 2003 Feb;30(1 Suppl 2):34-9
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] Rituximab in chronic lymphocytic leukemia.
  • Chronic lymphocytic leukemia (CLL) is the most common adult leukemia but is currently incurable by conventional therapeutic interventions.
  • Rituximab has proven efficacy and tolerability in non-Hodgkin's lymphoma, achieving response rates of 73% and 48% in previously untreated or relapsed/refractory indolent non-Hodgkin's lymphoma, respectively.
  • However, the standard dose and schedule (375 mg/m(2) once-weekly for 4 weeks) may not be optimal for patients with previously treated small lymphocytic lymphoma, the lymphomatous equivalent of CLL.
  • Nevertheless, good response rates have been achieved in untreated CLL and small lymphocytic lymphoma using the standard dose and schedule and also using higher or more frequent dosing, indicating that rituximab is an active agent in this setting.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Vidarabine / analogs & derivatives
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials as Topic. Drug Administration Schedule. Humans. Rituximab

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. VIDARABINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2003, Elsevier Science (USA). All rights reserved.
  • (PMID = 12652463.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
  • [Number-of-references] 28
  •  go-up   go-down


17. Plosker GL, Figgitt DP: Rituximab: a review of its use in non-Hodgkin's lymphoma and chronic lymphocytic leukaemia. Drugs; 2003;63(8):803-43
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] Rituximab: a review of its use in non-Hodgkin's lymphoma and chronic lymphocytic leukaemia.
  • Rituximab is an anti-CD20 monoclonal antibody that has demonstrated efficacy in patients with various lymphoid malignancies, including indolent and aggressive forms of B-cell non-Hodgkin's lymphoma (NHL) and B-cell chronic lymphocytic leukaemia (CLL).
  • While the optimal use of the drug in many clinical settings has yet to be clarified, two pivotal trials have established rituximab as a viable treatment option in patients with relapsed or refractory indolent NHL, and as a standard first-line treatment option when combined with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy in elderly patients with diffuse large B-cell lymphoma (the most common type of aggressive NHL).
  • The former was a noncomparative trial in relapsed indolent NHL (follicular and small lymphocytic subtypes) with clinical responses achieved in about half of patients treated with rituximab 375 mg/m(2) intravenously once weekly for 4 weeks, which was similar to some of the most encouraging results reported with traditional chemotherapeutic agents.
  • The latter was a randomised comparison of eight cycles of CHOP plus rituximab 375 mg/m(2) intravenously (one dose per cycle) versus CHOP alone in previously untreated elderly patients (60 to 80 years of age) with diffuse large B-cell lymphoma.
  • Treatment with rituximab is generally well tolerated, particularly in terms of adverse haematological effects and serious or opportunistic infections relative to standard chemotherapy.
  • CONCLUSIONS: Clinical trials with rituximab indicate that the drug has broad application to B-cell malignancies, although further clarification is needed to determine its optimal use in many of these clinical settings.
  • Importantly, rituximab in combination with CHOP chemotherapy has emerged as a new treatment standard for previously untreated diffuse large B-cell lymphoma, at least in elderly patients.
  • Compared with conventional chemotherapy, rituximab is associated with markedly reduced haematological events such as severe neutropenia, as well as associated infections.
  • Rituximab may be particularly suitable for elderly patients or those with poor performance status, and its tolerability profile facilitates its use in combination with cytotoxic drugs.
  • PHARMACODYNAMIC PROPERTIES: Rituximab is a mouse/human chimaeric IgG(1)-kappa monoclonal antibody that targets the CD20 antigen found on the surface of malignant and normal B lymphocytes.
  • Although treatment with rituximab induces lymphopenia in most patients, typically lasting about 6 months, a full recovery of B lymphocytes in the peripheral blood is usually seen 9-12 months after therapy, as CD20 is not expressed on haematopoietic stem cells.
  • CD20 is, however, expressed on >90% of B-cell non-Hodgkin's lymphomas (NHL) and to a lesser degree on B-cell chronic lymphocytic leukaemia (CLL) cells.
  • In addition, in vitro data indicate that rituximab sensitises tumour cells to the effects of conventional chemotherapeutic drugs.
  • PHARMACOKINETIC PROPERTIES: Serum rituximab concentrations increased in proportion to dose across a wide range of single- and multiple-dose intravenous regimens in patients with B-cell NHL.
  • When administered at a dose of 375 mg/m(2) once weekly for 4 weeks in a pivotal trial in patients with relapsed or refractory indolent B-cell NHL (follicular or small lymphocytic subtypes), peak serum concentrations essentially doubled from the first (239.1 mg/L) to the fourth (460.7 mg/L) infusion, while elimination half-life (t(1/2)) increased from 76.3 to 205.8 hours (3.2 to 8.6 days).
  • The pharmacokinetic properties of rituximab are also characterised by wide inter-individual variability, and serum drug concentrations that are correlated with clinical response.
  • Although pharmacokinetic data are limited in patients with aggressive forms of NHL, such as diffuse large B-cell lymphoma, rituximab appears to have a similar pharmacokinetic profile in these patients to that in patients with indolent B-cell NHL.
  • The pharmacokinetics of rituximab are also reported to be similar whether the drug is administered with or without cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy.
  • THERAPEUTIC USE: A number of studies have demonstrated efficacy of intravenous rituximab in patients with various lymphoid malignancies of B-cell origin, including indolent (e.g. follicular lymphoma) and aggressive (e.g. diffuse large B-cell lymphoma) forms of NHL, and CLL, but the drug has not yet been approved for use in CLL, and approved indications in NHL vary between countries.
  • In the US, for example, rituximab is available for the treatment of patients with low-grade or follicular, relapsed or refractory, CD20-positive B-cell NHL.
  • In Europe, the drug has similar approval for relapsed or refractory follicular NHL as in the US, but has also been approved for use in combination with CHOP chemotherapy for the most common aggressive form of NHL (CD20-positive, diffuse large B-cell lymphoma).
  • In Japan, rituximab has been approved for indolent B-cell NHL and mantle cell lymphoma (an aggressive form of B-cell NHL), primarily on the basis of results of a Japanese phase II trial.
  • Indolent NHL: Results of several studies evaluating rituximab 375 mg/m(2) once weekly for 4 weeks in patients with indolent forms of B-cell NHL (primarily follicular and small lymphocytic lymphomas) showed objective response (OR) rates ranging from approximately 40-60% in those receiving the drug for relapsed or refractory indolent B-cell NHL, and slightly higher (50-70%) for those receiving rituximab as first-line therapy.
  • In a pivotal trial in 166 patients with relapsed or refractory low-grade or follicular B-cell NHL, intent-to-treat (ITT) analysis showed an OR rate of 48%, and a projected median time to progression of 13 months.
  • CHOP, fludarabine-containing regimens) or other drugs (e.g. interferon-alpha2a) in previously untreated patients with indolent forms of B-cell NHL (primarily follicular and small lymphocytic subtypes).
  • Follow-up data from a study in 40 patients with low-grade or follicular B-cell NHL treated with rituximab plus CHOP as first-line therapy showed that responses were durable with a progression-free survival and median duration of response >5 years.Bcl-2 gene rearrangement (t14;18) occurs in malignant cells in up to 85% of patients with follicular lymphoma, and minimal residual disease in peripheral blood and bone marrow can be monitored using polymerase chain reaction (PCR).
  • Aggressive NHL: Studies with rituximab as monotherapy in aggressive B-cell NHL, a potentially curable disorder, have generally been restricted to patients with relapsed or recurrent disease, since CHOP has traditionally been the standard first-line treatment regimen.
  • However, promising results from phase II monotherapy studies prompted further clinical investigation of rituximab in conjunction with chemotherapy.
  • Thus, most studies with rituximab in patients with aggressive forms of B-cell NHL have involved combination therapy, including a pivotal randomised trial comparing eight cycles of standard CHOP therapy plus rituximab 375 mg/m(2) (one dose per cycle) versus CHOP alone in 399 previously untreated elderly patients (60-80 years of age) with diffuse large B-cell lymphoma.
  • Other, smaller trials with rituximab in combination with CHOP or other chemotherapeutic regimens, either as first-line therapy or for patients with relapsed or refractory aggressive B-cell NHL, have also shown promising results in terms of clinical response rates.CLL: In relatively small trials (n < 40) conducted primarily in patients with relapsed or refractory B-cell CLL, rituximab monotherapy (various regimens) achieved OR rates of 23-45%, with median duration of response ranging from approximately 3-10 months. (ABSTRACT TRUNCATED)
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Clinical Trials as Topic. Drug Administration Schedule. Humans. Rituximab

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • 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] Blood. 1994 Oct 15;84(8):2457-66 [7522629.001]
  • [Cites] N Engl J Med. 1993 Sep 30;329(14 ):987-94 [8141877.001]
  • [Cites] Cancer Immunol Immunother. 2000 Mar;48(12):673-83 [10752475.001]
  • [Cites] J Clin Oncol. 1997 Oct;15(10):3266-74 [9336364.001]
  • [Cites] Blood. 2000 Jun 15;95(12):3900-8 [10845926.001]
  • [Cites] J Clin Oncol. 1999 Apr;17(4):1244 [10561185.001]
  • [Cites] Semin Oncol. 1999 Oct;26(5 Suppl 14):88-96 [10561023.001]
  • [Cites] Eur J Haematol. 2002 Jul;69(1):21-6 [12270058.001]
  • [Cites] Leuk Lymphoma. 2003 Mar;44(3):477-81 [12688318.001]
  • [Cites] J Clin Oncol. 2001 Jan 15;19(2):389-97 [11208830.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2153-64 [11304767.001]
  • [Cites] Semin Oncol. 2002 Feb;29(1S2):2-9 [28140087.001]
  • [Cites] Clin Cancer Res. 2001 Mar;7(3):709-23 [11297268.001]
  • [Cites] Ann Hematol. 2000 Jun;79(6):332-5 [10901614.001]
  • [Cites] Anticancer Res. 2000 Sep-Oct;20(5A):2961-6 [11062708.001]
  • [Cites] Blood. 1994 Jan 15;83(2):435-45 [7506951.001]
  • [Cites] Semin Oncol. 2002 Feb;29(1S2):30-35 [28140089.001]
  • [Cites] Ann Oncol. 1999 Jun;10(6):655-61 [10442187.001]
  • [Cites] Cell Immunol. 2000 Aug 25;204(1):55-63 [11006018.001]
  • [Cites] Semin Oncol. 2000 Dec;27(6 Suppl 12):53-61 [11226001.001]
  • [Cites] Blood. 1984 Jun;63(6):1424-33 [6609729.001]
  • [Cites] Blood. 2002 Feb 1;99(3):1038-43 [11807010.001]
  • [Cites] J Clin Oncol. 2002 May 15;20(10 ):2453-63 [12011122.001]
  • [Cites] Br J Haematol. 2000 Apr;109(1):81-8 [10848785.001]
  • [Cites] Blood. 2003 Jan 1;101(1):6-14 [12393429.001]
  • [Cites] Blood. 2002 Nov 1;100(9):3115-20 [12384407.001]
  • [Cites] Scand J Immunol. 2000 Jun;51(6):634-41 [10849376.001]
  • [Cites] Semin Oncol. 1999 Oct;26(5 Suppl 14):79-87 [10561022.001]
  • [Cites] Clin Cancer Res. 2000 Jul;6(7):2644-52 [10914705.001]
  • [Cites] Blood. 1999 Oct 1;94(7):2217-24 [10498591.001]
  • [Cites] Ann Oncol. 1998 Sep;9(9):995-1001 [9818074.001]
  • [Cites] Clin Cancer Res. 2002 Mar;8(3):836-45 [11895917.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1326-31 [11520778.001]
  • [Cites] Blood. 2002 Jan 1;99(1):67-74 [11756154.001]
  • [Cites] Semin Oncol. 2002 Feb;29(1S2):105-112 [28140083.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1658-64 [12886256.001]
  • [Cites] Jpn J Cancer Res. 1998 Jul;89(7):748-56 [9738982.001]
  • [Cites] Blood. 2002 Feb 1;99(3):1096-7 [11822361.001]
  • [Cites] Haematologica. 2002 Jan;87(1):33-43 [11801463.001]
  • [Cites] Ann Oncol. 2002 Jun;13(6):928-43 [12123339.001]
  • [Cites] Blood. 2001 Mar 1;97(5):1392-8 [11222385.001]
  • [Cites] J Clin Oncol. 1999 Jan;17(1):268-76 [10458242.001]
  • [Cites] J Clin Oncol. 2002 Mar 1;20(5):1288-94 [11870171.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1991-2 [11565541.001]
  • [Cites] Ann Oncol. 2000 Apr;11(4):399-408 [10847457.001]
  • [Cites] Ann Oncol. 2000 Mar;11(3):374-5 [10811510.001]
  • [Cites] J Clin Oncol. 2005 Feb 20;23(6):1103-8 [15657404.001]
  • [Cites] Haematologica. 2002 Nov;87(11):1229-30 [12414357.001]
  • [Cites] Eur J Health Econ. 2002;3(3):166-72 [15609141.001]
  • [Cites] Eur J Haematol. 2002 Sep;69(3):129-34 [12406005.001]
  • [Cites] Cancer J. 2002 Sep-Oct;8(5):371-6 [12416894.001]
  • [Cites] J Clin Oncol. 1999 Dec;17(12):3793-803 [10577851.001]
  • [Cites] Semin Oncol. 2002 Feb;29(1S2):70-74 [28140094.001]
  • [Cites] Semin Oncol. 2002 Apr;29(2 Suppl 6):18-22 [12040530.001]
  • [Cites] Am J Hematol. 1992 Aug;40(4):259-63 [1380203.001]
  • [Cites] Blood. 1997 Sep 15;90(6):2188-95 [9310469.001]
  • [Cites] Clin Lymphoma. 2000 Sep;1(2):146-51; discussion 152-3 [11707827.001]
  • [Cites] Br J Haematol. 1999 Jul;106(1):47-54 [10444162.001]
  • [Cites] J Immunol Methods. 1997 Mar 28;202(2):163-71 [9107305.001]
  • [Cites] Leukemia. 2002 Sep;16(9):1735-44 [12200688.001]
  • [Cites] J Clin Oncol. 2002 Oct 15;20(20):4261-7 [12377971.001]
  • [Cites] Blood Cells Mol Dis. 2000 Apr;26(2):133-43 [10753604.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Haematologica. 2002 Jul;87(7):719-29; discussion 729 [12091123.001]
  • [Cites] Blood. 2002 Oct 1;100(7):2672; author reply 2673 [12360978.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1314-9 [11830481.001]
  • [Cites] Oncology (Williston Park). 1998 May;12(5):697-714; discussion 714, 717, 721 [9597680.001]
  • [Cites] Semin Oncol. 2002 Feb;29(1S2):56-69 [28140093.001]
  • [Cites] J Clin Oncol. 2000 Jan;18(2):317-24 [10637245.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):791-5 [10071268.001]
  • [Cites] Drugs. 1999 Jul;58(1):79-88; discussion 89-90 [10439931.001]
  • [Cites] Bone Marrow Transplant. 2002 Feb;29 Suppl 1:S14-7 [11840156.001]
  • [Cites] Ann Oncol. 2001 Jan;12(1):109-14 [11249036.001]
  • [Cites] N Engl J Med. 2002 Jan 24;346(4):280-2 [11807154.001]
  • [Cites] Blood. 2001 Nov 1;98(9):2771-7 [11675350.001]
  • [Cites] Blood. 2001 Dec 1;98(12):3383-9 [11719378.001]
  • [Cites] Blood. 2003 May 1;101(9):3413-5 [12522009.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):7170-6 [11156427.001]
  • [Cites] Semin Oncol. 2002 Feb;29(1S2):41-47 [28140091.001]
  • [Cites] Blood. 1994 Jun 15;83(12):3800-7 [8204898.001]
  • [Cites] J Clin Oncol. 1999 Jun;17(6):1851-7 [10561225.001]
  • [Cites] Semin Oncol. 2002 Feb;29(1S2):75-80 [28140095.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2165-70 [11304768.001]
  • [Cites] Br J Haematol. 2002 Jun;117(4):828-34 [12060117.001]
  • [Cites] N Engl J Med. 2002 Jan 24;346(4):235-42 [11807147.001]
  • [Cites] Blood. 1998 Sep 15;92(6):1927-32 [9731049.001]
  • [Cites] Clin Lymphoma. 2000 Dec;1(3):186-94; discussion 195-6 [11707828.001]
  • [Cites] Haematologica. 1998 Mar;83(3):209-16 [9573674.001]
  • [Cites] Ann Hematol. 2000 Sep;79(9):493-500 [11043420.001]
  • [Cites] Ann Oncol. 2000;11 Suppl 1:123-6 [10707793.001]
  • [Cites] J Clin Oncol. 2000 Sep;18(17):3135-43 [10963642.001]
  • [Cites] Blood. 2001 Jan 1;97(1):101-6 [11133748.001]
  • [Cites] Blood. 2002 Jun 15;99(12 ):4336-42 [12036859.001]
  • [Cites] Leuk Res. 2000 May;24(5):411-5 [10785263.001]
  • [Cites] J Clin Oncol. 1998 Aug;16(8):2825-33 [9704735.001]
  • [Cites] Blood. 1993 Jun 15;81(12):3449-57 [8507880.001]
  • [Cites] Bone Marrow Transplant. 1999 Sep;24(5):521-6 [10482937.001]
  • [Cites] J Clin Invest. 1981 Jan;67(1):134-40 [6969730.001]
  • [Cites] Cancer Biother Radiopharm. 1997 Jun;12(3):177-86 [10851464.001]
  • [Cites] Eur J Haematol. 1999 Feb;62(2):76-82 [10052709.001]
  • [Cites] Blood. 2002 Feb 1;99(3):856-62 [11806987.001]
  • [Cites] Semin Oncol. 2002 Feb;29(1S2):36-40 [28140090.001]
  • [Cites] CA Cancer J Clin. 2001 Jan-Feb;51(1):15-36 [11577478.001]
  • [Cites] J Clin Oncol. 2002 Aug 1;20(15):3262-9 [12149300.001]
  • (PMID = 12662126.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 177
  •  go-up   go-down


18. Perz J, Topaly J, Fruehauf S, Hensel M, Ho AD: Level of CD 20-expression and efficacy of rituximab treatment in patients with resistant or relapsing B-cell prolymphocytic leukemia and B-cell chronic lymphocytic leukemia. Leuk Lymphoma; 2002 Jan;43(1):149-51
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Level of CD 20-expression and efficacy of rituximab treatment in patients with resistant or relapsing B-cell prolymphocytic leukemia and B-cell chronic lymphocytic leukemia.
  • Rituximab (IDEC C2B8) is a chimeric human-mouse monoclonal anti-CD20 antibody that has been proven to be effective for the treatment of patients with CD20 positive leukemia and lymphoma.
  • The level of CD20-expression in patients with B-cell chronic lymphocytic leukemia (B-CLL) is low in comparison to other B-cell lymphomas and normal B-cells.
  • Previous experience with rituximab treatment in small series of patients with B-CLL suggest that it is less effective in B-CLL than in follicular lymphomas.
  • We analyzed the correlation between CD20-expression level and efficacy of rituximab treatment in eight patients with refractory or relapsed B-CLL and two patients with B-cell prolymphocytic leukemia (B-PLL).
  • We could not identify any correlation between CD20-expression and efficacy of rituximab treatment.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD20 / metabolism. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Aged. Antibodies, Monoclonal, Murine-Derived. Biomarkers / analysis. Disease-Free Survival. Drug Evaluation. Flow Cytometry. Humans. Leukemia, Prolymphocytic / diagnosis. Leukemia, Prolymphocytic / drug therapy. Leukemia, Prolymphocytic / mortality. Male. Middle Aged. Rituximab. Salvage Therapy. Survival Rate. Therapeutic Equivalency. Treatment Outcome


19. Hainsworth JD, Litchy S, Barton JH, Houston GA, Hermann RC, Bradof JE, Greco FA, Minnie Pearl Cancer Research Network: Single-agent rituximab as first-line and maintenance treatment for patients with chronic lymphocytic leukemia or small lymphocytic lymphoma: a phase II trial of the Minnie Pearl Cancer Research Network. J Clin Oncol; 2003 May 1;21(9):1746-51
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] Single-agent rituximab as first-line and maintenance treatment for patients with chronic lymphocytic leukemia or small lymphocytic lymphoma: a phase II trial of the Minnie Pearl Cancer Research Network.
  • PURPOSE: To assess the efficacy and toxicity of first-line single-agent rituximab, followed by re-treatment with rituximab at 6-month intervals, in previously untreated patients with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL).
  • All patients were required to have one or more indications for treatment.
  • After a median follow-up of 20 months, the median progression-free survival (PFS) time was 18.6 months, and the 1- and 2-year PFS rates were 62% and 49%, respectively.
  • Treatment was well tolerated, with only two episodes of grade 3 to 4 infusion-related toxicity.
  • CONCLUSION: Single-agent rituximab, used at a standard dose and schedule, is active in the first-line treatment of patients with CLL/SLL, producing substantially higher response rates than previously reported in relapsed or refractory patients (51% v 13%, respectively).
  • Re-treatment with rituximab at 6-month intervals is well tolerated.
  • The PFS time of 18.6 months in patients with CLL/SLL seems shorter than the 36- to 40-month median PFSs previously reported with first-line plus maintenance rituximab in patients with follicular lymphoma.
  • Additional follow-up is required to fully assess the impact of this treatment strategy.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antineoplastic Agents / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal, Murine-Derived. Disease Progression. Disease-Free Survival. Drug Administration Schedule. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Rituximab. Treatment Outcome

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. RITUXIMAB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12721250.001).
  • [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; Clinical Trial, Phase II; 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; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  •  go-up   go-down


20. Lin TS, Naumovski L, Lecane PS, Lucas MS, Moran ME, Cheney C, Lucas DM, Phan SC, Miller RA, Byrd JC: Effects of motexafin gadolinium in a phase II trial in refractory chronic lymphocytic leukemia. Leuk Lymphoma; 2009 Dec;50(12):1977-82
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] Effects of motexafin gadolinium in a phase II trial in refractory chronic lymphocytic leukemia.
  • Chronic lymphocytic leukemia (CLL) cells are susceptible to oxidative stress.
  • A phase II trial administered MGd 5 mg/kg/day IV for 5 days every 3 weeks until disease progression to patients with previously treated CLL and small lymphocytic lymphoma.
  • Thirteen patients (median age 66 years) with a median of four prior therapies (range 2-9) were enrolled.
  • Serial increase in AKT phosphorylation in patient samples following MGd treatment was not observed, suggesting intracellular generation of ROS was not optimal.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Metalloporphyrins / therapeutic use
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Agents / adverse effects. Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / therapeutic use. Chromosome Deletion. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 17 / genetics. Drug Administration Schedule. Drug Resistance, Neoplasm. Female. Flow Cytometry. Humans. Immunoblotting. In Situ Hybridization, Fluorescence. Male. Middle Aged. Phosphorylation / drug effects. Proto-Oncogene Proteins c-akt / metabolism. Treatment Outcome

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19860624.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Metalloporphyrins; 6433A42F4F / motexafin gadolinium; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  •  go-up   go-down


21. Petryk M, Grossbard ML: Rituximab therapy of B-cell neoplasms. Clin Lymphoma; 2000 Dec;1(3):186-94; discussion 195-6
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 therapy of B-cell neoplasms.
  • The development of rituximab, an anti-CD20 monoclonal antibody, represents a revolutionary advance in the therapy of hematological malignancies.
  • Rituximab was approved in 1997 by the Food and Drug Administration for the treatment of relapsed or refractory, CD20(+), B-cell, low-grade or follicular non-Hodgkin's lymphoma (NHL).
  • Recent studies have documented activity of rituximab in other CD20-expressing hematological malignancies including mantle cell lymphoma, small lymphocytic lymphoma, aggressive NHL, chronic lymphocytic leukemia, and Waldenstrom's macroglobulinemia.
  • When used in combination with cytotoxic chemotherapy, rituximab achieves response rates of 90%-95% in low-grade follicular and aggressive NHL patients.
  • Currently, rituximab is undergoing intensive investigation in several large phase II and III trials, both as a single agent and in combination with chemotherapy.
  • Clinical research will help define the ultimate role of this agent and its potential impact on survival of patients with B-cell neoplasms.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Lymphoma, B-Cell / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Clinical Trials as Topic. Combined Modality Therapy. Humans. Rituximab

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11707828.001).
  • [ISSN] 1526-9655
  • [Journal-full-title] Clinical lymphoma
  • [ISO-abbreviation] Clin Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 53
  •  go-up   go-down


22. O'Brien S, Osterborg A: Ofatumumab: a new CD20 monoclonal antibody therapy for B-cell chronic lymphocytic leukemia. Clin Lymphoma Myeloma Leuk; 2010 Oct;10(5):361-8
The Weizmann Institute of Science GeneCards and MalaCards databases. gene/protein/disease-specific - MalaCards for b-cell chronic lymphocytic leukemia .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ofatumumab: a new CD20 monoclonal antibody therapy for B-cell chronic lymphocytic leukemia.
  • Though most patients with chronic lymphocytic leukemia (CLL) respond to first-line therapy, all patients eventually relapse, after which therapeutic options are limited.
  • Fludarabine-refractory patients have a particularly poor prognosis.
  • The addition of the CD20 monoclonal antibody (MoAb) rituximab to chemotherapy in CLL has improved outcomes, particularly in early lines of therapy; however, the efficacy of rituximab monotherapy in CLL is limited, potentially in part because of reduced cell lysis via complement-dependent cytotoxicity (CDC) in this setting.
  • Ofatumumab is a human MoAb that targets an epitope encompassing the membrane-proximal small-loop on the CD20 molecule, which differs from the binding location of rituximab.
  • In vitro studies with ofatumumab have demonstrated that it is significantly more effective than rituximab at corresponding dose levels at lysing CLL cells and B-cell lines, especially those with low CD20 copy numbers.
  • In patients with CLL refractory to both fludarabine and alemtuzumab or refractory to fludarabine with bulky lymphadenopathy and, therefore, less suitable for treatment with the CD52 MoAb alemtuzumab, results from the planned interim analysis showed an encouraging response rate with ofatumumab (Independent Endpoint Review Committee evaluated) and survival parameters, which seemed to be higher than those reported from a historical assessment of other salvage therapies in a corresponding group of patients.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • Genetic Alliance. consumer health - Leukemia, B-cell, chronic.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21030349.001).
  • [ISSN] 2152-2669
  • [Journal-full-title] Clinical lymphoma, myeloma & leukemia
  • [ISO-abbreviation] Clin Lymphoma Myeloma Leuk
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD20; 0 / ofatumumab
  •  go-up   go-down


23. Bosly A, Keating MJ, Stasi R, Bradstock K: Rituximab in B-cell disorders other than non-Hodgkin's lymphoma. Anticancer Drugs; 2002 Nov;13 Suppl 2:S25-33
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] Rituximab in B-cell disorders other than non-Hodgkin's lymphoma.
  • Rituximab is a human/mouse chimeric monoclonal antibody that binds to the CD20 antigen and is expressed at all stages of B-cell development.
  • Rituximab has demonstrated efficacy as monotherapy and in combination with chemotherapy in the treatment of both indolent and aggressive non-Hodgkin's lymphoma (NHL).
  • Rituximab treatment results in rapid depletion of B-cells and this has led to the consideration of other B-cell disorders as candidates for rituximab therapy.
  • Recent studies have demonstrated the efficacy of rituximab in a variety of such disorders, including chronic lymphocytic leukemia (CLL), post-transplant lymphoproliferative disorder (PTLD), Waldenström's macroglobulinemia (WM), multiple myeloma (MM), idiopathic thrombocytopenic purpura (ITP), hairy-cell leukemia (HCL) and cold agglutinin disease (CAD).
  • In patients with CLL, increasing the dose and/or frequency of rituximab treatment has given improved response rates compared with the standard dose schedule used in NHL, and combination immunochemotherapy has yielded an overall response rate of 92% (with a 60% complete response rate).
  • Clinical trials have also demonstrated evidence of efficacy for rituximab in PTLD, WM and relapsed or refractory ITP.
  • Efficacy of rituximab in CAD and relapsed or refractory HCL has also been demonstrated in small studies and case reports.
  • Available data thus indicate that rituximab can be an effective therapy in a wide range of CD20+ lymphoid disorders.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. B-Lymphocytes / pathology. Hematologic Diseases / drug therapy. Lymphoproliferative Disorders / drug therapy
  • [MeSH-minor] Anemia, Hemolytic, Autoimmune / drug therapy. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Agents / therapeutic use. Clinical Trials as Topic. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy. Organ Transplantation / adverse effects. Paraproteinemias / drug therapy. Purpura, Thrombocytopenic, Idiopathic / drug therapy. Rituximab

  • MedlinePlus Health Information. consumer health - Blood Disorders.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • 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
  • [CommentIn] Curr Rheumatol Rep. 2003 Oct;5(5):381-2 [12967521.001]
  • (PMID = 12710588.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 43
  •  go-up   go-down


24. Hagenbeek A, Gadeberg O, Johnson P, Pedersen LM, Walewski J, Hellmann A, Link BK, Robak T, Wojtukiewicz M, Pfreundschuh M, Kneba M, Engert A, Sonneveld P, Flensburg M, Petersen J, Losic N, Radford J: First clinical use of ofatumumab, a novel fully human anti-CD20 monoclonal antibody in relapsed or refractory follicular lymphoma: results of a phase 1/2 trial. Blood; 2008 Jun 15;111(12):5486-95
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] First clinical use of ofatumumab, a novel fully human anti-CD20 monoclonal antibody in relapsed or refractory follicular lymphoma: results of a phase 1/2 trial.
  • Ofatumumab is a unique monoclonal antibody that targets a distinct small loop epitope on the CD20 molecule.
  • Preclinical data show that ofatumumab is active against B-cell lymphoma/chronic lymphocytic leukemia cells with low CD20-antigen density and high expression of complement inhibitory molecules.
  • In a phase 1/2 trial evaluating safety and efficacy of ofatumumab in relapsed or refractory follicular non-Hodgkin lymphoma (FL) grade 1 or 2, 4 dose groups of 10 patients received 4 weekly infusions of 300, 500, 700, or 1000 mg.
  • Patients had a median of 2 prior FL therapies and 13% had elevated lactate dehydrogenase.
  • Treatment caused immediate and profound B-cell depletion, and 65% of patients reverted to negative BCL2 status.
  • Median time to progression for all patients/responders was 8.8/32.6 months, and median duration of response was 29.9 months at a median/maximum follow-up of 9.2/38.6 months.
  • Ofatumumab is currently being evaluated in patients with rituximab-refractory FL.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antigens, CD20 / immunology. Lymphoma, Follicular / drug therapy. Lymphoma, Follicular / immunology
  • [MeSH-minor] Adult. Aged. B-Lymphocytes / immunology. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Female. Follow-Up Studies. Humans. Infection / immunology. Kaplan-Meier Estimate. Male. Middle Aged. Recurrence. Treatment Outcome

  • Genetic Alliance. consumer health - Follicular Lymphoma.
  • Genetic Alliance. consumer health - Follicular lymphoma 1.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Blood. 2008 Sep 15;112(6):2584-5; author reply 2585 [18779407.001]
  • (PMID = 18390837.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00092274
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD20; 0 / ofatumumab
  •  go-up   go-down


25. Lin TS: Novel agents in chronic lymphocytic leukemia: efficacy and tolerability of new therapies. Clin Lymphoma Myeloma; 2008 Aug;8 Suppl 4:S137-43
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] Novel agents in chronic lymphocytic leukemia: efficacy and tolerability of new therapies.
  • Alkylating agents and purine analogues have been the mainstays of therapy for chronic lymphocytic leukemia (CLL) for decades.
  • The past decade witnessed the general clinical use of monoclonal antibodies such as rituximab and alemtuzumab, both as single agents and in combination regimens with cytotoxic drugs, for previously untreated and relapsed CLL.
  • Despite these advances in first-line therapy, patients with CLL invariably experience relapse and often acquire high-risk chromosomal abnormalities, such as del(11q22) and del(17p13), which result in resistance to current therapies.
  • Patients who are refractory to fludarabine-based therapy have a median survival of <1 year.
  • Therefore, new agents with novel mechanisms of action are needed for the treatment of patients with relapsed CLL, particularly for patients with high-risk genetic features.
  • (1) the alkylator bendamustine, (2) the cyclin-dependent kinase inhibitor flavopiridol, (3) the immunomodulating drug lenalidomide, (4) the bcl-2 antisense oligonucleotide oblimersen, and (5) the Bcl-2 small-molecule inhibitor obatoclax.
  • While these agents have demonstrated exciting clinical activity against genetically high-risk CLL, they have also induced toxicities that have not been commonly observed with previous CLL therapies.
  • The most notable toxicities have been tumor lysis syndrome and tumor flare, which are potentially serious or even fatal complications of these new therapies.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Bendamustine Hydrochloride. Flavonoids / adverse effects. Flavonoids / therapeutic use. Humans. Maximum Tolerated Dose. Nitrogen Mustard Compounds / adverse effects. Nitrogen Mustard Compounds / therapeutic use. Piperidines / adverse effects. Piperidines / therapeutic use. Pyrroles / adverse effects. Pyrroles / therapeutic use. Thalidomide / adverse effects. Thalidomide / analogs & derivatives. Thalidomide / therapeutic use. Thionucleotides / adverse effects. Thionucleotides / therapeutic use. Treatment Outcome

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Bendamustine .
  • Hazardous Substances Data Bank. THALIDOMIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18952544.001).
  • [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
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Flavonoids; 0 / Nitrogen Mustard Compounds; 0 / Piperidines; 0 / Pyrroles; 0 / Thionucleotides; 0 / obatoclax; 45AD6X575G / alvocidib; 4Z8R6ORS6L / Thalidomide; 85J5ZP6YSL / oblimersen; 981Y8SX18M / Bendamustine Hydrochloride; F0P408N6V4 / lenalidomide
  • [Number-of-references] 30
  •  go-up   go-down


28. Oertel J, Oertel B, Dörken B: Detection of small numbers of cells characteristic for haematological disorders in peripheral blood (the deep diff). Clin Lab Haematol; 2002 Apr;24(2):73-80
Hazardous Substances Data Bank. METHYLENE BLUE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of small numbers of cells characteristic for haematological disorders in peripheral blood (the deep diff).
  • We studied cytocentrifuge preparations of peripheral blood mononuclear leucocytes in haematological patients with nondiagnostic white cell differential counts.
  • This approach (the 'deep diff') enabled the detection of small numbers of diagnostically significant cells in a majority of patients.
  • We observed centrocytes in seven patients with follicular lymphoma, mantle cells in five patients with mantle cell lymphoma and marginal zone cells in five patients with nodal marginal zone lymphoma.
  • We detected small percentages of lymphoma cells in cytospins of mononuclear leucocytes in 12 patients with large B-cell lymphoma, Burkitt's lymphoma and anaplastic large-cell lymphoma.
  • The deep diff was nondiagnostic in 5/6 patients with hairy cell leukaemia and in 9/10 patients with Waldenström's macroglobulinaemia and small lymphocytic lymphoma.
  • Increased counts of leukaemic cells were found in 12/13 patients with acute leukaemia with < 3% blasts in the conventional white cell differential.
  • Increased blasts were also observed in six patients with refractory anaemia with excess of blasts (RAEB).
  • Decreased blasts were found in five patients with aplastic anaemia and in nine patients with bone marrow aplasia after intensive chemotherapy.
  • Increased plasma cell counts were observed in 13/14 patients with advanced plasma cell myeloma.
  • [MeSH-major] Blood Cell Count. Hematologic Diseases / blood
  • [MeSH-minor] Anemia / blood. Anemia, Refractory, with Excess of Blasts / blood. Centrifugation. Coloring Agents. Eosine Yellowish-(YS). Humans. Leukemia / blood. Lymphoma, Non-Hodgkin / blood. Methylene Blue. Neoplastic Cells, Circulating. Retrospective Studies. Staining and Labeling / methods. Waldenstrom Macroglobulinemia / blood

  • MedlinePlus Health Information. consumer health - Blood Count Tests.
  • MedlinePlus Health Information. consumer health - Blood Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11985551.001).
  • [ISSN] 0141-9854
  • [Journal-full-title] Clinical and laboratory haematology
  • [ISO-abbreviation] Clin Lab Haematol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Coloring Agents; 0 / May-Grunwald Giemsa; T42P99266K / Methylene Blue; TDQ283MPCW / Eosine Yellowish-(YS)
  •  go-up   go-down


29. Hainsworth JD: First-line and maintenance treatment with rituximab for patients with indolent non-Hodgkin's lymphoma. Semin Oncol; 2003 Feb;30(1 Suppl 2):9-15
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] First-line and maintenance treatment with rituximab for patients with indolent non-Hodgkin's lymphoma.
  • The chimeric human-mouse anti-CD20 monoclonal antibody rituximab has durable single-agent activity in patients with relapsed and refractory indolent non-Hodgkin's lymphoma.
  • The focus of this report is a phase II trial evaluating the efficacy of single-agent rituximab as first-line therapy in patients with indolent lymphoma and scheduled maintenance treatment in prolonging duration of remission.
  • Of 62 patients entered in the trial, 61% had follicular lymphoma while 39% had small lymphocytic lymphoma (SLL).
  • The response rate improved to 73% (37% complete response) following maintenance rituximab therapy and was similar in patients with follicular lymphoma and SLL (76% v 70%, respectively).
  • Single-agent therapy was well tolerated and maintenance rituximab was administered without grade 3/4 toxicity.
  • Because of the higher activity of rituximab in this study compared with previous results in patients with relapsed or refractory SLL, a second phase II trial of identical design but limited to patients with SLL and chronic lymphocytic leukemia was initiated.
  • In summary, rituximab appears highly active as first-line single-agent therapy for indolent non-Hodgkin's lymphoma and responses may be improved with maintenance courses of rituximab.
  • Results suggest a higher response rate to rituximab when used as first-line compared with second/third-line treatment, particularly in the subset of patients with SLL and chronic lymphocytic leukemia.
  • Further follow-up will provide important information regarding the impact of first-line and maintenance rituximab on progression-free survival in patients with indolent non-Hodgkin's lymphoma.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2003, Elsevier Science (USA). All rights reserved.
  • (PMID = 12652459.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 18
  •  go-up   go-down


30. Robak T, Robak P, Smolewski P: TRU-016, a humanized anti-CD37 IgG fusion protein for the potential treatment of B-cell malignancies. Curr Opin Investig Drugs; 2009 Dec;10(12):1383-90
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] TRU-016, a humanized anti-CD37 IgG fusion protein for the potential treatment of B-cell malignancies.
  • TRU-016, under development by Trubion Pharmaceuticals Inc and Facet Biotech Corp, is an intravenously administered anti-CD37 IgG fusion protein for the potential treatment of B-cell malignancies, including chronic lymphocytic leukemia (CLL) and non-Hodgkin's lymphoma (NHL), as well as for autoimmune and inflammatory diseases.
  • TRU-016 was created by humanizing SMIP-016, a mouse/human chimeric protein that demonstrated antitumor activity against lymphoid malignancies in preclinical studies, including in human B-cell tumor mouse xenograft models.
  • In a phase I/II clinical trial in refractory or relapsed patients with CLL or small lymphocytic lymphoma, TRU-016 was well tolerated, with clinical benefit and a reduced absolute lymphocyte count observed in all cohorts dosed at > 0.1 mg/kg.
  • TRU-016 is a promising therapeutic agent for patients with B-cell lymphoid malignancies, especially patients refractory to standard treatment.
  • [MeSH-major] Antigens, CD / immunology. Antigens, Neoplasm / immunology. Antineoplastic Agents / therapeutic use. Immunoglobulin G / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, B-Cell / drug therapy. Recombinant Fusion Proteins / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Autoimmune Diseases / drug therapy. Autoimmune Diseases / immunology. Clinical Trials as Topic. Drug Evaluation, Preclinical. Humans. Inflammation / drug therapy. Inflammation / immunology. Mice. Tetraspanins

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19943209.001).
  • [ISSN] 2040-3429
  • [Journal-full-title] Current opinion in investigational drugs (London, England : 2000)
  • [ISO-abbreviation] Curr Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD37 protein, human; 0 / Immunoglobulin G; 0 / Recombinant Fusion Proteins; 0 / TRU 016; 0 / Tetraspanins
  • [Number-of-references] 73
  •  go-up   go-down


31. Giles FJ, Cortes J, Jones D, Bergstrom D, Kantarjian H, Freedman SJ: MK-0457, a novel kinase inhibitor, is active in patients with chronic myeloid leukemia or acute lymphocytic leukemia with the T315I BCR-ABL mutation. Blood; 2007 Jan 15;109(2):500-2
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] MK-0457, a novel kinase inhibitor, is active in patients with chronic myeloid leukemia or acute lymphocytic leukemia with the T315I BCR-ABL mutation.
  • MK-0457 (VX-680) is a small-molecule aurora kinase (AK) inhibitor with preclinical antileukemia activity.
  • MK-0457 has in vitro activity against cells expressing wild-type or mutated BCR-ABL, including the T315I BCR-ABL mutation.
  • Three patients with T315I abl-mutated chronic myeloid leukemia (CML) or Philadelphia chromosome (Ph)-positive acute lymphocytic leukemia (ALL) have achieved clinical responses to doses of MK-04547 that are not associated with adverse events.
  • The observation of responses in 3 patients with T315I phenotype-refractory CML or Ph-positive ALL, at doses of MK-0457 associated with no significant extramedullary toxicity, is very encouraging.
  • [MeSH-major] Fusion Proteins, bcr-abl / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Protein Kinase Inhibitors / therapeutic use
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / drug effects. Adaptor Proteins, Signal Transducing / metabolism. Adult. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Female. Humans. Infusions, Intravenous. Male. Maximum Tolerated Dose. Middle Aged. Mutation. Nuclear Proteins / drug effects. Nuclear Proteins / metabolism. Phenotype. Phosphorylation. Treatment Outcome


32. Clavio M, Quintino S, Venturino C, Ballerini F, Varaldo R, Gatto S, Galbusera V, Garrone A, Grasso R, Canepa L, Miglino M, Pierri I, Gobbi M: Lymphoplasmacytic lymphoma/immunocytoma: towards a disease-targeted treatment? J Exp Clin Cancer Res; 2001 Sep;20(3):351-8
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] Lymphoplasmacytic lymphoma/immunocytoma: towards a disease-targeted treatment?
  • Lymphoplasmacytic-lymphoplasmacytoid lymphoma (LPL)/Waldenstrom's macroglobulinemia (WM) or immunocytoma (IMC) consists of diffuse proliferation of small mature B lymphocytes, plasmacytoid lymphocytes, and plasma-cells.
  • The nosographic definition includes the lack of histological, immunophenotypic, cytogenetic, and molecular markers considered specific of other types of lymphoma.
  • The cells show surface Ig (usually IgM), B-cell-associated antigens and display the CD5-, CD23- and CD10- phenotype, which allows for differential diagnosis from B-CLL and mantle cell lymphoma. t(9;14)(p13;q32) chromosomal translocation has been found in 50% of all LPL cases.
  • The cytogenetic rearrangement juxtaposes the PAX-5 gene, which encodes for an essential transcription factor for B-cell proliferation and differention, to the Ig heavy chain gene.
  • The combination of chlorambucil and prednisone holds as the standard treatment and seems to guarantee good control of the disease in most patients.
  • Similar therapeutic results have been described with the combination of cyclophosphamide, vincristine, prednisone with (CHOP) or without doxorubicin (CVP), or with a combination of other alkylating agents and prednisone.
  • Nucleoside analogues, alone or in combination with alkylating agents and anthracyclines, provide good salvage therapy for IMC and being increasingly employed as first line therapy.
  • Therapy was well tolerated by all patients, and there was no decrease in cellular immune function, or significant infectious morbidity.
  • Partial responses were noted in three of these patients, including two with fludarabine-refractory disease.
  • Furthermore, Weide et al. first reported that WM-associated polyneuropathy can be treated effectively with a combination of chemotherapy and the anti-CD20 monoclonal antibody rituximab.
  • Most published trials exploring the efficacy of high dose treatment as salvage therapy for relapsed or refractory low grade non Hodgkin's lymphoma have included prevalently follicular or lymphocytic lymphomas.
  • In selected high risk patients radioimmunotherapy with autologous stem-cell rescue, and myeloablative therapy followed either by autologous stem cell transplantation (SCT) or allogeneic SCT might represent an alternative strategy.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Lymphoma, B-Cell / therapy
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. B-Lymphocytes / pathology. Diagnosis, Differential. Humans. Immunophenotyping. Immunotherapy. Lymphoproliferative Disorders / immunology. Rituximab

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11718214.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 46
  •  go-up   go-down


33. Robak T, Lech-Maranda E, Janus A, Blonski J, Wierzbowska A, Gora-Tybor J: Cladribine combined with cyclophosphamide and mitoxantrone is an active salvage therapy in advanced non-Hodgkin's lymphoma. Leuk Lymphoma; 2007 Jun;48(6):1092-101
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cladribine combined with cyclophosphamide and mitoxantrone is an active salvage therapy in advanced non-Hodgkin's lymphoma.
  • The aim of this study was to determine the feasibility, efficacy and toxicity of the combined therapy consisting of cladribine (2-CdA), mitoxantrone and cyclophosphamide (CMC regimen) in patients with refractory or relapsed non-Hodgkin's lymphoma (NHL).
  • Thirty six patients, 14 with mantle cell lymphoma (MCL), 10 with diffuse large B-cell lymphoma (DLBCL), 5 with follicular lymphoma (FL), 3 with small lymphocytic lymphoma (SLL), and 4 with T-cell lymphoma were enrolled to the study.
  • Seven of 19 patients with CR/PR are still in remission with a median follow-up of 3 months (range, 2-17 months).
  • The median overall survival (OS) for the entire group was 9 months (range, 0.1-7 months).
  • There was a significant difference in OS between responders and nonresponders after CMC therapy (log rank test, P = 0.015).
  • When different disease status before CMC treatment was considered, a trend toward longer survival of recurrent patients was observed (log rank test, P = 0.08).
  • Grade 3-4 neutropenia developed in 14 (39%) patients, and 16 episodes (15%) of grade 3-4 infections were observed.
  • The results of our study show that the CMC regimen is effective salvage therapy with acceptable toxicity in heavily pretreated patients with NHL including MCL and DLBCL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cladribine / adverse effects. Cladribine / therapeutic use. Cyclophosphamide / adverse effects. Cyclophosphamide / therapeutic use. Feasibility Studies. Female. Humans. Male. Middle Aged. Mitoxantrone / adverse effects. Mitoxantrone / therapeutic use. Salvage Therapy / adverse effects. Survival Analysis. Treatment Outcome

  • Hazardous Substances Data Bank. CLADRIBINE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17577772.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 47M74X9YT5 / Cladribine; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; CMC protocol 2
  •  go-up   go-down


34. Paoluzzi L, O'Connor OA: Mechanistic rationale and clinical evidence for the efficacy of proteasome inhibitors against indolent and mantle cell lymphomas. BioDrugs; 2006;20(1):13-23
Hazardous Substances Data Bank. BORTEZOMIB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanistic rationale and clinical evidence for the efficacy of proteasome inhibitors against indolent and mantle cell lymphomas.
  • Proteasome inhibitors represent a new approach for the treatment of many forms of cancer, especially select hematological malignancies.
  • While only some of the consequences of inhibiting this activity are understood, a growing amount of data suggests that inhibition of the proteasome is associated with a remarkable panoply of different biological effects that include cell cycle arrest, apoptosis, changes in cell surface adhesion markers, and an increased sensitivity to standard chemotherapy and radiation therapy.
  • Bortezomib was recently approved by the US FDA for the treatment of relapsed or refractory multiple myeloma.
  • In addition, bortezomib has also shown encouraging results in the treatment of select types of non-Hodgkin lymphomas (NHLs).
  • Ongoing phase II clinical trials in pretreated patients are exploring bortezomib in different histologies of NHLs and in combination with conventional chemotherapy.
  • Preliminary data have shown interesting activity, especially in patients with follicular, marginal zone, and mantle cell lymphoma; in these populations, durable complete and partial remissions have been reported.
  • The toxicity profile of this drug, coupled with its unusual mechanism of action, make it a potentially important agent warranting further preclinical and clinical attention.
  • However, many unanswered questions remain regarding how best to employ bortezomib in the conventional treatment of lymphoma.
  • The apparent lack of activity in different subtypes of lymphoma, such as small lymphocytic lymphoma/chronic lymphocytic leukemia and diffuse large B-cell lymphoma, as well as a lack of understanding about the best way to combine bortezomib with standard therapies for indolent NHLs, raises important questions regarding the mechanistic basis for its effects.
  • We will undoubtedly need to understand these effects better in order to fully exploit the potential of this new class of drugs.
  • [MeSH-major] Boronic Acids / therapeutic use. Lymphoma, Non-Hodgkin / drug therapy. Protease Inhibitors / therapeutic use. Pyrazines / therapeutic use

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16573348.001).
  • [ISSN] 1173-8804
  • [Journal-full-title] BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy
  • [ISO-abbreviation] BioDrugs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / UO1 CA 69913
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  • [Number-of-references] 87
  •  go-up   go-down


35. Cowan RA, Murby B, Gunton D, Owens SE, Hoyes KP, Sharma HL, Smith AM, Chang J, van Kessel B, Nuttall PM, Crowther D: Autologous lymphocytes as vectors to target therapeutic radiation, using indium-114m, in patients with lymphoid cell malignancy. Br J Haematol; 2002 Nov;119(2):459-66
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autologous lymphocytes as vectors to target therapeutic radiation, using indium-114m, in patients with lymphoid cell malignancy.
  • Autologous lymphocytes provide a potential vector for the delivery of a cytotoxic agent in patients with lymphoid cell malignancy.
  • This report describes a phase I-II study using autologous lymphocytes to target the radionuclide indium-114m ((114m)In) in patients with refractory chronic lymphocytic leukaemia or small lymphocytic non-Hodgkin's lymphoma.
  • Nineteen patients, the majority of whom had been heavily pretreated with conventional chemotherapy and radiotherapy, received between 69 and 211 MBq (114m)In-labelled autologous lymphocytes.
  • The first notable response in every patient was a fall in peripheral lymphocyte count.
  • The indium treatment was not associated with any subjective toxicity, although all patients suffered from myelosuppression, with thrombocytopenia being the dose-limiting factor.
  • [MeSH-major] Indium Radioisotopes / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / radiotherapy. Lymphocytes. Radioimmunotherapy / methods

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12406086.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Indium Radioisotopes
  •  go-up   go-down


36. Eklund JW, Kuzel TM: Denileukin diftitox: a concise clinical review. Expert Rev Anticancer Ther; 2005 Feb;5(1):33-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Denileukin diftitox (DAB389IL-2; Ontak) is a novel recombinant fusion protein approved by the US Food and Drug Administration for the treatment of relapsed or refractory cutaneous T-cell lymphoma.
  • This article will review the clinical trials leading to the approval of denileukin diftitox for cutaneous T-cell lymphoma, and discuss the potential future role of this novel drug in patients with both malignant and nonmalignant diseases, including non-Hodgkin's lymphoma, chronic lymphocytic leukemia, solid tumors, psoriasis and graft-versus-host disease.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Diphtheria Toxin / therapeutic use. Interleukin-2 / therapeutic use. Lymphoma, T-Cell, Cutaneous / drug therapy
  • [MeSH-minor] Carcinoma, Non-Small-Cell Lung / drug therapy. Clinical Trials as Topic. Graft vs Host Disease / drug therapy. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lung Neoplasms / drug therapy. Lymphoma, Non-Hodgkin / drug therapy. Psoriasis / drug therapy. Recombinant Fusion Proteins / therapeutic use. Survival

  • 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 = 15757436.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Diphtheria Toxin; 0 / Interleukin-2; 0 / Recombinant Fusion Proteins; 25E79B5CTM / denileukin diftitox
  • [Number-of-references] 26
  •  go-up   go-down


37. Rodig SJ, Abramson JS, Pinkus GS, Treon SP, Dorfman DM, Dong HY, Shipp MA, Kutok JL: Heterogeneous CD52 expression among hematologic neoplasms: implications for the use of alemtuzumab (CAMPATH-1H). Clin Cancer Res; 2006 Dec 1;12(23):7174-9
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.
  • The humanized monoclonal antibody alemtuzumab (CAMPATH-1H) is specific for CD52 and is Food and Drug Administration - approved for the treatment of relapsed or refractory chronic lymphocytic leukemia (CLL).
  • The utility of CAMPATH in the treatment of other hematologic neoplasms has been explored; however, a comprehensive survey of CD52 expression among a broad spectrum of WHO-defined tumor types has not been completed.
  • RESULTS: The vast majority of low-grade B cell lymphoproliferative disorders (CLL/small lymphocytic leukemia, follicular lymphoma, lymphoplasmacytic lymphoma, hairy cell leukemia, and mucosa-associated lymphoid tissue lymphomas) express CD52.
  • In addition, we found that the majority of precursor B cell acute lymphoblastic leukemia/lymphomas express this antigen.
  • In contrast, there is surprising heterogeneity in CD52 expression among more aggressive B cell lymphomas, with 25% of cases of diffuse large B cell lymphoma and Burkitt lymphoma demonstrating no detectable CD52.
  • In addition, the majority of neoplasms of the T cell lineage are negative for the antigen, including most cases of precursor T cell acute lymphoblastic leukemia/lymphoma, anaplastic large cell lymphoma, and peripheral T cell lymphoma, not otherwise specified.
  • Finally, the vast majority of cases of acute myeloid leukemia, Hodgkin lymphoma, and multiple myeloma are negative for CD52 expression.
  • CONCLUSION: In contrast with CLL, the variable expression of CD52 among other hematologic malignancies suggests that target validation on a case-by-case basis will likely be necessary to guide the rational analysis of CAMPATH therapy.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antigens, CD / biosynthesis. Antigens, Neoplasm / biosynthesis. Glycoproteins / biosynthesis. Leukemia, Myeloid. Lymphoma, B-Cell. Lymphoma, T-Cell. Lymphoproliferative Disorders
  • [MeSH-minor] Acute Disease. Antibodies, Monoclonal, Humanized. Humans. Immunohistochemistry. Treatment Outcome

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17145843.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Glycoproteins; 3A189DH42V / alemtuzumab
  •  go-up   go-down


38. O'Connor OA, Heaney ML, Schwartz L, Richardson S, Willim R, MacGregor-Cortelli B, Curly T, Moskowitz C, Portlock C, Horwitz S, Zelenetz AD, Frankel S, Richon V, Marks P, Kelly WK: Clinical experience with intravenous and oral formulations of the novel histone deacetylase inhibitor suberoylanilide hydroxamic acid in patients with advanced hematologic malignancies. J Clin Oncol; 2006 Jan 1;24(1):166-73
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The spectrum of diseases included patients with diffuse large B-cell lymphoma (n = 12), Hodgkin's disease (HD; n = 12), multiple myeloma (n = 2), T-cell lymphoma (n = 3), mantle cell lymphoma (n = 2), small lymphocytic lymphoma (n = 2), and myeloid leukemia (n = 2).
  • One patient with transformed small lymphocytic lymphoma met criteria for complete response, whereas another met the criteria for partial response (PR).
  • One patient with refractory HD had a PR, whereas three patients had stable disease for up to 9 months.
  • CONCLUSION: These results suggest that SAHA has activity in hematologic malignancies including HD and select subtypes of non-Hodgkin's lymphoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Hematologic Neoplasms / drug therapy. Histone Deacetylase Inhibitors. Hydroxamic Acids / administration & dosage


39. Frankel SR: Oblimersen sodium (G3139 Bcl-2 antisense oligonucleotide) therapy in Waldenstrom's macroglobulinemia: a targeted approach to enhance apoptosis. Semin Oncol; 2003 Apr;30(2):300-4
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] Oblimersen sodium (G3139 Bcl-2 antisense oligonucleotide) therapy in Waldenstrom's macroglobulinemia: a targeted approach to enhance apoptosis.
  • The components of the apoptotic pathway are targets for anticancer therapy.
  • Bcl-2 protein inhibits apoptosis and confers resistance to treatment with traditional cytotoxic chemotherapy, radiotherapy, and monoclonal antibodies.
  • Randomized clinical trials are currently underway to evaluate the efficacy and tolerability of oblimersen in combination with cytotoxic chemotherapy in chronic lymphocytic leukemia (CLL), multiple myeloma (MM), malignant melanoma, and non-small cell lung cancer.
  • In addition, nonrandomized trials are underway to evaluate oblimersen in non-Hodgkin's lymphoma (NHL), acute myeloid leukemia (AML), and hormone-refractory prostate cancer.
  • Preclinical data support the clinical evaluation of oblimersen in additional tumor types, including chronic myelogenous leukemia, and breast, small cell lung, gastric, colon, bladder (CML), and Merkel cell cancers.
  • Enhancement of the efficacy of anticancer treatments with oblimersen Bcl-2 antisense therapy represents a promising new apoptosis-modulating strategy, and ongoing clinical trials will test this therapeutic approach.
  • [MeSH-major] Apoptosis. Down-Regulation / drug effects. Genes, bcl-2 / genetics. Oligonucleotides, Antisense / therapeutic use. Thionucleotides / therapeutic use. Waldenstrom Macroglobulinemia / drug therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2003 Elsevier Inc. All rights reserved.
  • (PMID = 12720157.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Thionucleotides; 85J5ZP6YSL / oblimersen
  • [Number-of-references] 45
  •  go-up   go-down


40. Klasa RJ, Gillum AM, Klem RE, Frankel SR: Oblimersen Bcl-2 antisense: facilitating apoptosis in anticancer treatment. Antisense Nucleic Acid Drug Dev; 2002 Jun;12(3):193-213
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] Oblimersen Bcl-2 antisense: facilitating apoptosis in anticancer treatment.
  • The components of the apoptotic program are targets for anticancer therapy.
  • Bcl-2 protein inhibits apoptosis and confers resistance to treatment with traditional cytotoxic chemotherapy, radiotherapy, and monoclonal antibodies (mAb).
  • Randomized clinical trials are currently underway to evaluate the efficacy and tolerability of oblimersen in combination with cytotoxic chemotherapy in chronic lymphocytic leukemia, multiple myeloma, malignant melanoma, and non-small cell lung cancer.
  • In addition, nonrandomized trials are under way to evaluate oblimersen in non-Hodgkin's lymphoma, acute myeloid leukemia, and hormone-refractory prostate cancer.
  • Preclinical data also support the clinical evaluation of oblimersen in additional tumor types, including chronic myelogenous leukemia and breast, small cell lung, gastric, colon, bladder, and Merkel cell cancers.
  • Enhancement of the efficacy of anticancer treatments with oblimersen Bcl-2 antisense therapy represents a promising new apoptosis-modulating strategy, and ongoing clinical trials will test this therapeutic approach.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Oligonucleotides, Antisense / pharmacology. Proto-Oncogene Proteins c-bcl-2 / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12162702.001).
  • [ISSN] 1087-2906
  • [Journal-full-title] Antisense & nucleic acid drug development
  • [ISO-abbreviation] Antisense Nucleic Acid Drug Dev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger
  • [Number-of-references] 124
  •  go-up   go-down


41. Uppenkamp M, Engert A, Diehl V, Bunjes D, Huhn D, Brittinger G: Monoclonal antibody therapy with CAMPATH-1H in patients with relapsed high- and low-grade non-Hodgkin's lymphomas: a multicenter phase I/II study. Ann Hematol; 2002 Jan;81(1):26-32
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] Monoclonal antibody therapy with CAMPATH-1H in patients with relapsed high- and low-grade non-Hodgkin's lymphomas: a multicenter phase I/II study.
  • CAMPATH-1H (CP-1H) is a humanized monoclonal antibody directed against the CD52 antigen with promising therapeutic effects in patients with small cell lymphocytic non-Hodgkin's lymphomas (NHL) of B- and T-cell type.
  • We report about the response and toxicity of CP-1H in 18 patients with B-cell NHL who were treated in four clinical centers in Germany.
  • All patients had received chemotherapy before and had either relapsed or were refractory to conventional therapy.
  • Two patients received CP-1H in a dose-range finding trial once weekly and 16 patients as a fixed dose of 30 mg three times weekly.
  • Prophylactic treatment of the side effects is strongly recommended for patients treated either with CP-1H alone or in combination with chemotherapy.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antibodies, Neoplasm / administration & dosage. Antineoplastic Agents / administration & dosage. Lymphoma, Non-Hodgkin / drug therapy
  • [MeSH-minor] Aged. Antibodies, Monoclonal, Humanized. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Recurrence. Treatment Outcome

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11807632.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 3A189DH42V / alemtuzumab
  •  go-up   go-down


42. Senderowicz AM: Novel direct and indirect cyclin-dependent kinase modulators for the prevention and treatment of human neoplasms. Cancer Chemother Pharmacol; 2003 Jul;52 Suppl 1:S61-73
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] Novel direct and indirect cyclin-dependent kinase modulators for the prevention and treatment of human neoplasms.
  • Abnormalities in the cell cycle are responsible for the majority of human neoplasias.
  • Most abnormalities occur due to hyperphosphorylation of the tumor suppressor gene Rb by the key regulators of the cell cycle, the cyclin-dependent kinases (CDKs).
  • Thus, a pharmacological CDK inhibitor may be useful in the prevention and/or treatment of human neoplasms.
  • Antitumor activity was observed in some patients with non-Hodgkin's lymphoma and renal, colon, and prostate cancers.
  • Concentrations between 300 and 500 n M-necessary to inhibit CDK-were achieved safely.
  • Phase II trials with infusional flavopiridol and phase I infusional trials in combination with standard chemotherapy are being completed with encouraging results.
  • Phase II/III trials using this 1-h schedule in several tumor types including non-small-cell lung cancer, chronic lymphocytic leukemia, mantle cell lymphoma, and head and neck cancer are being conducted worldwide.
  • (2) it promotes cell-cycle arrest by accumulation in p21/p27;.
  • In the initial UCN-01 clinical trial (continuous infusion for 72 h), a prolonged half-life of about 600 h (100 times longer than in preclinical models) was observed.
  • Another patient with refractory anaplastic large-cell lymphoma had no evidence of disease at >4 years.
  • " Moreover, it is still unclear which pharmacodynamic endpoint reflects loss of CDK activity in tissue samples from patients in these trials.
  • Despite these caveats, we feel that CDKs are sensible targets for cancer therapy and that there are several small-molecule CDK modulators in clinical trials with encouraging results.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclin-Dependent Kinases / antagonists & inhibitors. Enzyme Inhibitors / therapeutic use. Neoplasms / drug therapy
  • [MeSH-minor] Alkaloids / administration & dosage. Animals. Cell Cycle / drug effects. Clinical Trials as Topic. Flavonoids / administration & dosage. Humans. Piperidines / administration & dosage. Staurosporine / analogs & derivatives. Tumor Cells, Cultured


43. Sternberg DW, Licht JD: Therapeutic intervention in leukemias that express the activated fms-like tyrosine kinase 3 (FLT3): opportunities and challenges. Curr Opin Hematol; 2005 Jan;12(1):7-13
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] Therapeutic intervention in leukemias that express the activated fms-like tyrosine kinase 3 (FLT3): opportunities and challenges.
  • This article reviews recent efforts to disrupt FLT3 signaling in acute myelogenous leukemia and to identify potential therapeutic challenges posed by the acquisition of resistance mutations in these malignancies.
  • Although the agents are well tolerated by patients, clinical responses in relapsed or refractory acute myelogenous leukemia (AML) are limited and transient.
  • Nevertheless, these agents may hold promise when combined with traditional chemotherapy.
  • Use of tyrosine kinase inhibitors for AML therapy is hindered by the acquisition of mutations in the kinase catalytic domain, and in the case of BCR-ABL, these mutations confer resistance to imatinib.
  • New efforts focus on blocking the binding of FLT3 ligand to its receptor as a means of inhibiting autocrine stimulation in leukemogenesis.
  • SUMMARY: FLT3 is widely expressed in AML and some cases of acute lymphocytic leukemia.
  • The development of FLT3 small molecule kinase inhibitors follows from research efforts to understand signal transduction and profiles of gene expression in leukemia pathogenesis.
  • Thus, FLT3 is a promising target for therapeutic intervention.
  • Research priorities will include (1) identification of other groups of patients likely to benefit from FLT3 inhibition, (2) the optimal use of FLT3 inhibitors in combination with other agents, and (3) development of molecules that overcome resistance to FLT3 inhibitors that arise as a result of further acquired mutations in the receptor.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Proto-Oncogene Proteins / antagonists & inhibitors. Proto-Oncogene Proteins / genetics. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptor Protein-Tyrosine Kinases / genetics
  • [MeSH-minor] Animals. Combined Modality Therapy. Humans. Structure-Activity Relationship. fms-Like Tyrosine Kinase 3

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • 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 = 15604885.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K08 CA82261; United States / NCI NIH HHS / CA / R01 CA59936
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 69
  •  go-up   go-down


44. Pangalis GA, Dimopoulou MN, Angelopoulou MK, Tsekouras C, Vassilakopoulos TP, Vaiopoulos G, Siakantaris MP: Campath-1H (anti-CD52) monoclonal antibody therapy in lymphoproliferative disorders. Med Oncol; 2001;18(2):99-107
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] Campath-1H (anti-CD52) monoclonal antibody therapy in lymphoproliferative disorders.
  • Campath-1H is a humanized monoclonal antibody targeted against the CDw52 membrane antigen of lymphocytes, which causes complement and antibody-dependent cell-mediated cytotoxicity.
  • Campath-1H has been used in B-chronic lymphocytic leukemia (B-CLL), T-prolymphocytic leukemia (T-PLL), and low-grade non-Hodgkin's lymphoma (LGNHL).
  • Because of the antibody's higher activity on circulating lymphocytes, it has been used for in vivo purging of residual disease in B-CLL, followed by autologous stem-cell transplantation.
  • Promising results have been reported in a small number of patients with refractory autoimmune thrombocytopenia of lymphoproliferative disorders.
  • The main complications of Campath-1H treatment are caused by tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 release, usually during the first intravenous infusion, and include fever, rigor, nausea, vomiting, and hypotension responsive to steroids.
  • Immunosupression resulting from normal B- and T-lymphocyte depletion is frequent, resulting in an increased risk for opportunistic infections.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, B-Cell / drug therapy. Leukemia, Prolymphocytic / drug therapy. Lymphoma, Non-Hodgkin / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Dose-Response Relationship, Drug. Humans. Immunosuppression. Infection. Infusions, Intravenous. Interleukin-6 / adverse effects. Interleukin-6 / secretion. Phenotype. Risk Factors. Treatment Outcome. Tumor Necrosis Factor-alpha / adverse effects. Tumor Necrosis Factor-alpha / secretion

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Invest. 1996 Dec 15;98(12):2819-26 [8981930.001]
  • [Cites] Br J Haematol. 1997 Jun;97(3):669-72 [9207420.001]
  • [Cites] Br J Haematol. 1996 Apr;93(1):151-3 [8611450.001]
  • [Cites] Med Oncol. 2000 Feb;17(1):70-3 [10713664.001]
  • [Cites] Tissue Antigens. 1990 Mar;35(3):118-27 [2165283.001]
  • [Cites] Leuk Lymphoma. 1996 Dec;24(1-2):93-101 [9049965.001]
  • [Cites] Lancet. 1992 Sep 26;340(8822):748-52 [1356177.001]
  • [Cites] Transplantation. 1988 Apr;45(4):753-9 [3282358.001]
  • [Cites] Biotechnology (N Y). 1991 Jan;9(1):64-8 [1367214.001]
  • [Cites] Semin Oncol. 1998 Feb;25(1):65-74 [9482528.001]
  • [Cites] Bone Marrow Transplant. 1996 May;17(5):819-24 [8733704.001]
  • [Cites] Leuk Lymphoma. 1991;5 Suppl 1:113-7 [27463491.001]
  • [Cites] Blood. 1998 Dec 15;92(12):4581-90 [9845524.001]
  • [Cites] J Clin Oncol. 1997 Jul;15(7):2667-72 [9215839.001]
  • [Cites] Semin Hematol. 1999 Oct;36(4 Suppl 5):12-7 [10528911.001]
  • [Cites] Br J Haematol. 2000 Mar;108(4):754-60 [10792280.001]
  • [Cites] J Clin Pathol. 1994 Apr;47(4):313-7 [8027367.001]
  • [Cites] Ann Oncol. 1995 Mar;6(3):219-35 [7612488.001]
  • [Cites] Blood. 1983 Oct;62(4):873-82 [6349718.001]
  • [Cites] Br J Haematol. 1995 Mar;89(3):506-15 [7734348.001]
  • [Cites] Semin Oncol. 1999 Oct;26(5 Suppl 14):52-7 [10561018.001]
  • [Cites] Semin Hematol. 1999 Apr;36(2):198-208 [10319388.001]
  • [Cites] Blood. 1989 May 1;73(6):1431-9 [2713487.001]
  • [Cites] Bone Marrow Transplant. 1996 Mar;17(3):305-8 [8704678.001]
  • [Cites] Blood. 1984 Nov;64(5):1085-93 [6333257.001]
  • [Cites] Lancet. 1988 Dec 17;2(8625):1394-9 [2904526.001]
  • [Cites] Leuk Lymphoma. 1994 Sep;15(1-2):61-4 [7858503.001]
  • [Cites] J Rheumatol. 1996 Jun;23(6):1103-6 [8782148.001]
  • [Cites] J Clin Oncol. 1998 Oct;16(10):3257-63 [9779699.001]
  • [Cites] Br J Haematol. 1997 Mar;96(3):617-9 [9054672.001]
  • [Cites] Eur J Immunol. 1991 Jul;21(7):1677-84 [1711975.001]
  • [Cites] Br J Haematol. 1993 Jul;84(3):542-4 [8217808.001]
  • [Cites] Lancet. 1993 Apr 17;341(8851):1037 [8096935.001]
  • [Cites] Mol Biol Med. 1983 Oct;1(3):305-19 [6390085.001]
  • [Cites] Semin Hematol. 1999 Apr;36(2):104-14 [10319379.001]
  • [Cites] Leuk Lymphoma. 1997 May;25(5-6):479-86 [9250818.001]
  • [Cites] Exp Hematol. 1999 Jul;27(7):1210-8 [10390197.001]
  • [Cites] Leuk Res. 1998 Feb;22(2):185-91 [9593475.001]
  • [Cites] Eur J Immunol. 1988 Oct;18(10):1507-14 [2973413.001]
  • [Cites] Curr Opin Oncol. 1996 Sep;8(5):353-9 [8914801.001]
  • [Cites] Transplantation. 1999 Feb 27;67(4):620-6 [10071037.001]
  • [Cites] Eur J Haematol. 1997 Jan;58(1):5-13 [9020367.001]
  • [Cites] N Engl J Med. 1990 Jul 26;323(4):250-4 [2366834.001]
  • [Cites] Leuk Lymphoma. 1990;2(3-4):179-93 [27456733.001]
  • [Cites] Curr Opin Hematol. 1998 Jul;5(4):237-43 [9747629.001]
  • [Cites] Nature. 1988 Mar 24;332(6162):323-7 [3127726.001]
  • [Cites] Semin Hematol. 1999 Apr;36(2):209-16 [10319389.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1165-71 [9694704.001]
  • [Cites] J Clin Oncol. 1997 Apr;15(4):1567-74 [9193354.001]
  • (PMID = 11778765.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 3A189DH42V / alemtuzumab
  • [Number-of-references] 60
  •  go-up   go-down


45. Cheson BD, Rummel MJ: Bendamustine: rebirth of an old drug. J Clin Oncol; 2009 Mar 20;27(9):1492-501
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] Bendamustine: rebirth of an old drug.
  • Bendamustine is a unique cytotoxic agent with structural similarities to alkylating agents and antimetabolites, but which is non-cross-resistant with alkylating agents and other drugs in vitro and in the clinic.
  • Early clinical studies conducted in the German Democratic Republic more than 30 years ago suggested promising activity in indolent non-Hodgkin's lymphoma (NHL).
  • Two North American trials reported responses in more than 70% of patients with chemotherapy- and rituximab-refractory disease, suggesting that bendamustine may be the most effective drug available for this patient population.
  • Response rates of 90% to 92%, with complete remission in 55% to 60%, have been reported in patients with follicular and mantle-cell lymphoma with the combination of bendamustine and rituximab.
  • Superiority over chlorambucil in previously untreated patients with chronic lymphocytic leukemia (CLL) led to its recent approval for this disease in the United States.
  • Bendamustine is approved in Germany for the treatment of patients with indolent NHL, CLL, and multiple myeloma.
  • Activity has also been noted in patients with breast cancer and small-cell lung cancer [corrected].
  • Questions related to the optimization of bendamustine therapy, including dose and schedule, role relative to other available agents, and management of toxicities, are being investigated.
  • However, the availability of bendamustine provides another effective treatment option for patients with lymphoid malignancies.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neoplasms / drug therapy. Nitrogen Mustard Compounds / therapeutic use

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. Bendamustine .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] J Clin Oncol. 2009 Jun 10;27(17):2892
  • (PMID = 19224851.001).
  • [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; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Nitrogen Mustard Compounds; 981Y8SX18M / Bendamustine Hydrochloride
  • [Number-of-references] 66
  •  go-up   go-down


46. Galustian C, Dalgleish A: Lenalidomide: a novel anticancer drug with multiple modalities. Expert Opin Pharmacother; 2009 Jan;10(1):125-33
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] Lenalidomide: a novel anticancer drug with multiple modalities.
  • Over the past 5 years, lenalidomide (Revlimid, Celgene Co., Summit, NJ, USA), a member of a class of drugs termed immunomodulatory drugs, has emerged as a significant weapon in the arsenal of cancer-therapeutics.
  • It is a lead therapeutic in multiple myeloma and del-5q myelodysplastic syndromes and has also been trialed for acute leukaemia and chronic lymphocytic leukaemia, relapsed or refractory Hodgkin's lymphoma, T-cell non-Hodgkin's lymphoma, prostate cancer, non-small cell lung cancer, malignant melanoma, renal cancer, advanced ovarian and peritoneal carcinoma.
  • The following review describes key clinical and mechanistic breakthroughs that have made lenalidomide a leading cancer therapeutic.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neoplasms / drug therapy. Thalidomide / analogs & derivatives

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. THALIDOMIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19236186.001).
  • [ISSN] 1744-7666
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
  • [Number-of-references] 78
  •  go-up   go-down


47. Roccaro AM, Vacca A, Ribatti D: Bortezomib in the treatment of cancer. Recent Pat Anticancer Drug Discov; 2006 Nov;1(3):397-403
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 the treatment of cancer.
  • It blocks activation of nuclear factor-kappa B (NF-kB), resulting in increased apoptosis, decreased angiogenic cytokine production, and inhibition of tumor cell adhesion to stroma.
  • Multiple myeloma is the prototype of cancer where bortezomib has shown marked in vitro activity, which was followed by rapid translation to phase I, II and III clinical trials, and resulted in accelerated approval by the FDA for the treatment of patients with relapsed refractory disease.
  • Different clinical trials are currently ongoing in multiple myeloma as well as in many others haematologic and solid tumors (mantle cell and follicular non-Hodgkin's lymphoma; peripheral T-cell lymphoma; Waldenström's macroglobulinemia, chronic lymphocytic leukemia; head and neck / gastroesophageal junction / stomach /colo-rectal / prostate / non-small cell lung cancer).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Neoplasms / drug therapy. Pyrazines / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Bortezomib. Clinical Trials as Topic. Humans. Patents as Topic. Proteasome Inhibitors. Signal Transduction / drug effects

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • 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 = 18221049.001).
  • [ISSN] 1574-8928
  • [Journal-full-title] Recent patents on anti-cancer drug discovery
  • [ISO-abbreviation] Recent Pat Anticancer Drug Discov
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  • [Number-of-references] 53
  •  go-up   go-down






Advertisement