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6. Kernt M, Hirneiss C, Neubauer AS, Kampik A: Minocycline is cytoprotective in human corneal endothelial cells and induces anti-apoptotic B-cell CLL/lymphoma 2 (Bcl-2) and X-linked inhibitor of apoptosis (XIAP). Br J Ophthalmol; 2010 Jul;94(7):940-6
Hazardous Substances Data Bank. MINOCYCLINE .

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  • [Title] Minocycline is cytoprotective in human corneal endothelial cells and induces anti-apoptotic B-cell CLL/lymphoma 2 (Bcl-2) and X-linked inhibitor of apoptosis (XIAP).
  • This study investigates the possible anti-apoptotic and cytoprotective effects of minocycline on a human corneal endothelial cell line (HCEC-SV40) cultured under oxidative stress and with transforming growth factor beta (TGF-beta).
  • Cell viability and the median inhibitory concentration (IC(50)) were evaluated after 48 h and after H(2)O(2) treatment (tetrazolium dye reduction assay and live-dead assay).
  • Expression of B-cell CLL/lymphoma 2 (Bcl-2) and X-linked inhibitor of apoptosis (XIAP) and their mRNA were assessed by reverse transcriptase (RT)-PCR and western blot analysis after treatment with minocycline alone and consecutive incubation with 200 microM H(2)O(2) and TGF-beta2.
  • CONCLUSION: In this study minocycline prevented apoptotic cell death in cultured CECs in vitro.

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  • (PMID = 20606027.001).
  • [ISSN] 1468-2079
  • [Journal-full-title] The British journal of ophthalmology
  • [ISO-abbreviation] Br J Ophthalmol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human; FYY3R43WGO / Minocycline
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7. Bagchi S: Alemtuzumab shows promise for CLL. Lancet Oncol; 2007 Dec;8(12):1060

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alemtuzumab shows promise for CLL.

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  • (PMID = 28581422.001).
  • [ISSN] 1474-5488
  • [Journal-full-title] The Lancet. Oncology
  • [ISO-abbreviation] Lancet Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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8. Chipuk JE, Moldoveanu T, Llambi F, Parsons MJ, Green DR: The BCL-2 family reunion. Mol Cell; 2010 Feb 12;37(3):299-310
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • B cell CLL/lymphoma-2 (BCL-2) and its relatives comprise the BCL-2 family of proteins, which were originally characterized with respect to their roles in controlling outer mitochondrial membrane integrity and apoptosis.
  • Here we will discuss the mechanisms and functions of the BCL-2 family in the context of these pathways, highlighting the complex integration and regulation of the BCL-2 family in cell fate decisions.

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  • [Cites] Mol Cell. 2009 Nov 13;36(3):355-63 [19917245.001]
  • [Cites] Mol Cell. 2009 Nov 13;36(3):487-99 [19917256.001]
  • [Cites] Mol Cell. 2009 Nov 25;36(4):696-703 [19941828.001]
  • [Cites] Nature. 2010 Jan 7;463(7277):103-7 [20023629.001]
  • [Cites] J Biol Chem. 2008 Apr 18;283(16):10892-903 [18281291.001]
  • [Cites] J Biol Chem. 2007 Apr 27;282(17):13123-32 [17337444.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 May;8(5):405-13 [17377525.001]
  • [Cites] Apoptosis. 2007 May;12(5):897-911 [17453159.001]
  • [Cites] J Cell Biol. 2007 Apr 23;177(2):277-87 [17452531.001]
  • [Cites] EMBO J. 2007 May 16;26(10):2527-39 [17446862.001]
  • [Cites] Cell Death Differ. 2007 Jun;14(6):1086-94 [17332775.001]
  • [Cites] Autophagy. 2007 Jul-Aug;3(4):374-6 [17438366.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jul 10;104(28):11649-54 [17606912.001]
  • [Cites] Genes Dev. 2007 Aug 1;21(15):1937-48 [17671092.001]
  • [Cites] Nat Cell Biol. 2007 Sep;9(9):1057-65 [17721514.001]
  • [Cites] Autophagy. 2007 Nov-Dec;3(6):561-8 [17643073.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19500-5 [18048346.001]
  • [Cites] Cell. 2008 Jan 11;132(1):27-42 [18191218.001]
  • [Cites] J Biol Chem. 2000 May 26;275(21):16202-12 [10821866.001]
  • [Cites] Genes Dev. 2000 Aug 15;14(16):2060-71 [10950869.001]
  • [Cites] J Biol Chem. 2001 Mar 2;276(9):6453-62 [11102440.001]
  • [Cites] Dev Cell. 2001 Oct;1(4):515-25 [11703942.001]
  • [Cites] Dev Cell. 2002 Jan;2(1):55-67 [11782314.001]
  • [Cites] Cancer Cell. 2002 Feb;1(1):19-30 [12086884.001]
  • [Cites] Cancer Cell. 2002 Sep;2(3):183-92 [12242151.001]
  • [Cites] Cell. 2002 Nov 1;111(3):331-42 [12419244.001]
  • [Cites] J Cell Biol. 2002 Dec 23;159(6):931-8 [12499352.001]
  • [Cites] Mol Cell. 2003 Mar;11(3):577-90 [12667443.001]
  • [Cites] Science. 2003 Apr 4;300(5616):135-9 [12624178.001]
  • [Cites] J Biol Chem. 2003 Sep 19;278(38):36373-9 [12783892.001]
  • [Cites] Science. 2004 Feb 13;303(5660):1010-4 [14963330.001]
  • [Cites] Biochim Biophys Acta. 2004 Mar 1;1644(2-3):83-94 [14996493.001]
  • [Cites] Nat Cell Biol. 2004 May;6(5):443-50 [15077116.001]
  • [Cites] Mol Biol Cell. 2004 Nov;15(11):5001-11 [15356267.001]
  • [Cites] Nature. 1988 Sep 29;335(6189):440-2 [3262202.001]
  • [Cites] Cell. 1989 Apr 7;57(1):79-88 [2649247.001]
  • [Cites] Nature. 1990 Nov 22;348(6299):331-3 [2250704.001]
  • [Cites] J Biol Chem. 1997 May 23;272(21):13829-34 [9153240.001]
  • [Cites] J Virol. 1998 Nov;72(11):8586-96 [9765397.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 4;102(1):105-10 [15613488.001]
  • [Cites] Mol Cell. 2005 Feb 4;17(3):393-403 [15694340.001]
  • [Cites] Science. 2005 Feb 18;307(5712):1101-4 [15718471.001]
  • [Cites] Mol Cell. 2005 Feb 18;17(4):525-35 [15721256.001]
  • [Cites] Nature. 2005 Jun 2;435(7042):677-81 [15902208.001]
  • [Cites] Science. 2005 Sep 9;309(5741):1732-5 [16151013.001]
  • [Cites] J Biol Chem. 2005 Oct 21;280(42):35742-50 [16115883.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 13;102(50):17975-80 [16330765.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Feb;7(2):97-108 [16493416.001]
  • [Cites] Mol Cell. 2006 Mar 17;21(6):761-73 [16543146.001]
  • [Cites] Science. 2006 Apr 28;312(5773):572-6 [16645094.001]
  • [Cites] Cancer Cell. 2006 May;9(5):351-65 [16697956.001]
  • [Cites] Cell. 2006 Jul 14;126(1):163-75 [16839884.001]
  • [Cites] Cell. 2006 Jul 14;126(1):177-89 [16839885.001]
  • [Cites] J Cell Biol. 2006 Sep 25;174(7):915-21 [16982799.001]
  • [Cites] Mol Cell Biol. 2006 Oct;26(20):7397-408 [17015472.001]
  • [Cites] J Clin Oncol. 2006 Oct 10;24(29):4738-45 [16966688.001]
  • [Cites] Nature. 2006 Oct 12;443(7112):658-62 [17035996.001]
  • [Cites] Cancer Cell. 2006 Nov;10(5):389-99 [17097561.001]
  • [Cites] Nat Cell Biol. 2006 Dec;8(12):1348-58 [17115033.001]
  • [Cites] J Clin Invest. 2007 Jan;117(1):112-21 [17200714.001]
  • [Cites] Science. 2007 Feb 9;315(5813):856-9 [17289999.001]
  • [Cites] Nat Rev Cancer. 2008 Feb;8(2):121-32 [18202696.001]
  • [Cites] Dev Cell. 2008 Feb;14(2):193-204 [18267088.001]
  • [Cites] Nat Immunol. 2008 Apr;9(4):405-14 [18327259.001]
  • [Cites] Trends Cell Biol. 2008 Apr;18(4):157-64 [18314333.001]
  • [Cites] Mol Cell. 2008 May 9;30(3):369-80 [18471982.001]
  • [Cites] J Exp Med. 2008 May 12;205(5):1029-36 [18443228.001]
  • [Cites] Mol Biol Cell. 2008 Jun;19(6):2402-12 [18353969.001]
  • [Cites] Mol Cell. 2008 Jun 20;30(6):678-88 [18570871.001]
  • [Cites] Nature. 2008 Jul 10;454(7201):232-5 [18454133.001]
  • [Cites] J Biol Chem. 2008 Jul 25;283(30):21294-304 [18524770.001]
  • [Cites] Mol Cell. 2008 Aug 22;31(4):557-69 [18691924.001]
  • [Cites] Mol Cell. 2008 Aug 22;31(4):570-85 [18722181.001]
  • [Cites] Cell Death Differ. 2008 Oct;15(10):1564-71 [18551131.001]
  • [Cites] Nature. 2008 Oct 23;455(7216):1076-81 [18948948.001]
  • [Cites] Nature. 2008 Dec 4;456(7222):605-10 [19052620.001]
  • [Cites] Cell. 2008 Dec 12;135(6):1074-84 [19062087.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 23;105(51):20327-32 [19074266.001]
  • [Cites] Mol Cell. 2009 Jan 16;33(1):15-29 [19150424.001]
  • [Cites] J Biol Chem. 2009 Jan 30;284(5):2719-28 [19029119.001]
  • [Cites] Clin Cancer Res. 2009 Feb 15;15(4):1126-32 [19228717.001]
  • [Cites] Nature. 2009 May 21;459(7245):428-32 [19363473.001]
  • [Cites] Autophagy. 2009 Jul;5(5):720-2 [19395874.001]
  • [Cites] Cell Death Differ. 2009 Aug;16(8):1135-45 [19300452.001]
  • [Cites] Science. 2009 Jul 24;325(5939):477-81 [19556461.001]
  • [Cites] Apoptosis. 2009 Aug;14(8):929-34 [19629695.001]
  • [Cites] Nat Cell Biol. 2009 Aug;11(8):958-66 [19578372.001]
  • [Cites] J Cell Biol. 2009 Aug 10;186(3):355-62 [19651893.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Aug 25;106(34):14397-402 [19706527.001]
  • (PMID = 20159550.001).
  • [ISSN] 1097-4164
  • [Journal-full-title] Molecular cell
  • [ISO-abbreviation] Mol. Cell
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / F32 CA101444; United States / NIAID NIH HHS / AI / R01 AI040646; United States / NIAID NIH HHS / AI / R01 AI040646-16
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2
  • [Number-of-references] 89
  • [Other-IDs] NLM/ NIHMS337530; NLM/ PMC3222298
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9. Bartel C, Obermüller N, Rummel MJ, Geiger H, Hauser IA: Remission of a B cell CLL-associated membranoproliferative glomerulonephritis Type I with rituximab and bendamustine. Clin Nephrol; 2008 Apr;69(4):285-9
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Remission of a B cell CLL-associated membranoproliferative glomerulonephritis Type I with rituximab and bendamustine.
  • In a 56-year-old white male patient, a membranoproliferative glomerulonephritis Type I was diagnosed after a 12-month history of low grade B cell lymphoma (Binet A).
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Glomerulonephritis, Membranoproliferative / drug therapy. Glomerulonephritis, Membranoproliferative / etiology. Immunologic Factors / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / complications. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Nitrogen Mustard Compounds / therapeutic use

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  • (PMID = 18397703.001).
  • [ISSN] 0301-0430
  • [Journal-full-title] Clinical nephrology
  • [ISO-abbreviation] Clin. Nephrol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Immunologic Factors; 0 / Nitrogen Mustard Compounds; 4F4X42SYQ6 / Rituximab; 981Y8SX18M / Bendamustine Hydrochloride
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10. Antić D, Dencić-Fekete M, Tomin D, Djunić I: Monosomy 12 and deletion of 13q34 in a case of chronic lymphocytic leukemia with concomitant lung cancer. Vojnosanit Pregl; 2010 Oct;67(10):864-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monosomy 12 and deletion of 13q34 in a case of chronic lymphocytic leukemia with concomitant lung cancer.
  • BACKGROUND: We described a patient with chronic lymphocytic leukemia (CLL) and lung cancer and unusual chromosomal aberrations.
  • CASE REPORT: At the same time with the diagnosis of B-cell CLL, squamocellular lung carcinoma diagnosis was established.
  • One month after the beginning of examination the patient died unexpectedly during sleep immediately before we applied a specific treatment for CLL or lung carcinoma.
  • CONCLUSION: Simultaneous occurrence of monosomy 12 and deletion of 13q34 in a patient with B-cell CLL has been described only once before, but as a part of a complex karyotype.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 12. Chromosomes, Human, Pair 13. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lung Neoplasms / complications. Monosomy

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  • (PMID = 21061845.001).
  • [ISSN] 0042-8450
  • [Journal-full-title] Vojnosanitetski pregled
  • [ISO-abbreviation] Vojnosanit Pregl
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Serbia
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16. Ganesan P, Raina V, Kumar R: A phase II pilot study of valproic acid in relapsed/refractory chronic lymphocytic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7081

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II pilot study of valproic acid in relapsed/refractory chronic lymphocytic leukemia.
  • : 7081 Background: Valproic acid (VA) has demonstrated cell-kill by triggering pro-apoptotic pathways in chronic lymphocytic leukemia (CLL) in preclinical studies.
  • We studied the safety and efficacy of VA in patients with relapsed and refractory CLL.
  • METHODS: Adult patients with CLL diagnosed by the NCI-WG criteria who had received at least one previous fludarabine-based therapy and subsequently progressed or relapsed with ECOG performance status (PS) ≤3 and normal organ functions were included.
  • RESULTS: Five patients have so far been included, age 48-70 years (mean 62 years); sex: 3 males/ 2 females; disease duration: 2-16 years (mean 5.4 years).
  • One patient had partial response and one had stable disease.
  • Grade 3 hypersensitivity skin rashes developed in one patient at one month and the therapy was discontinued.
  • Most patients had mild drowsiness and two patients had significant weight gain of grade 2.
  • CONCLUSIONS: VA produces very impressive palliation in advanced/ refractory CLL in terms of improvement of hemoglobin, ANC, platelets, PS, and a reduction in the number of infective episodes -apparently a sequel to significant rise in neutrophils.

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  • (PMID = 27961474.001).
  • [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
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17. Kumar A, Mhaskar A, Vadaparampil S, Djulbegovic B, Quinn G, Moffitt Fertility Preservation Group: Fertility preservation and timing of cancer treatment. J Clin Oncol; 2009 May 20;27(15_suppl):e20629

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 3 RCTs assessed the efficacy of early versus deferred treatment in prostate cancer, 3 in multiple myeloma, and 1 each in lung cancer and chronic lymphocytic leukemia (CLL).
  • There was no survival difference between early and deferred treatment in multiple myeloma (HR=1.11,95%CI 0.67-1.84), CLL (HR=0.89,95%CI 0.49-1.59) or lung cancer (HR=0.95,95%CI 0.72-1.24).

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  • (PMID = 27961594.001).
  • [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
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18. Lu L, Schafer P, Bartlett JB: Inhibition by lenalidomide of growth factor and hypoxia-induced signaling in endothelial and epithelial tumor cells, and effects within the tumor cell microenvironment. J Clin Oncol; 2009 May 20;27(15_suppl):e14620

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition by lenalidomide of growth factor and hypoxia-induced signaling in endothelial and epithelial tumor cells, and effects within the tumor cell microenvironment.
  • Lenalidomide studies in CLL and MM suggest that it may also attenuate pro-survival signals generated by interaction of stroma with the malignant cell itself.
  • Ovarian cancer cell lines SKOV-3 and OVCAR-3 were treated with LPA and the effect of lenalidomide on invasiveness via enhanced p-Akt was investigated.
  • Treatment of ovarian tumor cells with LPA increased tumor cell invasiveness via enhanced p-Akt.
  • Lenalidomide strongly inhibited invasion and p-Akt (at S308 but not T473) in a dose-dependent manner.

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  • (PMID = 27964203.001).
  • [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
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19. Townsend AR, Millward M, Price T, Mainwaring P, Spencer A, Longenecker A, Palladino MA, Lloyd GK, Spear MA, Padrik P: Clinical trial of NPI-0052 in advanced malignancies including lymphoma and leukemia (advanced malignancies arm). J Clin Oncol; 2009 May 20;27(15_suppl):3582

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical trial of NPI-0052 in advanced malignancies including lymphoma and leukemia (advanced malignancies arm).
  • Preclinical research suggests improvements in therapeutic ratio and activity in hematologic and solid tumor models, leading to clinical trials in patients with myeloma, lymphomas, leukemias, and solid tumors.
  • METHODS: Patients with solid tumor, lymphoma or leukemia diagnoses without standard treatment options were treated with IV NPI on Days 1, 8 and 15 of 28-day cycles in a 3+3 design dose escalation to a Recommended Phase 2 Dose (RP2D).
  • Enrollment then began in 10 patient lymphoma and CLL RP2D cohorts.
  • RESULTS: 30 patients were treated at doses ranging from 0.1 mg/m<sup>2</sup> to 0.9 mg/m<sup>2</sup>.
  • 0.7 mg/m<sup>2</sup> was selected as the RP2D secondary to DLT of transient "hallucinations" (visual imprints when eyes closed) and dizziness/unsteady gait at 0.9 mg/m<sup>2</sup>.
  • At the RP2D PK data showed: half-life = 31 ± 28 min; AUC<sub>total</sub> = 270 ± 219 ng/mL*min; Cmax = 33.4 ± 34.2 ng/mL; clearance = 7.17 ± 0.40 L/min; volume of distribution (Vz) = 223.3 ± 229.7 L.
  • Stable disease was induced in 31% of patients, including one each with mantle cell, Hodgkin's lymphoma, follicular lymphoma, sarcoma, prostate carcinoma, and two with melanoma.

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  • (PMID = 27961753.001).
  • [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
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20. Cole J, Pantanowitz L, Aboulafia DM: Chronic lymphocytic leukemia (CLL) coexistent with HIV: An increasing association? J Clin Oncol; 2009 May 20;27(15_suppl):7078

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic lymphocytic leukemia (CLL) coexistent with HIV: An increasing association?
  • CLL is the most common leukemia in Western countries, yet very little has been published regarding HIV coexistent with CLL.
  • Therefore, the aim of this study was to evaluate the clinicopathological findings and outcome of HIV-associated CLL in a series of cases.
  • METHODS: Cases of HIV-associated CLL/small lymphocytic leukemia (SLL) were collected from the authors' archives and published case reports (using PubMed search).
  • Information regarding patient demographics (age, gender), mode of HIV acquisition, HAART use, immunosuppression (HIV Viral load [VL], CD4+ cell count), clinical presentation, pathology, and outcome were abstracted and analyzed.
  • Immunologic parameters available for 4 patients showed a median CD4+ count of 930 cells/mm3 (range, 396-1374) and mean HIV VL of 2,103 copies/ml (range, <75-5,297).
  • CLL/SLL was diagnosed by lymph node biopsy (n = 1) and/or flow cytometry (n = 5).
  • Two patients remained well without treatment and 4 required therapy due to either hemolytic anemia, CLL- induced renal failure, pancytopenia, or hypogammaglobulinemia with recurrent infections.
  • CONCLUSIONS: CLL/SLL may occur in association with HIV infection in the elderly without significant concomitant immunosuppression.
  • CLL-related complications in our small series were frequent (67%), including mortality (50%).
  • Additional cases of CLL/SLL are anticipated as HIV-infected patients in the HAART era are reported to be living longer.
  • The association between HIV and CLL is deserving of further attention and we encourage clinicians to report their findings.

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  • (PMID = 27961484.001).
  • [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
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21. Soliman HH, Antonia S, Sullivan D, Vanahanian N, Link C: Overcoming tumor antigen anergy in human malignancies using the novel indeolamine 2,3-dioxygenase (IDO) enzyme inhibitor, 1-methyl-D-tryptophan (1MT). J Clin Oncol; 2009 May 20;27(15_suppl):3004

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 3004 Background: The limited effect of cancer immunotherapy is due to the tumor's ability to induce host anergy towards its antigens.
  • The preclinical data support the activity of 1-MT in preventing T-cell anergy in TDLN, slowing growth of LLC mouse xenografts, and synergizing with chemotherapy in regression of autochthonous breast tumors in MMTV-Neu mice.
  • Correlative studies include serum kyn/trp levels, T-reg cell quantification by flow, tumor IDO expression by IHC, and humoral immune response using a proprietary tumor antigen microarray.
  • Attributable toxicities were 1 case of grade 1 fatigue and 2 cases of grade 2 hypophysitis.
  • CONCLUSIONS: 1-MT appears to be an active, orally bioavailable, and reasonably well tolerated immunomodulator at 200mg daily.

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  • (PMID = 27962050.001).
  • [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
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22. Kurosumi M, Kobayashi Y, Takei H: The utility of a real-time RT-PCR assay for the detection of metastases greater than 0.2 mm in sentinel lymph nodes of breast cancer patients confirmed by detailed histological analysis. J Clin Oncol; 2009 May 20;27(15_suppl):628

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The utility of a real-time RT-PCR assay for the detection of metastases greater than 0.2 mm in sentinel lymph nodes of breast cancer patients confirmed by detailed histological analysis.
  • Our study confirms the reliability of the cutoff values of a real-time RT-PCR assay (GeneSearch, Veridex LLC) to detect metastases larger than 0.2 mm by detailed 0.2 mm frozen section histological diagnosis.
  • One half of each LN was used for routine intra-operative diagnosis.
  • These sections were then re-stained immunohistochemically using a pancytokeratin antibody (AE1/AE3) for detecting submicrometastses.
  • Cutoff values were pre-set in a large US study (n = 304).
  • RESULTS: Compared to the histological diagnosis using 0.2 mm interval frozen sections, the real-time RT-PCR results were as follows; sensitivity of 100.0% (34/34), specificity of 93.7% (89/95), and overall accuracy of 95.3% (123/129).

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  • (PMID = 27961430.001).
  • [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
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23. McGregor BA, Gorrebeeck A, Struble E, Harroff A: The effects of sildenafil citrate on malignant B-cells in patients with chronic lymphocytic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7076

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effects of sildenafil citrate on malignant B-cells in patients with chronic lymphocytic leukemia.
  • : 7076 Background: Chronic lymphocytic leukemia (CLL) is the most common form of leukemia in the Western Hemisphere, with over 10,000 cases diagnosed annually in the United States.
  • It is characterized by progressive accumulation of functionally incompetent long-lived lymphocytes, shown to be secondary to a defect in programmed cell death or apoptosis.
  • The phosphodiesterase inhibitor sildenafil induces capsase dependent apoptosis of malignant B lymphocytes in vitro.
  • This study will test the hypothesis that sildenafil reduces the expression of BCL-2 and increases the spontaneous apoptosis rate of malignant B-cells in patients with CLL.
  • METHODS: Thirteen patients with Rai Stage 0 CLL were enrolled.
  • RESULTS: The median age of patients enrolled in the study was 74 with a median white blood cell count of 18 x10<sup>3</sup>/mL.
  • While one patient withdrew due to blehparitis, not felt to be a side effect of sildenafil, all other patients tolerated the medication well without any adverse effects.
  • There was no significant decrease in white blood cell count or Bcl-2 expression; capsase 3 activity and apoptosis rates remained undetectable on presentation and throughout treatment.
  • CONCLUSIONS: At a dose of 25 to 50 mg weekly, sildenafil does not appear to have any effects on the malignant B cells in CLL.
  • While this dose may not produce a measurable clinical or cellular response, higher doses may still have an effect on the malignant B cells of CLL.

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  • (PMID = 27961459.001).
  • [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
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4. Andritsos L, Furman R, Flinn IW, Foreno-Torres A, Flynn JM, Stromatt SC, Byrd JC: A phase I trial of TRU-016, an anti-CD37 small modular immunopharmaceutical (SMIP) in relapsed and refractory CLL. J Clin Oncol; 2009 May 20;27(15_suppl):3017

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I trial of TRU-016, an anti-CD37 small modular immunopharmaceutical (SMIP) in relapsed and refractory CLL.
  • Pre-clinical studies have demonstrated CD37 SMIP mediates significantly greater direct and NK-cell mediated killing of CLL cells as compared to other therapeutic antibodies used in CLL.
  • METHODS: Patients with relapsed/refractory CLL or SLL who had adequate organ function, platelets > 30,000/mm<sup>3</sup> were eligible.
  • Dose escalation and de-escalation is based on CTC AE toxicity grades.
  • Mild (grade 1-2) infusion toxicity has been observed in 3 patients.
  • Two patients had partial clearing of leukemia cutis, and the other six had 27-94% reduction in peripheral lymphocyte count.
  • CONCLUSIONS: To date, TRU-016 is a well tolerated treatment with minimal infusional toxicity and no observed dose limiting toxicity.
  • Encouraging reduction in tumor lymphocyte blood counts, lymph node/spleen size and improvement in normal hematopoeitic function in patients with high risk genomic CLL have already been observed at low, non-saturating doses of CD37.
  • Future single agent and combination studies of Tru16 in CLL are warranted.

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  • (PMID = 27962057.001).
  • [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
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25. Ghosh J, Kumar L, Saxena R, Raina V, Sharma A, Gupta R, Vivekanandhan S, Sreenivas V, Verma R: A study of the prevalence and type of anemia in lymphoid malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):e19556

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A study of the prevalence and type of anemia in lymphoid malignancies.
  • : e19556 Background: Anemia is a common and serious problem in patients with lymphoid malignancy.
  • METHODS: Newly diagnosed patients of lymphoid malignancy- non Hodgkins lymphoma (NHL), Hodgkins lymphoma (HL), and chronic lymphocytic leukemia (CLL) aged more than 15 years without renal failure and who had not received blood transfusion, iron, folic acid or vitamin B complex in the last 2 weeks were analyzed.
  • Of the anemic patients (hemoglobin <11gm/dl), 46 were studied for the type of anemia.
  • Anemia was categorized as due to either autoimmune hemolytic anemia (AIHA)-DCT positive with evidence of hemolysis on PBS, B12 and folate deficiency (<200 pgm/ml and < 4ngm/ml respectively), iron deficiency anemia (IDA)- psat <20% and SF315μgm/dl, anemia of chronic disease (ACD)-psat200μgm/L, a combination of IDA and ACD -psat <20%, SF -30-200 with TIBC ≤315 μgm/dl.
  • RESULTS: The prevalence of anemia in patients with lymphoid malignancy was 42.41% (134 /316, 95% CI-36.96% -47.85%).
  • CONCLUSIONS: Although anemia of chronic disease is the most common cause of anemia in patients with lymphoid malignancy, it is multifactorial in a large number of patients and hence it is important to rule out other causes of anemia like nutritional and AIHA in these patients.

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  • (PMID = 27961090.001).
  • [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
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26. Cadoo KA, Lowery MA, Cumiskey J, McCaffrey J, Carney DN: Long term follow-up of primary B and T cell non-Hodgkin's lymphoma (NHL) of the gastrointestinal (GI) tract. J Clin Oncol; 2009 May 20;27(15_suppl):e19516

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long term follow-up of primary B and T cell non-Hodgkin's lymphoma (NHL) of the gastrointestinal (GI) tract.
  • : e19516 Background: Anthracycline based chemotherapy is the treatment of choice for aggressive primary lymphomas of the GI tract, with surgery reserved for management of complications.
  • We report long term follow up of 71 cases of primary GI NHL treated with chemotherapy and/or surgery.
  • Median age at diagnosis was 60 (15-83).
  • 52 (73%) were DLBCL, 11 (16%) were T-cell, 8 (11%) were MALT.
  • Of the aggressive lymphomas (63), all patients with T cell lymphoma had small bowel as primary site and histological evidence of celiac associated enteropathy, even in the absence of known celiac disease.
  • Primary sites of DLBCL were stomach 35 (67%), small bowel 11 (21%) & colon 6 (12%).
  • 39 (62%) patients underwent surgery at diagnosis due to acute presentation with perforation, bleeding or obstruction, or to obtain histology.
  • Following confirmed diagnosis, 61 patients received anthracycline based chemotherapy.
  • 2 patients with T cell lymphoma presented with perforation, were treated with surgery only and died of rapid disease progression.
  • Of the 63 patients with aggressive NHL, 37 (59%) remain alive & disease free at median follow up of 13 years (1-24).
  • 35 (67%) patients with DLBCL are alive & disease free.
  • Only 2 (18%) of the T cell lymphomas are alive & disease free.
  • All deaths in the T cell group were due to progressive disease.
  • CONCLUSIONS: Patients with aggressive primary B cell GI NHL have almost 70 % survival following anthracycline based chemotherapy.
  • However, in contrast, coeliac enteropathy associated T-cell lymphomas present with rapidly progressive disease & have a survival of < 20% with chemotherapy and/or surgery.

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  • (PMID = 27960953.001).
  • [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
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27. Byrd JC, Lapalombella R, Ramanunni A, Andritsos LA, Flynn JM, Baum P, Thompson P, Muthusamy N: Effect of CD37 small modular immuno-pharmaceutical (SMIP) on direct apoptosis in chronic lymphocytic leukemia cells via transcriptional up-regulation of the BH3 family member BIM. J Clin Oncol; 2009 May 20;27(15_suppl):3035

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of CD37 small modular immuno-pharmaceutical (SMIP) on direct apoptosis in chronic lymphocytic leukemia cells via transcriptional up-regulation of the BH3 family member BIM.
  • A novel CD37<sup>SMIP</sup> was previously demonstrated to mediate superior direct apoptosis and NK-cell mediated killing of chronic lymphocytic leukemia (CLL) and other B-cell malignancies.
  • METHODS: Given the superior in vitro apoptosis observed with CD37<sup>SMIP</sup> treatment and early clinical activity observed in highly refractory CLL patients, we hypothesized that a unique mechanism of cell killing was utilized by CD37<sup>SMIP</sup>.
  • RESULTS: Unlike many other agents utilized to treat CLL, death mediated by CD37<sup>SMIP</sup> does not depend upon caspase activation.
  • Nonetheless, CD37<sup>SMIP</sup> treatment of CLL cells promotes time-dependent induction of mitochondrial membrane depolarization, mitochondrial translocation of Bax, and up-regulation of Bim protein.
  • CD37<sup>SMIP</sup> Bim protein induction occurred concomitantly with an increase in BIM mRNA levels.
  • Electrophoretic mobility shift assay using oligonucleotides of the BIM promoter demonstrated increased protein binding activity in nuclear extracts derived from CD37<sup>SMIP</sup> treated cells and the physical interaction of FoxO3a transcription factor with the FoxO3a responsive element in the BIM promoter was demonstrated using a "protein pull down" assay and confirmed by chromatin immunoprecipitation assays.
  • Furthermore, CD37<sup>SMIP</sup> treatment significantly increased BIM promoter regulated luciferase reporter expression in B-CLL cells.
  • Consistent with a primary role of Bim up-regulation in mitochondrial membrane destabilization and apoptosis, transfection of CLL cells with BIM siRNA resulted in inhibition of CD37<sup>SMIP</sup>-induced mitochondrial membrane depolarization and apoptosis.
  • CONCLUSIONS: These studies demonstrate CD37<sup>SMIP</sup> mediated apoptosis in CLL cells occurs via FoxO3a-dependent transcriptional up-regulation of BIM protein.
  • This distinct mechanism of apoptosis utilized by CD37<sup>SMIP</sup> contrasts it with other agents used for CLL treatment.
  • Additionally, it provides a mechanism for the promising clinical activity of TRU-016 (humanized CD37<sup>SMIP</sup>) observed to date in refractory CLL patients.

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  • (PMID = 27962079.001).
  • [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
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28. Kipps TJ, Österborg A, Mayer J, Stilgenbauer S, Hellmann A, Williams CD, Furman R, Chan G, Russell C, Wierda WG, 406 Study Investigators: Clinical improvement with a novel CD20 mAb, ofatumumab, in fludarabine-refractory chronic lymphocytic leukemia (CLL) also refractory to alemtuzumab or with bulky lymphadenopathy. J Clin Oncol; 2009 May 20;27(15_suppl):7043

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical improvement with a novel CD20 mAb, ofatumumab, in fludarabine-refractory chronic lymphocytic leukemia (CLL) also refractory to alemtuzumab or with bulky lymphadenopathy.
  • : 7043 Background: Patients (pts) with CLL refractory tofludarabine and alemtuzumab (double-refractory, DR) or refractory to fludarabine with bulky (>5 cm) lymphadenopathy (bulky fludarabine-refractory, BFR) have a poor prognosis.
  • Ofatumumab is a human mAb specific for a distinctive small-loop epitope of CD20 that appears more potent than rituximab in eliciting complement-dependent lysis of B cells in vitro.
  • We report, for the first time, results from the planned interim analysis of the clinical benefit observed in pts with DR or BFR CLL treated with ofatumumab in an international pivotal clinical study.
  • METHODS: Pts with DR or BFR CLL received 8 weekly then 4 monthly ofatumumab infusions (Dose 1, 300 mg; Doses 2-12, 2,000 mg).
  • RESULTS: Of 138 treated pts (DR: N = 59; BFR: N = 79; median age 64 and 62 yrs, respectively), 63% had Rai stage III/IV disease at screening.
  • Resolution of disease symptoms (maintained for ≥2 mo) were observed in a large proportion of pts (Table), including in pts considered nonresponders by NCI-WG criteria.
  • Pts with thrombocytopenia at baseline (n = 73) experienced sustained increases in median platelet counts from 65 × 10<sup>9</sup>/L to over 100 × 10<sup>9</sup>/L by Wk 8; a similar pattern of rapid improvement was observed in Hgb values.
  • CONCLUSIONS: Ofatumumab as single-agent achieves high ORR, and improves disease symptoms and hematologic parameters in heavily pretreated pts with DR and BFR disease who lack standard treatment options.

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  • (PMID = 27961406.001).
  • [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
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29. Tsimberidou AM, Wierda WG, Plunkett WK, O'Brien S, Lerner S, Smith SC, Kantarjian HM, Keating MJ: Phase I/II study of oxaliplatin, fludarabine, cytarabine, and rituximab in patients (OFAR2) with Richter's syndrome (RS), and relapsed or refractory B-cell chronic lymphocytic leukemia (CLL). J Clin Oncol; 2009 May 20;27(15_suppl):7031

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I/II study of oxaliplatin, fludarabine, cytarabine, and rituximab in patients (OFAR2) with Richter's syndrome (RS), and relapsed or refractory B-cell chronic lymphocytic leukemia (CLL).
  • : 7031 Background: The first Phase I-II clinical trial of oxaliplatin, fluradabine, Ara-C, and rituximab (OFAR1) demonstrated significant activity in refractory CLL and RS (Tsimberidou et al, J Clin Oncol, 2008;26:196).
  • To enhance the response rate with a decrease in myelosuppression, the dose of oxaliplatin was increased to 30 mg daily, the dose of Ara-C was decreased to 0.5g/m<sup>2</sup> daily and the optimal number of days of fluradabine and Ara-C administration was explored (OFAR2).
  • METHODS: The OFAR2 regimen consisted of oxaliplatin 30mg/m<sup>2</sup>, D1-4; fludarabine 30mg/m<sup>2</sup>, Ara-C 0.5 g/m<sup>2</sup>; rituximab 375mg/m<sup>2</sup>, D3; and pelfigrastim 6mg D6.
  • Forty-three pts were treated in the Phase II portion of the study (relapsed CLL, 35; RS, 8).
  • The median age was 64 yrs (range, 40- 81); 50 (91%) had β2-microglobulin > 3 mg/L; platelets were < 100 x10<sup>9</sup>/L in 22 pts; and 44 pts had > 1 prior therapies.
  • Eleven pts underwent stem cell transplantation as postremission or salvage therapy.

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  • (PMID = 27961393.001).
  • [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
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30. Baum PR, Cerveny C, Gordon B, Nilsson C, Wiens J, Rafiq S, Lapalombella R, Muthusamy N, Byrd JC, Wahl A: Evaluation of the effect of TRU-016, an anti-CD37 directed SMIP in combination with other therapeutic drugs in models of non-Hodgkin's lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):8571

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of the effect of TRU-016, an anti-CD37 directed SMIP in combination with other therapeutic drugs in models of non-Hodgkin's lymphoma.
  • : 8571 Background: TRU-016, a single chain anti-CD37 Fc fusion molecule has been shown to display pro-apoptotic and Fc-dependent cellular cytotoxicity activities against primary CLL cells and NHL cell lines.
  • The pro-apoptotic signal generated by TRU-016 binding to CD37 on CLL cells has been shown to be caspase-independent and distinct from the signal generated by many other therapeutics including rituximab.
  • We have tested drug combinations using the mantle cell lymphoma line Rec-1 and diffuse large B-cell lymphoma line SU-DHL-6 in vitro and extended these results to in vivo settings using the follicular lymphoma cell line DOHH2 treated with the combination of TRU-016 and bendamustine.
  • METHODS: To determine TRU-016 interactions with the established therapeutics rituximab, doxorubicin, rapamycin, and bendamustine, drugs were tested alone or in combination with TRU-016 and the anti-proliferative effects on cell lines measured after 96 hours.
  • To determine if in vitro synergy could be recapitulated in vivo, SCID mice were implanted with DOHH2 cells and therapeutic treatment was initiated when tumor volumes reached 200 mm<sup>3</sup>.
  • This demonstrates that the in vitro synergy results were extendable to a more complex in vivo disease model.
  • CONCLUSIONS: TRU-016 in combination with rituximab, rapamycin, or bendamustine increases cell killing of NHL cells.
  • Furthermore, the combination of TRU-016 and bendamustine displayed greater in vivo anti-tumor activity than either agent alone against a follicular lymphoma tumor model.

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  • (PMID = 27961015.001).
  • [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
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31. Tay K, Shapiro G, Disinski M, Chirieac LR, Pittaluga S, Jaffe ES, Janik JE, Wiestner A, Wilson WH, Dunleavy K: Phase I/II study of a hybrid schedule of flavopiridol in relapsed/refractory mantle cell lymphoma (MCL) and diffuse large B-cell lymphoma (DLBCL). J Clin Oncol; 2009 May 20;27(15_suppl):8563

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I/II study of a hybrid schedule of flavopiridol in relapsed/refractory mantle cell lymphoma (MCL) and diffuse large B-cell lymphoma (DLBCL).
  • However, a pharmacologically derived hybrid schedule of administration is effective in refractory, genetically high-risk CLL, though life-threatening tumor lysis syndrome (TLS) may occur in patients with very high lymphocyte counts.
  • Because flavopiridol decreases cyclin D1 and mcl-1 and induces apoptosis in MCL cells, is significantly toxic for cell lines derived from the activated B-cell-like type of DLBCL (OCI-Ly3) and down-regulates NF-kappa B, we investigated the hybrid schedule in MCL and DLBCL.
  • Other toxicities were grade 4 ANC (10 pts) requiring prophylactic G-CSF, TLS (1 pt) and bowel perforation (1 pt).
  • Analysis of cell cycle and transcriptional cdk targets is ongoing.

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  • (PMID = 27961020.001).
  • [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
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32. Melo-Cardenas J, Castro JE, Cox B, Sandoval-Sus JD, Darrah D, Urquiza M, Prussak CE, Kipps TJ: Ad-ISF35-transduced autologous cells promote in vitro and in vivo chemosensitization in patients with 17p-/P53-defective chronic lymphocytic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):e14552

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ad-ISF35-transduced autologous cells promote in vitro and in vivo chemosensitization in patients with 17p-/P53-defective chronic lymphocytic leukemia.
  • : e14552 Background: Transduction of chronic lymphocytic leukemia (CLL) cells with a replication-defective adenovirus (Ad) encoding recombinant CD154 (Ad-ISF35) induces expression of death receptors and Bid via a P53-independent pathway involving induction of P73.
  • Induction of P73 significantly enhances the sensitivity of P53-defective CLL cells to "P53-dependent" drugs, such as Fludarabine (F-ara-A).
  • Patients with P53-defective CLL who received iv infusions of autologous Ad-ISF35-transduced CLL cells were observed to achieve complete remissions (CR) with subsequent treatment using F-ara-A based treatment regimens, suggesting Ad-ISF35 could sensitize P53-defective CLL to chemotherapy.
  • METHODS: We examined patients with drug-resistant and/or P53-defective CLL before and after iv infusions of autologous Ad-ISF35-transduced CLL cells who were enrolled in a phase I study examining whether such treatment could sensitize patients to a truncated fludarabine, cyclophosphamide and rituximab (FCR) regimen.
  • We examined CLL cells for sensitivity to F-ara-A in vitro, expression of CD95, DR5, Bid, and P73 and correlated these with the response to treatment in vivo.
  • RESULTS: P53-defective CLL cells were resistant to F-ara-A induced apoptosis with IC50 > 10μM prior to treatment.
  • CLL cells collected from patients≥24 hours after IV infusion of autologous Ad-ISF35-trasduced CLL cells became sensitive to the cytotoxic effects of F-ara-A, with IC50 0.3-1 μM.
  • Enhanced sensitivity to F-ara-A was associated with induced expression of Bid, DR5, CD95, and P73 by circulating CLL cells, an effect lasting≥2 weeks following iv infusion.
  • Consistent with this, we observed complete resolution in lymphocytosis, lymphadenopathy and splenomegaly following 1 cycle of FCR administered 2 weeks after 3 biweekly infusions of Ad-ISF35- transduced CLL cells.
  • CONCLUSIONS: IV infusion of autologous Ad-ISF35-transduced CLL cells can induce de novo, systemic expression of death receptors and Bid on bystander CLL cells, which is associated with enhanced sensitivity of P53-defective CLL to the cytotoxic effects of standard chemotherapy [Table: see text].

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  • (PMID = 27963590.001).
  • [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
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33. Cotter F, Smith DA, Boyd TE, Richards DA, Alemany C, Loesch D, Salogub G, Tidmarsh GF, Gammon GM, Gribben J: Single-agent activity of GCS-100, a first-in-class galectin-3 antagonist, in elderly patients with relapsed chronic lymphocytic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):7006

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Single-agent activity of GCS-100, a first-in-class galectin-3 antagonist, in elderly patients with relapsed chronic lymphocytic leukemia.
  • GCS-100 has been shown to induce apoptosis of patient CLL cells ex vivo.
  • In addition, GCS-100 potentiates the in vitro activity of other agents commonly used to treat CLL, including rituximab.
  • This phase II clinical trial evaluated the potential of GCS-100 as a novel single-agent therapeutic for relapsed CLL.
  • METHODS: Patients with Rai Stage II or higher CLL who had relapsed after one or two prior therapies were eligible.
  • Patients received GCS-100 i.v. at 160 mg/m<sup>2</sup> for 5 days every 21 days until disease progression.
  • GCS-100 was well-tolerated.
  • There were no cases of drug-related grade 3 or 4 hematological toxicity or other serious AE.
  • CONCLUSIONS: GCS-100 has significant single-agent activity in relapsed CLL.
  • Its lack of myelosuppression and potential synergy with other agents makes GCS-100 a strong candidate for further development in CLL, particularly for elderly patients for whom there is a major need for less toxic agents.

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  • (PMID = 27961378.001).
  • [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
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34. Durbecq V, Majjaj S, Nogaret J, Sirtaine N, Schobbens J, Noterman D, Hertens D, Filipov V, Larsimont D, Veys I: Use of quantitative RT-PCR assay to predict metastases size of sentinel node from breast cancer patients. J Clin Oncol; 2009 May 20;27(15_suppl):621

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 621 Background: A RT-PCR Assay (GeneSearch, Veridex, LLC), FDA approved and CE marked to detect metastases > 0.2 mm in sentinel lymph nodes (SLNs) of breast cancer patients, has been in clinical use in our institute for 25 months.
  • An additional 74 patients were tested in a pilot study.
  • The marker Ct values are correlated with metastases size as determined by H&E on adjacent node pieces (r = -0.74 for MG and -0.77 for CK19, p < 0.001).
  • For example when CK19 and MG < 24 Cts, the non-SLN positivity rate jumps from 29% to 58%.

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  • (PMID = 27961419.001).
  • [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
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35. Ding W, Knox TR, Smoley SA, Van Dyke DL, Kay NE: Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects. J Clin Oncol; 2009 May 20;27(15_suppl):e22002

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic abnormalities in mesenchymal stem cells in chronic lymphocytic leukemia (CLL) patients and normal subjects.
  • : e22002 Background: Mesenchymal stem cells (MSC) residing in the marrow support hematopoiesis and protect cancer cells from undergoing cell death induced by chemotherapy.
  • Recent reports have described clonal cytogenetic abnormalities in the MSC of acute myeloid leukemia and myelodysplastic syndrome patients.
  • To determine if cytogenetic abnormalities are present in MSC from CLL patients, we analyzed karyotypes of MSC from 13 CLL patients and 5 normal subjects.
  • METHODS: Stromal cells from marrow core biopsies of 13 CLL patients and 5 normal control subjects were isolated, cultured and confirmed as MSC based on their immunophenotype and capacity to differentiate into three lineages.
  • After 3-4 non-stimulated cell culture passages, the karyotype was analyzed in 5-40 metaphase cells from each subject Abnormalities were considered clonal using the accepted convention of the same chromosomal gain or rearrangement in 2 or more cells or loss in at least 3 cells.
  • For each CLL patient, interphase FISH analysis to detect the common CLL-associated abnormalities was performed on freshly isolated peripheral blood mononuclear cells (PBMC).
  • RESULTS: Clonal cytogenetic abnormalities of the cultured MSC were observed in 6 of 13 CLL patients (46%) and 3 of 5 control subjects (60%).
  • The 6 CLL MSC had different clonal abnormalities than the PBMC CLL FISH studies.
  • One CLL MSC exhibited trisomy 5, one exhibited trisomy 8, and one had monosomy X clone.
  • There was no correlation of the chromosomal abnormalities in CLL MSC with clinical stage.
  • CONCLUSIONS: Marrow MSC derived from CLL patients and normal subjects do show an array of cytogenetic abnormalities including clonal chromosomal abnormalities.
  • However the genetic abnormalities found in both CLL and normal MSC could represent acquired genomic instability associated with advanced age, rather than oncogenesis associated with CLL.

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  • (PMID = 27963169.001).
  • [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
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36. Flinn IW, Byrd JC, Furman RR, Brown JR, Lin TS, Bello C, Giese NA, Yu AS: Preliminary evidence of clinical activity in a phase I study of CAL-101, a selective inhibitor of the p1108 isoform of phosphatidylinositol 3-kinase (P13K), in patients with select hematologic malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):3543

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preliminary evidence of clinical activity in a phase I study of CAL-101, a selective inhibitor of the p1108 isoform of phosphatidylinositol 3-kinase (P13K), in patients with select hematologic malignancies.
  • The PI3K p110δ isoform is highly expressed in cells of hematopoietic origin and plays a key role in B cell maturation and function.
  • CAL-101 is a potent inhibitor of PI3K p110δ (IC<sub>50</sub>=65 nM) with 40 to 300-fold selectivity compared to other PI3K isoforms.
  • In vitro studies of 0.1 to 10 μM CAL-101 showed inhibition of pAKT expression and/or apoptotic effects against primary chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML) cells and against a range of leukemia and lymphoma cell lines.
  • METHODS: In an ongoing phase 1 dose escalation study in sequential cohorts of 3 patients with relapsed/refractory CLL or select B-cell non-Hodgkin's lymphoma, CAL-101 is administered orally twice daily for 28 days per cycle.
  • No treatment-related adverse events greater than grade 1 have been seen, with 2 patients treated for >5 cycles.
  • Two of 6 patients attained partial response and 4 have stable disease.
  • Partial responses were observed after 2 cycles of 50 mg in a patient with mantle cell lymphoma with 6 prior therapies, and after 1 cycle of 100 mg in a patient with follicular lymphoma with 6 prior therapies, including autologous stem cell transplant.
  • Disease specific cohort expansion will occur at the maximally tolerated dose, and patients with AML will be added.
  • CONCLUSIONS: Early results from a phase 1 study of the oral PI3K p110δ inhibitor CAL-101 show that it is well tolerated and has preliminary clinical activity in patients with B-cell malignancies.

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  • (PMID = 27961357.001).
  • [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
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37. Wilson W, O'Connor OO, Roberts AW, Czuczman M, Brown J, Xiong H, Xiong H, Chiu Y, Krivoshik A, Enschede S, Humerickhouse R: ABT-263 activity and safety in patients with relapsed or refractory lymphoid malignancies in particular chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL). J Clin Oncol; 2009 May 20;27(15_suppl):8574

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ABT-263 activity and safety in patients with relapsed or refractory lymphoid malignancies in particular chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL).
  • : 8574 Background: ABT-263, a novel, orally bioavailable, BH3 mimetic, binds with high affinity (K<sub>i</sub> ≤ 1nM) and inhibits multiple antiapoptotic Bcl-2 family proteins.
  • ABT-263 displays activity (EC<sub>50</sub> ≤ 1μM) against human lymphoid and small cell lung cancer cell lines.
  • Mechanism based preclinical toxicities include reductions in circulating lymphocytes, apoptosis of circulating platelets, and decreased spermatogenesis, mediated by inhibition of Bcl-2, Bcl-X<sub>L</sub>, and Bcl-w, respectively.
  • METHODS: Safety and activity of ABT-263 in 2 enrolling phase I studies in relapsed/refractory lymphoid malignancies (M06-814) and CLL (M06-873) was evaluated.
  • Patients (pts) were dosed on days 1-14 of a 21 d cycle, 10-440mg (M06-814) or 10-250mg (M06-873).
  • Among 27 CLL/SLL pts, 3 have confirmed radiographic partial responses (PR) (99%, 92% and 72%) and 2 have unconfirmed regressions, 51% and 72%.
  • 6 pts maintained a ≥50% decrease in circulating lymphocytes for ≥ 2 months and 11 pts have stable disease; of these 5 experienced minor radiographic responses (range of 36% to 49%).
  • In addition, among 40 (M06-814) lymphoma pts, 3 with follicular lymphoma achieved PR and one had a minor response (49% regression).
  • With CD dosing (16 pts), activity includes 1 unconfirmed PR in SLL & and 3 CLL pts with ≥50% lymphocyte reduction for ≥2 months duration.
  • Pharmacodynamic toxicities included dose-dependent thrombocytopenia (TCP) resulting from on-target activity against Bcl-X<sub>L</sub>.
  • Dose limiting toxicities, 14/21 d dosing, in M06-814 occurred at 160mg (bronchitis), 315mg (elevated ALT and grade 4 TCP) and 440mg (worsening pleural effusion in a pt with underlying afib), and in M06-873 at 110mg (tumor lysis and grade 4 TCP) and 250mg (grade 4 TCP).
  • CONCLUSIONS: ABT-263 showed favorable PK and safety profiles with anti-tumor activity in relapsed/refractory CLL/SLL and follicular lymphoma.

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  • (PMID = 27962273.001).
  • [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
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38. Jones JA, Flynn J, Moran M, Lin T, Byrd J: Trends in pneumonia (PNA) hospitalization among patients (pts) with chronic lymphocytic leukemia (CLL). J Clin Oncol; 2009 May 20;27(15_suppl):e20500

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Trends in pneumonia (PNA) hospitalization among patients (pts) with chronic lymphocytic leukemia (CLL).
  • : e20500 Background: Despite recent therapeutic advances, PNA remains a significant source of morbidity and mortality among CLL pts.
  • Nationwide Inpatient Sample and ICD-9CM diagnosis codes, we identified all non-governmental hospitalizations of CLL pts for a primary dx of PNA in calendar years 1994 and 2004.
  • Admissions were described by pt demographics (age, gender, race) and comorbidity (Charlson index, presence of chronic lung disease).
  • Ten-year prevalence estimates for CLL were obtained from NCI SEER data and used as denominators in incidence calculations.
  • RESULTS: PNA was the primary dx for 7316 (13.1%) and 7651 (11.2%) CLL pt admissions in 1994 and 2004, respectively.
  • CLL pts admitted in 2004 were older (75.7 v. 74.2 years, p<0.001) and more likely to have at least one Charlson comorbidity (67.6% v. 56.2%, p<0.001) or comorbid chronic lung disease (40.6% v. 28.3%, p<0.001) than pts in 1994.
  • Intubation was rare in both cohorts (<1%) and did not significantly differ by year, but in-hospital mortality was significantly higher in 2004 (11.3% v. 8.2%, p=0.005).
  • However, LOS decreased significantly between 1994 and 2004 (9.2 v. 6.4 days, p<0.001).
  • CONCLUSIONS: PNA hospitalization rates for CLL pts have not significantly increased over the last decade despite more aggressive therapies, likely secondary to improved supportive care.
  • However, CLL pts hospitalized for PNA are now older, increasingly likely to suffer from chronic medical illness, and significantly more likely to die while in hospital.

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  • (PMID = 27960954.001).
  • [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
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39. Grubbs SS, Gonzalez M, Krasna M, Siegel R, Bryant D, Tschetter L, Hayenga L, Duggan B, St Germaine D, Denicoff A: Tracking clinical trial accrual strategies and barriers via a Web-based screening tool. J Clin Oncol; 2009 May 20;27(15_suppl):6586

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Seven NCCCP sites utilized the log during the 60 day open accrual period for the Wake Forrest WFU 07-02-03 cancer control trial (chronic lymphocytic leukemia COLD- fX) in Novermber 2008 and December 2008.
  • RESULTS: 327 chronic lymphocytic leukemia patients were screened mostly by chart review.

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  • (PMID = 27963861.001).
  • [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
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40. Ramaswamy B, Phelps M, Baiocchi R, Bekaii-Saab T, Wilkins D, Arbogast D, Campbell A, Doyle AL, Grever M, Shah M: A phase I study of flavopiridol using an alternative schedule in patients (pts) with advanced solid tumors. J Clin Oncol; 2009 May 20;27(15_suppl):2580

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 2580 Background: A phase I study of flavopiridol, a cyclin-dependent kinase inhibitor, using an alternative schedule was conducted in pts with solid tumors given its promising activity in pts with chronic lymphocytic leukemia (CLL).
  • DLT was defined as Gr 4 hematologic toxicity (HT) for > 7 days, > Gr 3 non-HT except Gr 3 fatigue or diarrhea resolving <4 days and cytokine release syndrome (CRS) > Gr 3 despite steroids.
  • Due to a grade 5 CRS/death in cohort 3, the protocol was amended to include 20 mg IV dexamethasone prior to flavopiridol to prevent CRS (cohorts 2B, 1B).
  • Of the 20 evaluable pts, 35% had stable- and 65% had progressive-disease.
  • CONCLUSIONS: There was a higher frequency of CRS, despite prophylactic steroids seen our pts with solid tumors compared to previous studies with CLL and this correlated with AUC.

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  • (PMID = 27961903.001).
  • [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
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41. Goldman S, Coiffier B, Reiter A, Younes A, Cairo MS, International TLS Expert Panel: A medical decision tree for the prophylaxis (P) and treatment (T) of tumor lysis syndrome (TLS): An international TLS consensus panel. J Clin Oncol; 2009 May 20;27(15_suppl):e17575

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Rasburicase (R), a recombinant urate oxidase, results in a more rapid and total reduction of uric acid (UA) compared to allopurinol (A) in children at high-risk of TLS (Goldman/Cairo et al, Blood.
  • METHODS: We convened an international panel (N = 17) of experts in pediatric and adult hematological malignancies and solid tumors (ST) to develop a medical decision tree for the P and T of TLS based on the risk classification (low, medium, high) and management recommendations of Coiffier et al (J Clin Oncol.
  • 2008) Results: Patients without evidence of LTLS were assigned to either low-risk disease (LRD), medium-risk (MRD), or high-risk (HRD).
  • Risk factors included pathological classification stage, bulk, disease burden (WBC/LDH) and renal impairment/involvement.
  • HRD was assigned to patients with either B-ALL, ALL/AML ≥100K/mm<sup>3</sup>, BL/LL stage III/IV, and/or high LDH, DLBCL/PTCL/MCL/ATL with bulky and elevated LDH and patients with MRD with renal impairment/involvement.
  • MRD consisted of ALL ≤100K/mm<sup>3</sup>, AML 25-100K/mm<sup>3</sup>, BL/LL stage I/II and low LDH, childhood ALCL, DLBCL/PTCL/MCL/ATL non-bulky but elevated LDH, CLL treated with targeted therapy, and LRD with renal impairment/involvement.
  • LRD consisted of ST (except bulky sensitive to cytotoxic therapy [MRD]), CML, MM, HL, other NHL and AML <25K/mm<sup>3</sup>.
  • CONCLUSIONS: This medical decision tree will facilitate the practice of management of the P and T of TLS and hopefully improve the quality of care in a cost effective manner.

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  • (PMID = 27963935.001).
  • [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
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42. Dennis RJ, Alberts JC: The implications of an incidental chronic lymphocytic leukaemia in a resection specimen for colorectal adenocarcinoma. World J Surg Oncol; 2007;5:126

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The implications of an incidental chronic lymphocytic leukaemia in a resection specimen for colorectal adenocarcinoma.
  • BACKGROUND: Colorectal cancer and B cell chronic lymphocytic leukaemia (CLL) have a significant incidence, which are increasing with the aging population.
  • Evidence has been presented in the literature to suggest that the synchronous presentation of colorectal cancer and B cell CLL may be more than simply coincidental for these two common malignancies.
  • We report an unusual case of a presumed B cell CLL diagnosed on the basis of histological analysis of lymph nodes recovered from a resection specimen for rectal adenocarcinoma.
  • We considered aetiological factors which may have linked the synchronous diagnosis of the two malignancies and the potential implications for the natural history of the two malignancies on one another.
  • CASE PRESENTATION: A 70-year-old male underwent low anterior resection with total mesorectal excision for a rectal adenocarcinoma.
  • His co-morbid conditions were chronic obstructive airways disease and ischaemic heart disease.
  • As well as confirming a pT3 N1 adenocarcinoma, histological analysis showed lymph nodes with an infiltrate of small lymphoid cells.
  • Immunohistochemical studies showed these cells to be in keeping with B cell CLL.
  • Examples such as our case of synchronous diagnosis of two malignancies in a patient are likely to increase with the aging population.
  • The potential affects of one malignancy on the natural history of the other warrants further study.
  • In our case, we considered that slow progression of the B cell CLL may increase the risk of recurrent rectal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Neoplasms, Second Primary / pathology. Neoplasms, Second Primary / surgery. Rectal Neoplasms / pathology

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  • [Cites] J Natl Cancer Inst. 2000 Mar 1;92(5):388-96 [10699069.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1979-81 [11535538.001]
  • [Cites] Dis Colon Rectum. 2002 Feb;45(2):273-9 [11852345.001]
  • [Cites] Leuk Lymphoma. 2004 Mar;45(3):507-13 [15160912.001]
  • [Cites] J Gastroenterol. 2004;39(5):479-83 [15175948.001]
  • [Cites] Leuk Lymphoma. 2006 Nov;47(11):2314-20 [17107903.001]
  • [Cites] Haematologica. 1976 Dec;61(4):456-69 [828608.001]
  • [Cites] J Natl Cancer Inst. 1978 Aug;61(2):337-40 [277720.001]
  • [Cites] Blood. 1995 Mar 15;85(6):1580-9 [7888675.001]
  • [Cites] J Am Coll Surg. 1995 Oct;181(4):335-46 [7551328.001]
  • [Cites] Am J Epidemiol. 1976 Nov;104(5):517-22 [984025.001]
  • (PMID = 17971235.001).
  • [ISSN] 1477-7819
  • [Journal-full-title] World journal of surgical oncology
  • [ISO-abbreviation] World J Surg Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2169241
  •  go-up   go-down


43. Dasanu CA, Alexandrescu DT: Risk for second nonlymphoid neoplasms in chronic lymphocytic leukemia. MedGenMed; 2007;9(4):35
MedlinePlus Health Information. consumer health - Skin Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Risk for second nonlymphoid neoplasms in chronic lymphocytic leukemia.
  • Major advances have occurred in understanding the biology, immunology, and modalities of treatment of chronic lymphocytic leukemia (CLL) in the last decade.
  • B-cell CLL is the most common type of leukemia occurring in the US and Western nations.
  • B-cell CLL is characterized by progressive defects in both cell-mediated and humoral-mediated immunity.
  • B-lymphocyte defects, low gammaglobulin levels, and quantitative and functional T-cell defects have been documented in the setting of CLL.
  • In concert with each other, they account for the increased susceptibility of the CLL patients to infectious agents.
  • Moreover, several recent surveys have pointed out that CLL patients are at high risk of developing a large variety of second malignant neoplasms.
  • Different therapeutic modalities used for CLL may further exacerbate immunosuppression by depleting both T- and B-immune effectors, thus favoring various infectious diseases and perhaps altering the immune surveillance.
  • The occurrence of 2 or more second cancers is increasingly reported in the context of CLL.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / epidemiology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Lung Neoplasms / epidemiology. Neoplasms, Second Primary / epidemiology. Skin Neoplasms / epidemiology

  • Genetic Alliance. consumer health - Chronic Lymphocytic Leukemia.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
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  • [Cites] Br J Dermatol. 2000 Mar;142(3):525-8 [10735964.001]
  • [Cites] J Natl Cancer Inst. 2007 Jun 20;99(12):962-72 [17565153.001]
  • [Cites] Clin Immunol. 2001 Feb;98(2):175-9 [11161973.001]
  • [Cites] Blood. 2001 Sep 15;98(6):1979-81 [11535538.001]
  • [Cites] Lung Cancer. 2001 Nov;34(2):227-32 [11679181.001]
  • [Cites] Semin Oncol. 2002 Feb;29(1 Suppl 2):70-4 [11842391.001]
  • [Cites] Am J Hematol. 2002 May;70(1):48-50 [11994981.001]
  • [Cites] Orbit. 2002 Jun;21(2):145-8 [12029570.001]
  • [Cites] Eur J Haematol. 2002 Feb;68(2):117-9 [12061321.001]
  • [Cites] Blood. 2002 Sep 15;100(6):2257-9 [12200395.001]
  • [Cites] Rinsho Ketsueki. 2002 Sep;43(9):862-4 [12412293.001]
  • [Cites] Clin Exp Immunol. 2002 Dec;130(3):495-500 [12452841.001]
  • [Cites] Blood. 2003 Jan 1;101(1):6-14 [12393429.001]
  • [Cites] Eur J Haematol. 1994 Oct;53(4):218-22 [7957806.001]
  • [Cites] Int J Cancer. 1995 Jun 9;61(6):773-9 [7790110.001]
  • [Cites] J Laryngol Otol. 1996 Jul;110(7):694-5 [8759553.001]
  • [Cites] Rinsho Ketsueki. 1997 Sep;38(9):740-4 [9364864.001]
  • [Cites] J Cutan Pathol. 1998 Mar;25(3):160-4 [9550315.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1165-71 [9694704.001]
  • [Cites] J Clin Oncol. 2003 May 1;21(9):1746-51 [12721250.001]
  • [Cites] Am J Hematol. 2003 Jul;73(3):184-9 [12827656.001]
  • [Cites] Am J Clin Oncol. 2003 Dec;26(6):531-4 [14663367.001]
  • [Cites] Rozhl Chir. 2003 Nov;82(11):583-6 [14686258.001]
  • [Cites] Eur J Cancer. 2004 Feb;40(3):383-9 [14746857.001]
  • [Cites] Leuk Lymphoma. 2004 Feb;45(2):205-19 [15101704.001]
  • [Cites] Leuk Lymphoma. 2004 Mar;45(3):507-13 [15160912.001]
  • [Cites] Blood. 2004 Jun 15;103(12):4389-95 [14962897.001]
  • [Cites] Pediatr Hematol Oncol. 2004 Jul-Aug;21(5):441-51 [15205088.001]
  • [Cites] Br J Dermatol. 2004 Jun;150(6):1129-35 [15214899.001]
  • [Cites] Arch Dermatol. 2004 Aug;140(8):985-8 [15313816.001]
  • [Cites] J Immunol. 2004 Sep 15;173(6):3901-8 [15356138.001]
  • [Cites] JAMA. 1975 Apr 21;232(3):267-9 [47401.001]
  • [Cites] J Natl Cancer Inst. 1978 Aug;61(2):337-40 [277720.001]
  • [Cites] J Dermatol Surg Oncol. 1979 Aug;5(8):609-14 [479446.001]
  • [Cites] Tumori. 1980 Aug 31;66(4):431-7 [7414709.001]
  • [Cites] Lancet. 1985 Feb 2;1(8423):263-6 [2857327.001]
  • [Cites] Am J Hematol. 1986 May;22(1):55-61 [3513551.001]
  • [Cites] Am J Clin Pathol. 1987 Jan;87(1):60-5 [2948384.001]
  • [Cites] Haematologia (Budap). 1990;23(1):49-56 [2397923.001]
  • [Cites] J Natl Cancer Inst. 1992 Sep 16;84(18):1422-7 [1512794.001]
  • [Cites] J Ky Med Assoc. 1994 May;92(5):183-7 [8027638.001]
  • [Cites] Hematol Cell Ther. 1999 Aug;41(4):145-51 [10543369.001]
  • [Cites] Cancer. 1999 Nov 1;86(9):1720-3 [10547544.001]
  • [Cites] J Clin Oncol. 1999 Aug;17(8):2454-60 [10561309.001]
  • [Cites] J Clin Gastroenterol. 1998 Oct;27(3):261-4 [9802460.001]
  • [Cites] Blood. 1999 Jul 15;94(2):448-54 [10397712.001]
  • [Cites] Cancer Immunol Immunother. 2006 Feb;55(2):197-209 [16025268.001]
  • [Cites] Immunol Rev. 2006 Feb;209:142-58 [16448540.001]
  • [Cites] Pol Arch Med Wewn. 2005 Dec;114(6):1217-9 [16789492.001]
  • [Cites] Actas Dermosifiliogr. 2006 May;97(4):264-6 [16801021.001]
  • [Cites] Nihon Rinsho Meneki Gakkai Kaishi. 2006 Jun;29(3):136-47 [16819262.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Aug;15(8):1545-9 [16896047.001]
  • [Cites] Transpl Int. 2006 Nov;19(11):927-36 [17018129.001]
  • [Cites] Leuk Lymphoma. 2006 Nov;47(11):2314-20 [17107903.001]
  • [Cites] Blood. 2000 Nov 1;96(9):3168-74 [11049999.001]
  • (PMID = 18311385.001).
  • [ISSN] 1531-0132
  • [Journal-full-title] MedGenMed : Medscape general medicine
  • [ISO-abbreviation] MedGenMed
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 58
  • [Other-IDs] NLM/ PMC2234297
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44. Faderl S, Rai K, Gribben J, Byrd JC, Flinn IW, O'Brien S, Sheng S, Esseltine DL, Keating MJ: Phase II study of single-agent bortezomib for the treatment of patients with fludarabine-refractory B-cell chronic lymphocytic leukemia. Cancer; 2006 Sep 1;107(5):916-24
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 II study of single-agent bortezomib for the treatment of patients with fludarabine-refractory B-cell chronic lymphocytic leukemia.
  • Therapeutic options are limited and the prognosis is poor for patients with fludarabine-refractory B-cell chronic lymphocytic leukemia (CLL).
  • Bortezomib induces apoptosis in vitro in CLL cells, both alone and in combination, including in cells resistant to fludarabine or other agents.
  • The aim of the current randomized, open-label, Phase II study was to investigate the clinical activity of bortezomib in patients with fludarabine-refractory B-cell CLL.
  • Twenty-two patients with histologically confirmed B-cell CLL were treated with bortezomib at doses of 1.0 mg/m2, 1.3 mg/m2, or 1.5 mg/m2 on Days 1, 4, 8, and 11 of a 21-day treatment cycle for a maximum of 9 cycles.
  • None of 19 patients evaluable for response achieved complete remission or partial response; however, signs of biologic activity based on disease site responses (e.g., reduction in lymphocytosis, splenomegaly, and lymphadenopathy) were observed.
  • In the 1.5 mg/m2 dose group, a higher proportion of patients had stable disease, and a lower proportion had progressive disease compared with the 2 lower-dose groups.
  • Eleven patients, all in the 2 higher dose groups, experienced Grade 3/4 adverse events (AEs) (according to National Cancer Institute Common Toxicity Criteria [version 2.0]); 2 patients experienced Grade 4 neutropenia.
  • Grade 3 hematologic AEs included anemia, neutropenia, thrombocytopenia, and hemolytic anemia; Grade 3 nervous system AEs included aphasia; peripheral neuropathy, not otherwise specified; and peripheral sensory neuropathy.
  • Although no objective responses were achieved in patients with fludarabine-refractory B-cell CLL, single-agent bortezomib demonstrated biologic activity.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Protease Inhibitors / therapeutic use. Pyrazines / therapeutic use

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  • (PMID = 16832816.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; 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; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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45. Colak D, Ozyilkan O, Akcali Z, Bilezikci B: Hodgkin's disease in an elderly patient with B-cell chronic lymphocytic leukemia. Indian J Cancer; 2005 Jul-Sep;42(3):158-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hodgkin's disease in an elderly patient with B-cell chronic lymphocytic leukemia.
  • Chronic lymphocytic leukemia (CLL) is the most common type of leukemia worldwide.
  • It is an indolent disease, almost exclusively of B-cell origin.
  • Some CLLs evolve into a more aggressive lymphoid malignancy.
  • Transformation to acute lymphoblastic leukemia, plasma cell leukemia, multiple myeloma, or Hodgkin's disease (HD) may also occur.
  • CLL patients are also at a significantly increased risk of developing a second malignant neoplasm later in life.
  • Herein, we report a case of HD in an elderly man with a history of B-cell CLL.
  • [MeSH-major] Hodgkin Disease / pathology. Leukemia, B-Cell / pathology
  • [MeSH-minor] Chronic Disease. Humans. Male. Middle Aged. Prognosis. Risk Assessment. Risk Factors


46. Aki Z, Aksoy O, Sucak G, Kuruoğlu R, Yağci M: Miller-Fisher syndrome associated with chronic lymphocytic leukemia. Neurol India; 2008 Apr-Jun;56(2):198-200
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Miller-Fisher syndrome associated with chronic lymphocytic leukemia.
  • Chronic lymphocytic leukemia (CLL) is a frequent hematological malignancy, with meningeal or peripheral nerve infiltrations being the most commonly encountered neurological complications.
  • In this report, we describe a CLL patient with Miller-Fisher syndrome (MFS) who responded to immune modulation with plasmapheresis.
  • A 47-year-old man diagnosed as B-cell CLL admitted with neutropenic fever.
  • Nerve conduction studies were indicative of a predominantly axonal sensori-motor peripheral neuropathy.
  • This association of CLL with MFS had not been previously reported in the literature.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / complications. Miller Fisher Syndrome / complications


47. Biderman B, Marakhonov A, Skoblov M, Birerdinc A, Nohelty E, Page S, Khomenkov V, Chandhoke V, Sudarikov A, Nikitin E, Baranova A: Inhibition of potassium currents as a pharmacologic target for investigation in chronic lymphocytic leukemia. Drug News Perspect; 2010 Dec;23(10):625-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of potassium currents as a pharmacologic target for investigation in chronic lymphocytic leukemia.
  • Chronic lymphocytic leukemia (CLL) represents 22-30% of all leukemia cases, thus being the most commonly diagnosed form of adult leukemia in the Western world.
  • On a cellular level, the disease progresses due to the prolonged survival of B-cell CLL cells arrested in the G₀ stage of the cell cycle.
  • The current standard treatment for CLL is a combination regimen containing purine analogues and monoclonal antibodies.
  • Although response rates to such regimens in previously untreated patients are high, patients with CLL invariably experience relapse and often acquire high-risk chromosomal abnormalities.
  • Therefore, the search for novel avenues in CLL treatment is warranted.
  • In this manuscript, we will describe theoretical premises and some preliminary data making the case for inhibitors of the potassium currents as possible proapoptotic agents that warrant investigation as a potential pharmacologic target in CLL.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Delivery Systems. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy

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  • [Copyright] Copyright 2010 Prous Science, S.A.U. or its licensors. All rights reserved.
  • (PMID = 21180648.001).
  • [ISSN] 0214-0934
  • [Journal-full-title] Drug news & perspectives
  • [ISO-abbreviation] Drug News Perspect.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R1R15CA113331-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Potassium Channel Blockers; 0 / Potassium Channels
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48. Bhattacharyya S, Pant N, Dudeja PK, Tobacman JK: Development, evaluation, and application of a highly sensitive microtiter plate ELISA for human Bcl10 protein. J Immunoassay Immunochem; 2007;28(3):173-88
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development, evaluation, and application of a highly sensitive microtiter plate ELISA for human Bcl10 protein.
  • Bcl10 (B-cell CLL/lymphoma 10) is a 233 amino acid CARD (caspase recruitment domain)-containing cellular protein, increasingly recognized as a mediator of NFkappaB activation in non-immune, as well as immune cells.
  • Due to the importance of Bcl10 in diverse cell types, we developed a solid-phase, enzyme-linked immunosorbent (ELISA) assay to precisely measure Bcl10 in small volume cell lysates, using recombinant Bcl10 to standardize the assay.
  • Standard curve measures Bcl10 from 0.25 ng/mL to 16 ng/mL, with very low intra- and inter-assay variation.

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  • (PMID = 17613665.001).
  • [ISSN] 1532-1819
  • [Journal-full-title] Journal of immunoassay & immunochemistry
  • [ISO-abbreviation] J Immunoassay Immunochem
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / BCL10 protein, human
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49. Klukowska-Rötzler J, Bugno M, Slota E, Robinson NE, Piumi F, Guérin G, Dolf G, Gerber V: The B-cell CLL lymphoma 2 (BCL2) gene maps to equine chromosome 8q22. Anim Genet; 2005 Dec;36(6):517-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The B-cell CLL lymphoma 2 (BCL2) gene maps to equine chromosome 8q22.

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  • (PMID = 16293130.001).
  • [ISSN] 0268-9146
  • [Journal-full-title] Animal genetics
  • [ISO-abbreviation] Anim. Genet.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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50. Willis CR, Goodrich A, Park K, Waselenko JK, Lucas M, Reese A, Diehl LF, Grever MR, Byrd JC, Flinn IW: A phase I/II study examining pentostatin, chlorambucil, and theophylline in patients with relapsed chronic lymphocytic leukemia and non-Hodgkin's lymphoma. Ann Hematol; 2006 May;85(5):301-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase I/II study examining pentostatin, chlorambucil, and theophylline in patients with relapsed chronic lymphocytic leukemia and non-Hodgkin's lymphoma.
  • In an attempt to exploit bcl-2 overexpression and aberrant p53 function, two frequently encountered aberrations that predict marked treatment resistance and worse prognosis in patients with chronic lymphocytic leukemia (CLL) and non-Hodgkin's lymphoma (NHL), we combined theophylline, pentostatin, and chlorambucil at two dose levels (cohort I: 30 mg/m(2); cohort II: 20 mg/m(2)) on a 21-day cycle for up to six courses.
  • We employed a phase I/II design to determine feasibility, define the maximum tolerated dose (MTD), and explore the impact of biologic modulation on response and time to progression (TTP) in 20 patients with relapsed or refractory CLL and NHL.
  • Because of myelotoxicity, this dose level defined the MTD, and de-escalation occurred.
  • An RR of 47% and a complete remission (CR) of 5% were observed for the entire group, although responses and TTP varied greatly by histology.
  • Significant activity was observed in patients with B-cell CLL and follicular lymphoma (FL).
  • RR and TTP for fludarabine-sensitive/naïve and fludarabine-refractory (FR) B-cell CLL patients were 66 vs 25% and 20 vs 8.5 months, respectively.
  • Both FL patients responded (one with partial remission and one with CR), with a 22.5-monthly median TTP.
  • For responding patients, median TTP and overall survival (OS) was 21 and 69 months, respectively, compared to a median TTP of 2 months and an OS of 13.5 months for nonresponders.
  • The combination of pentostatin, chlorambucil, and theophylline is the active regimen in patients with FL and B-cell CLL.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chlorambucil / administration & dosage. Chlorambucil / adverse effects. Disease-Free Survival. Female. Follow-Up Studies. Humans. Male. Maximum Tolerated Dose. Middle Aged. Pentostatin / administration & dosage. Pentostatin / adverse effects. Recurrence. Remission Induction. Survival Rate. Theophylline / administration & dosage. Theophylline / adverse effects

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  • (PMID = 16518606.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Clinical Trial, Phase III; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 18D0SL7309 / Chlorambucil; 395575MZO7 / Pentostatin; C137DTR5RG / Theophylline
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51. Kadia TM, Faderl S, Estrov Z, Konopleva M, George S, Lee W, Puzanov I, Chen A, Kantarjian H, Ravandi F: Final results of phase I and pharmacokinetic study of SJG-136 administered on a daily x 5 schedule. J Clin Oncol; 2009 May 20;27(15_suppl):e13506

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e13506 Background: SJG-136 is a pyrrolobenzodiazepine dimer that forms covalent DNA crosslinks in a sequence-specific manner in the minor groove.
  • A phase I study in patients (pts) with solid tumors revealed clinical activity, defined MTD as 30 mg/m<sup>2</sup>/d administered on daily x 3 schedule, and confirmed manageable toxicity.
  • Here we report the results of a CTEP-sponsored phase I trial of SJG-136 administered on a daily x 5 schedule in pts with relapsed or refractory (R/R) leukemias.
  • METHODS: Previously treated pts with R/R acute leukemias (AML, ALL, high risk MDS, CML blast phase) or R/R CLL with adequate organ function and ECOG performance status of ≤ 2 were eligible for the study.
  • The starting dose level was 6 mcg/m<sup>2</sup> given intravenously daily x 5 days on a 21 day cycle.
  • Pts were sequentially enrolled in cohorts of 3 and the dose was escalated in a classic 3+3 schema at the dose levels: 6, 12, 24, and 36 mcg/m<sup>2</sup>.
  • Pts enrolled at each dose level (mcg/m<sup>2</sup>) were: 6 (3 pts), 12 (5 pts), 24 (4 pts), 36 (4 pts).
  • The dose of 36 mcg/m<sup>2</sup> was found to be above the MTD, with the DLT being grade 3 soft tissue edema.
  • Other manifestations of vascular leak including grade I, II hypoalbuminemia, edema, and pleural effusions were seen in a number of patients starting at dose level 24 mcg/m<sup>2</sup> and above.
  • One pt had a PR, 8 pts had stable disease, and 6 had progression.
  • CONCLUSIONS: SJG-136 is safe and active in patients with advanced leukemias.
  • 24 mcg/m<sup>2</sup> is the recommended phase II dose for the daily x 5 schedule.

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  • (PMID = 27961262.001).
  • [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
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52. De Beuf A, Hou XH, D'Haese PC, Verhulst A: Epoetin delta reduces oxidative stress in primary human renal tubular cells. J Biomed Biotechnol; 2010;2010:395785
Hazardous Substances Data Bank. EPOETIN ALFA .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Whilst three of these, heme oxygenase-1 (HO-1), aquaporin-1 (AQP-1), and B-cell CLL/lymphoma 2 (Bcl-2) have already been associated with EPO-induced renoprotection, this study for the first time suggests carboxypeptidase M (CPM), dipeptidyl peptidase IV (DPPIV), and cytoglobin (Cygb) to play a role in this process.

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  • [Cites] J Biol Chem. 1999 Oct 29;274(44):31632-40 [10531371.001]
  • [Cites] Am J Respir Cell Mol Biol. 2009 Sep;41(3):251-60 [19617398.001]
  • [Cites] Arch Biochem Biophys. 2001 May 1;389(1):84-93 [11370676.001]
  • [Cites] Physiol Rev. 2002 Jan;82(1):205-44 [11773613.001]
  • [Cites] Free Radic Biol Med. 2002 Sep 1;33(5):691-702 [12208356.001]
  • [Cites] EMBO Rep. 2002 Dec;3(12):1146-51 [12475928.001]
  • [Cites] J Am Soc Nephrol. 2003 Mar;14(3):745-54 [12595512.001]
  • [Cites] Kidney Int. 2003 Apr;63(4):1564-73 [12631374.001]
  • [Cites] Crit Rev Clin Lab Sci. 2003 Jun;40(3):209-94 [12892317.001]
  • [Cites] FASEB J. 2003 Sep;17(12):1754-5 [12958199.001]
  • [Cites] Mol Hum Reprod. 2003 Dec;9(12):799-806 [14614042.001]
  • [Cites] Exp Cell Res. 2003 Dec 10;291(2):386-97 [14644160.001]
  • [Cites] Nephrol Dial Transplant. 2004 Feb;19(2):348-55 [14736958.001]
  • [Cites] J Mol Biol. 2004 Apr 23;338(2):257-69 [15066430.001]
  • [Cites] Kidney Int. 2004 Aug;66(2):683-95 [15253723.001]
  • [Cites] J Am Soc Nephrol. 2004 Aug;15(8):2115-24 [15284297.001]
  • [Cites] Biochem J. 1976 Jul 1;157(1):169-82 [962853.001]
  • [Cites] In Vitro Cell Dev Biol. 1987 Apr;23(4):279-87 [2437097.001]
  • [Cites] Free Radic Res. 1995 Apr;22(4):375-83 [7633567.001]
  • [Cites] Kidney Int. 1997 Aug;52(2):414-28 [9263997.001]
  • [Cites] J Med Chem. 1999 Mar 25;42(6):1041-52 [10090787.001]
  • [Cites] Oncogene. 2004 Nov 25;23(55):8987-91 [15480420.001]
  • [Cites] IUBMB Life. 2004 Nov-Dec;56(11-12):681-7 [15804832.001]
  • [Cites] Curr Gastroenterol Rep. 2005 Aug;7(4):308-16 [16042916.001]
  • [Cites] Biochim Biophys Acta. 2005 Aug 1;1751(1):26-32 [15897020.001]
  • [Cites] Am J Physiol Renal Physiol. 2006 Mar;290(3):F563-71 [16461755.001]
  • [Cites] Mol Ther. 2006 Jun;13(6):1093-100 [16581302.001]
  • [Cites] Cardiovasc Res. 2006 Sep 1;71(4):684-94 [16828072.001]
  • [Cites] J Heart Lung Transplant. 2006 Sep;25(9):1109-16 [16962474.001]
  • [Cites] J Heart Lung Transplant. 2007 Feb;26(2):174-80 [17258152.001]
  • [Cites] Biochim Biophys Acta. 2007 Feb;1774(2):267-77 [17208058.001]
  • [Cites] J Neurosci Methods. 2007 Aug 15;164(1):50-8 [17524492.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Aug 10;359(4):928-34 [17560935.001]
  • [Cites] J Biol Chem. 2007 Oct 12;282(41):30207-15 [17673462.001]
  • [Cites] Kidney Int Suppl. 2007 Nov;(107):S10-5 [17943138.001]
  • [Cites] Adv Exp Med Biol. 2007;618:169-80 [18269196.001]
  • [Cites] Hemoglobin. 2008;32(3):287-96 [18473245.001]
  • [Cites] Mutagenesis. 2008 Jul;23(4):293-8 [18353768.001]
  • [Cites] Biochem Pharmacol. 2008 Dec 15;76(12):1637-43 [18755155.001]
  • [Cites] Clin Chim Acta. 2009 Jan;399(1-2):24-39 [18957287.001]
  • [Cites] Curr Opin Nephrol Hypertens. 2009 Jan;18(1):15-20 [19077684.001]
  • [Cites] Kidney Int. 2001 Feb;59(2):554-64 [11168937.001]
  • (PMID = 20454536.001).
  • [ISSN] 1110-7251
  • [Journal-full-title] Journal of biomedicine & biotechnology
  • [ISO-abbreviation] J. Biomed. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GPI-Linked Proteins; 0 / Protective Agents; 0 / RNA, Messenger; 0 / Receptors, Erythropoietin; 0 / Recombinant Proteins; 0 / cytoglobin; 0 / epoetin delta; 11096-26-7 / Erythropoietin; 64FS3BFH5W / Epoetin Alfa; 9004-22-2 / Globins; EC 1.1.3.4 / Glucose Oxidase; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.4.17.12 / carboxypeptidase M; EC 3.4.24.- / Metalloendopeptidases
  • [Other-IDs] NLM/ PMC2864893
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53. Park HJ, Kim MJ, Ha E, Chung JH: Apoptotic effect of hesperidin through caspase3 activation in human colon cancer cells, SNU-C4. Phytomedicine; 2008 Jan;15(1-2):147-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • At 100 microM, hesperidin reduced cell viability to 65.00+/-0.05% of control values in a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.
  • Cell death induced by hesperidin showed apoptotic features in 4,6-diamidino-2-phenylindole (DAPI) staining and in terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assays.
  • Examination of the expression of apoptosis-regulating genes indicated that hesperidin treatment decreased the expression of B-cell CLL/lymphoma 2 (BCL2) mRNA, and increased the expression of BCL2-associated X protein (BAX).
  • [MeSH-minor] Cell Line, Tumor. Cell Survival / drug effects. Citrus / chemistry. Enzyme Activation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Molecular Structure. Proto-Oncogene Proteins c-bcl-2 / genetics. RNA, Messenger / metabolism. bcl-2-Associated X Protein / genetics

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  • (PMID = 17897817.001).
  • [ISSN] 0944-7113
  • [Journal-full-title] Phytomedicine : international journal of phytotherapy and phytopharmacology
  • [ISO-abbreviation] Phytomedicine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / bcl-2-Associated X Protein; E750O06Y6O / Hesperidin; EC 3.4.22.- / Caspase 3
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54. Lam QL, Wang S, Ko OK, Kincade PW, Lu L: Leptin signaling maintains B-cell homeostasis via induction of Bcl-2 and Cyclin D1. Proc Natl Acad Sci U S A; 2010 Aug 3;107(31):13812-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Leptin signaling maintains B-cell homeostasis via induction of Bcl-2 and Cyclin D1.
  • Regulation of apoptosis and cell cycle progression plays an essential role in the maintenance of B-cell homeostasis, because a fine balance of survival and expansion is critical for preventing lymphocytic disorders.
  • Although remarkable progress in understanding B-cell development has been achieved, much less is known concerning niches that are critical to the maintenance of B-cell homeostasis.
  • Leptin has recently been recognized to be important for modulating the immune responses, but it has remained unclear how leptin signaling influences B-cell physiology.
  • A variety of lymphocytic malignancies have been reported to be linked to leptin, and therefore it is necessary to elucidate the mechanisms involved.
  • Here we demonstrate that leptin promotes B-cell homeostasis by inhibiting apoptosis and by inducing cell cycle entry through the activation of expressions of B-cell CLL/lymphoma 2 (Bcl-2) and cyclin D1.
  • Amplification of these leptin-modulated miRNAs inhibited B lymphoma cell growth.
  • [MeSH-major] B-Lymphocytes / immunology. Cyclin D1 / immunology. Homeostasis. Leptin / immunology. Proto-Oncogene Proteins c-bcl-2 / immunology. Signal Transduction
  • [MeSH-minor] 3' Untranslated Regions. Animals. Cell Line. Cell Proliferation. Gene Expression Regulation. Humans. Male. Mice. Mice, Inbred C57BL. MicroRNAs / genetics. Promoter Regions, Genetic. Receptors, Leptin / immunology. Receptors, Leptin / metabolism

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  • [Cites] J Immunol. 2002 Jan 15;168(2):875-82 [11777985.001]
  • [Cites] Annu Rev Immunol. 2003;21:71-105 [12414721.001]
  • [Cites] Cell. 2002 Apr;109 Suppl:S97-107 [11983156.001]
  • [Cites] Trends Immunol. 2003 Mar;24(3):104-8 [12615201.001]
  • [Cites] Immunol Res. 2003;27(1):31-52 [12637767.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 May;13(5):779-86 [15159310.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 10;101(32):11755-60 [15284443.001]
  • [Cites] Cell. 1989 Apr 7;57(1):79-88 [2649247.001]
  • [Cites] Cell. 1993 Oct 22;75(2):229-40 [8402909.001]
  • [Cites] EMBO J. 1994 May 1;13(9):2124-30 [8187765.001]
  • [Cites] Am J Pathol. 1994 Aug;145(2):330-7 [7519826.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Aug 6;93(16):8374-8 [8710878.001]
  • [Cites] Leuk Res. 1998 May;22(5):395-404 [9652725.001]
  • [Cites] Blood. 2006 Nov 1;108(9):3005-11 [16825489.001]
  • [Cites] J Exp Med. 2006 Oct 30;203(11):2551-62 [17060474.001]
  • [Cites] Exp Oncol. 2006 Sep;28(3):241-4 [17080020.001]
  • [Cites] Eur J Immunol. 2006 Dec;36(12):3118-30 [17125143.001]
  • [Cites] Cell Mol Immunol. 2007 Feb;4(1):1-13 [17349207.001]
  • [Cites] J Biol Chem. 2007 Sep 21;282(38):27587-97 [17660512.001]
  • [Cites] Curr Opin Immunol. 2007 Oct;19(5):516-21 [17644328.001]
  • [Cites] PLoS One. 2009;4(3):e4699 [19259271.001]
  • [Cites] Cell Mol Immunol. 2009 Oct;6(5):353-60 [19887048.001]
  • [Cites] Recent Pat Inflamm Allergy Drug Discov. 2009 Nov;3(3):160-6 [19594439.001]
  • [Cites] J Exp Med. 2009 Nov 23;206(12):2671-83 [19917778.001]
  • [Cites] Cytokine Growth Factor Rev. 2010 Feb;21(1):11-9 [20018552.001]
  • [Cites] Trends Biochem Sci. 2003 Feb;28(2):91-8 [12575997.001]
  • [Cites] J Immunol. 2002 Apr 15;168(8):4018-24 [11937559.001]
  • (PMID = 20643953.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI020069
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3' Untranslated Regions; 0 / Ccnd1 protein, mouse; 0 / Leptin; 0 / MicroRNAs; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Leptin; 0 / leptin receptor, mouse; 136601-57-5 / Cyclin D1
  • [Other-IDs] NLM/ PMC2922219
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55. Kudo I, Esumi M, Kida A, Ikeda M: p53 mutation, but not in vitro predictor genes of therapeutic efficacy of cisplatin, is clinically relevant in comparing partial and complete responder cases of maxillary squamous cell carcinoma. Oncol Rep; 2010 Oct;24(4):851-6
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  • [Title] p53 mutation, but not in vitro predictor genes of therapeutic efficacy of cisplatin, is clinically relevant in comparing partial and complete responder cases of maxillary squamous cell carcinoma.
  • To predict the efficacy of cisplatin and radiation therapy for maxillary squamous cell carcinoma, we examined the mRNA expression of 14 cisplatin-resistant genes and p53 mutation in specimens biopsied from patients prior to initiation of therapy.
  • Six genes including multidrug resistance protein 1 (MDR-1), multidrug resistance associated protein 1 (MRP-1), Cu++ transporting, beta polypeptide (ATP7B), xeroderma pigmentosum, complementation group A (XPA), excision repair cross-complementing rodent repair deficiency, complementation group 1 (ERCC-1) and B-cell CLL/lymphoma 2 (BCL2) were down-regulated in cases of recurrent cancers.
  • In responder cases, the drug-resistant genes that were determined in cell lines by culture do not necessarily translate into clinical relevance.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Squamous Cell / genetics. Cisplatin / therapeutic use. Genes, p53 / genetics. Maxillary Neoplasms / genetics
  • [MeSH-minor] Aged. Aged, 80 and over. Base Sequence. Cell Line, Tumor. Drug Resistance, Neoplasm / genetics. Humans. Middle Aged. Mutation. Neoplasm Staging. Reverse Transcriptase Polymerase Chain Reaction


56. García-Sáez AJ, Ries J, Orzáez M, Pérez-Payà E, Schwille P: Membrane promotes tBID interaction with BCL(XL). Nat Struct Mol Biol; 2009 Nov;16(11):1178-85
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  • Two important questions on the molecular mechanism of the B cell CLL/lymphoma 2 (BCL2) proteins involve the interaction network between pro- and antiapoptotic members and the role of their translocation to the mitochondrial membrane during apoptosis.
  • We used fluorescence correlation spectroscopy to quantify the molecular interactions of BH3-interacting domain death agonist (BID) and its truncated form tBID with the B cell lymphoma extra-large protein truncated at the C terminus (BCL(XL)DeltaCt) in solution and in membranes, and we found that (i) only the active form tBID binds to BCL(XL)DeltaCt and (ii) that the membrane strongly promotes binding between them.

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  • (PMID = 19820711.001).
  • [ISSN] 1545-9985
  • [Journal-full-title] Nature structural & molecular biology
  • [ISO-abbreviation] Nat. Struct. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BH3 Interacting Domain Death Agonist Protein; 0 / bcl-X Protein
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57. Palanduz S, Serakinci N, Cefle K, Aktan M, Tutkan G, Ozturk S, Bozkurt G, Dincol G, Pekcelen Y, Koch J: A different approach to telomere analysis with ddPRINS in chronic lymphocytic leukemia. Eur J Med Genet; 2006 Jan-Feb;49(1):63-9
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  • [Title] A different approach to telomere analysis with ddPRINS in chronic lymphocytic leukemia.
  • Telomeric sequences, located at the very end of the chromosomes, compensate for the chromosomal shortening as it happens after each round of cell division.
  • It has been reported that telomeres are shortened in acute leukemias where the cell turnover is high.
  • B-cell chronic lymphocytic leukemia (CLL) is a particularly interesting haematological malignancy in regard to telomere dynamics because most of the malignant cells in CLL are mitotically inactive.
  • In this study, we analysed the telomere length in patients with B-cell CLL in a comparison with the control group by using ddPRINS technique.
  • Twenty patients with CLL and four healthy donors as a control group were included.
  • We hypothesise that the telomeric erosion in CLL may reflect the dominance of malignant cells with an abnormally long life span.
  • Our findings imply that shortened telomeres in CLL may be reflecting the "history" of the disease and serve as an independent prognostic factor.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Primed In Situ Labeling / methods. Repetitive Sequences, Nucleic Acid. Telomere / genetics

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  • (PMID = 16473311.001).
  • [ISSN] 1769-7212
  • [Journal-full-title] European journal of medical genetics
  • [ISO-abbreviation] Eur J Med Genet
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
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58. Bagic A, Lupu VD, Kessler CM, Tornatore C: Isolated Richter's transformation of the brain. J Neurooncol; 2007 Jul;83(3):325-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Patients with B-cell chronic lymphocytic leukemia (CLL) have an increased risk of second malignancy and may develop diffuse large-cell non-Hodgkin's lymphoma (DLCL) also known as Richter's syndrome (RS).
  • Only seven cases of isolated brain RS without evidence of systemic lymphoma have been reported to date.
  • We describe a case of isolated DLCL of the brain in a 58-year-old female patient with a 3 year history of B-cell CLL.
  • The patient presented with falls due to left leg paresis and showed non-specific neuroimaging findings.
  • Brain biopsy confirmed the diagnosis of DLCL and CLL restaging failed to demonstrate evidence of RS outside the CNS.
  • [MeSH-major] Cell Transformation, Neoplastic / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Lymphoma, Large B-Cell, Diffuse / diagnosis. Neoplasms, Second Primary / etiology

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  • (PMID = 17570037.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
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59. Holgersson G, Ekman S, Reizenstein J, Bergqvist M, Pontén F, Uhlén M, Magnusson K, Jonnalagadda P, Asplund A, Strömberg S, Linder A, Blomquist E, Liljeholm M, Lödén B, Hellström K, Bergström S: Molecular profiling using tissue microarrays as a tool to identify predictive biomarkers in laryngeal cancer treated with radiotherapy. Cancer Genomics Proteomics; 2010 Jan-Feb;7(1):1-7
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  • The expression of Ki-67, MutS homolog 2, (MSH2), p53, B-cell CLL/lymphoma 2 (Bcl-2) and cyclin D1 in the cancer cells was assessed immunohistochemically using tissue microarrays (TMAs) and its predicitve value on survival and relapse was analyzed using Cox regression models.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Squamous Cell / metabolism. Laryngeal Neoplasms / metabolism

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  • (PMID = 20181625.001).
  • [ISSN] 1790-6245
  • [Journal-full-title] Cancer genomics & proteomics
  • [ISO-abbreviation] Cancer Genomics Proteomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 136601-57-5 / Cyclin D1; EC 3.6.1.3 / MutS Homolog 2 Protein
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60. Kim HJ, Song JY, Park HJ, Park HK, Yun DH, Chung JH: Naringin Protects against Rotenone-induced Apoptosis in Human Neuroblastoma SH-SY5Y Cells. Korean J Physiol Pharmacol; 2009 Aug;13(4):281-5
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  • Rotenone, a mitochondrial complex I inhibitor, can induce the pathological features of Parkinson's disease (PD).
  • In the present study, naringin, a grapefruit flavonoid, inhibited rotenone-induced cell death in human neuroblastoma SH-SY5Y cells.
  • We assessed cell death and apoptosis by measuring mitogen-activated protein kinase (MAPKs) and caspase (CASPs) activities and by performing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, 4,6-diamidino-2-phenylindole (DAPI) staining, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining.
  • Naringin also blocked rotenone-induced phosphorylation of Jun NH2-terminal protein kinase (JNK) and P38, and prevented changes in B-cell CLL/lymphoma 2 (BCL2) and BCL2-associated X protein (BAX) expression levels.
  • These results suggest that naringin has a neuroprotective effect on rotenone-induced cell death in human neuroblastoma SH-SY5Y cells.

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  • [Cites] J Pharmacol Sci. 2003 Jun;92(2):166-70 [12832847.001]
  • [Cites] J Neurosci Res. 2003 Nov 15;74(4):589-97 [14598303.001]
  • [Cites] J Neurochem. 2002 Dec;83(5):1094-102 [12437580.001]
  • [Cites] IUBMB Life. 2001 Sep-Nov;52(3-5):135-41 [11798025.001]
  • [Cites] Neurosci Res. 2001 Sep;41(1):5-12 [11535288.001]
  • [Cites] J Neurochem. 2001 Jul;78(2):374-83 [11461973.001]
  • [Cites] Nature. 2001 Mar 1;410(6824):37-40 [11242034.001]
  • [Cites] Cell. 2000 Oct 13;103(2):239-52 [11057897.001]
  • [Cites] J Neurochem. 2000 Sep;75(3):1200-8 [10936203.001]
  • [Cites] Life Sci. 2000 Jan 14;66(8):709-23 [10680579.001]
  • [Cites] Exp Neurol. 2007 Nov;208(1):1-25 [17720159.001]
  • [Cites] Neurosci Bull. 2007 Mar;23(2):125-30 [17592536.001]
  • [Cites] Toxicol Sci. 2007 May;97(1):149-62 [17324951.001]
  • [Cites] Drugs Aging. 2007;24(2):95-105 [17313198.001]
  • [Cites] Life Sci. 2006 May 8;78(24):2826-32 [16445947.001]
  • [Cites] J Neurosci. 1998 Sep 15;18(18):7296-305 [9736650.001]
  • [Cites] Br J Pharmacol. 1999 Feb;126(3):673-80 [10188978.001]
  • [Cites] J Pharmacol Exp Ther. 1999 Feb;288(2):421-7 [9918541.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Jul 30;236(3):591-3 [9245694.001]
  • [Cites] Cell. 1997 Nov 14;91(4):479-89 [9390557.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Aug 15;92(17):7686-9 [7644477.001]
  • [Cites] J Med Virol. 1985 Jan;15(1):71-9 [2981979.001]
  • [Cites] Pharmacol Res Commun. 1986 Jan;18(1):61-72 [3006093.001]
  • [Cites] Lancet Neurol. 2004 Aug;3(8):496-503 [15261611.001]
  • [Cites] Toxicol Sci. 2004 May;79(1):137-46 [14976342.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 2004 Mar;75(3):382-7 [14966152.001]
  • [Cites] FASEB J. 2003 Mar;17(3):520-2 [12551850.001]
  • (PMID = 19885011.001).
  • [ISSN] 2093-3827
  • [Journal-full-title] The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology
  • [ISO-abbreviation] Korean J. Physiol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Other-IDs] NLM/ PMC2766708
  • [Keywords] NOTNLM ; Apoptosis / Naringin / Parkinson's disease / Rotenone / SH-SY5Y
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61. Floros KV, Talieri M, Scorilas A: Topotecan and methotrexate alter expression of the apoptosis-related genes BCL2, FAS and BCL2L12 in leukemic HL-60 cells. Biol Chem; 2006 Dec;387(12):1629-33
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  • The BCL2 family of genes (B-cell CLL/lymphoma 2; Bcl-2) plays a pivotal role in the highly regulated process of apoptosis.
  • In the present study we investigated the expression profile of the novel apoptotic gene BCL2L12 in relation to other apoptotic genes in the human leukemic cell line HL-60, after treatment with topotecan or methotrexate.
  • The kinetics of apoptosis induction and cell toxicity were investigated by DNA laddering and the MTT method, respectively.

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  • (PMID = 17132110.001).
  • [ISSN] 1431-6730
  • [Journal-full-title] Biological chemistry
  • [ISO-abbreviation] Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / BCL2L12 protein, human; 0 / Muscle Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 7M7YKX2N15 / Topotecan; YL5FZ2Y5U1 / Methotrexate
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62. Blonska M, Lin X: CARMA1-mediated NF-kappaB and JNK activation in lymphocytes. Immunol Rev; 2009 Mar;228(1):199-211
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  • [Title] CARMA1-mediated NF-kappaB and JNK activation in lymphocytes.
  • Deregulation of these signaling pathways leads to inappropriate immune response and contributes to the development of leukemia/lymphoma.
  • The scaffold protein CARMA1 [caspase-recruitment domain (CARD) membrane-associated guanylate kinase (MAGUK) protein 1] has a central role in regulation of NF-kappaB and the JNK2/c-Jun complex in both B and T lymphocytes.
  • During last several years, tremendous work has been done to reveal the mechanism by which CARMA1 and its signaling partners, B cell CLL-lymphoma 10 and mucosa-associated lymphoid tissue 1, are activated and mediate NF-kappaB and JNK activation.

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  • [Cites] J Biol Chem. 2004 Jan 9;279(2):1570-4 [14638696.001]
  • [Cites] Nature. 2004 Jan 8;427(6970):167-71 [14695475.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jan 27;101(4):1004-9 [14724296.001]
  • [Cites] J Biol Chem. 2004 Apr 16;279(16):15870-6 [14754896.001]
  • [Cites] Mol Cell Biol. 2004 May;24(9):3860-73 [15082780.001]
  • [Cites] Mol Cell. 2004 May 7;14(3):289-301 [15125833.001]
  • [Cites] Mol Cell. 2004 Sep 10;15(5):713-25 [15350216.001]
  • [Cites] Science. 2004 Oct 8;306(5694):271-5 [15358865.001]
  • [Cites] Genes Dev. 2007 Apr 15;21(8):984-96 [17438001.001]
  • [Cites] Science. 2007 May 4;316(5825):754-8 [17478723.001]
  • [Cites] Oncogene. 2007 May 14;26(22):3159-71 [17496913.001]
  • [Cites] J Biol Chem. 2007 Jun 8;282(23):17141-7 [17428801.001]
  • [Cites] Mol Cell Biol. 2007 Jul;27(14):5235-45 [17502353.001]
  • [Cites] Blood. 2007 Sep 1;110(5):1621-30 [17416736.001]
  • [Cites] Nat Immunol. 2007 Sep;8(9):984-91 [17660823.001]
  • [Cites] EMBO J. 2007 Nov 14;26(22):4634-45 [17948050.001]
  • [Cites] J Exp Med. 2000 Jan 3;191(1):139-46 [10620612.001]
  • [Cites] Mol Cell Biol. 2000 Apr;20(8):2933-40 [10733597.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3394-9 [10716728.001]
  • [Cites] Nature. 2000 Mar 23;404(6776):402-7 [10746729.001]
  • [Cites] Nature. 2000 May 4;405(6782):91-4 [10811224.001]
  • [Cites] Annu Rev Immunol. 2000;18:621-63 [10837071.001]
  • [Cites] Cell. 2000 Oct 13;103(2):239-52 [11057897.001]
  • [Cites] Mol Cell. 2000 Oct;6(4):961-7 [11090634.001]
  • [Cites] Cell. 2001 Jan 12;104(1):33-42 [11163238.001]
  • [Cites] Annu Rev Immunol. 2001;19:375-96 [11244041.001]
  • [Cites] J Biol Chem. 2001 Apr 13;276(15):11877-82 [11278692.001]
  • [Cites] FEBS Lett. 2001 May 11;496(2-3):121-7 [11356195.001]
  • [Cites] J Biol Chem. 2001 Jun 15;276(24):21405-9 [11259443.001]
  • [Cites] Oncogene. 2001 Apr 30;20(19):2390-400 [11402335.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):346-51 [11460167.001]
  • [Cites] J Biol Chem. 2001 Aug 17;276(33):30589-97 [11387339.001]
  • [Cites] Annu Rev Immunol. 2002;20:55-72 [11861597.001]
  • [Cites] Annu Rev Immunol. 2002;20:371-94 [11861607.001]
  • [Cites] Nat Immunol. 2002 Mar;3(3):221-7 [11875461.001]
  • [Cites] Nat Cell Biol. 2002 May;4(5):E131-6 [11988758.001]
  • [Cites] EMBO J. 2002 Aug 1;21(15):4104-13 [12145210.001]
  • [Cites] Nat Immunol. 2002 Aug;3(8):780-6 [12118249.001]
  • [Cites] J Biol Chem. 2002 Aug 16;277(33):29710-8 [12052834.001]
  • [Cites] Nat Immunol. 2002 Sep;3(9):830-5 [12154356.001]
  • [Cites] Nat Immunol. 2002 Sep;3(9):836-43 [12154360.001]
  • [Cites] EMBO J. 2002 Oct 1;21(19):5184-94 [12356734.001]
  • [Cites] Ann N Y Acad Sci. 2003 Apr;987:125-34 [12727631.001]
  • [Cites] Immunity. 2003 Jun;18(6):751-62 [12818157.001]
  • [Cites] Immunity. 2003 Jun;18(6):763-75 [12818158.001]
  • [Cites] Mol Cell. 2003 Jun;11(6):1479-89 [12820962.001]
  • [Cites] Curr Biol. 2003 Jul 15;13(14):1247-51 [12867037.001]
  • [Cites] Curr Biol. 2003 Jul 15;13(14):1252-8 [12867038.001]
  • [Cites] Immunity. 2003 Nov;19(5):749-58 [14614861.001]
  • [Cites] Science. 2003 Nov 28;302(5650):1581-4 [14576442.001]
  • [Cites] Nat Rev Cancer. 2003 Nov;3(11):859-68 [14668816.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(1):164-71 [14673152.001]
  • [Cites] J Mol Diagn. 2004 Nov;6(4):297-307 [15507668.001]
  • [Cites] Cell. 1988 Dec 2;55(5):875-85 [3142689.001]
  • [Cites] Blood. 1993 Mar 15;81(6):1540-8 [8453101.001]
  • [Cites] Cell. 1994 Mar 25;76(6):1025-37 [8137421.001]
  • [Cites] Cell. 1994 Jun 3;77(5):727-36 [8205621.001]
  • [Cites] Genes Dev. 1994 Dec 15;8(24):2996-3007 [8001819.001]
  • [Cites] Immunity. 1994 Apr;1(1):65-72 [7889400.001]
  • [Cites] EMBO J. 1996 Jun 3;15(11):2760-70 [8654373.001]
  • [Cites] Oncogene. 1996 Oct 3;13(7):1531-5 [8875991.001]
  • [Cites] Nature. 1997 Jan 2;385(6611):83-6 [8985252.001]
  • [Cites] Science. 1997 Jan 17;275(5298):400-2 [8994040.001]
  • [Cites] J Biol Chem. 1997 Dec 19;272(51):32163-8 [9405416.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):3792-7 [9520446.001]
  • [Cites] Cell. 1998 Sep 4;94(5):667-77 [9741631.001]
  • [Cites] Immunity. 1998 Oct;9(4):575-85 [9806643.001]
  • [Cites] Science. 1998 Dec 11;282(5396):2092-5 [9851932.001]
  • [Cites] Cell. 1999 Jan 8;96(1):35-45 [9989495.001]
  • [Cites] Nature. 1999 Mar 18;398(6724):252-6 [10094049.001]
  • [Cites] Science. 1999 Apr 9;284(5412):309-13 [10195894.001]
  • [Cites] J Biol Chem. 1999 Apr 9;274(15):9955-61 [10187770.001]
  • [Cites] J Biol Chem. 1999 Apr 9;274(15):9962-8 [10187771.001]
  • [Cites] J Biol Chem. 1999 Apr 9;274(15):10287-92 [10187815.001]
  • [Cites] Nat Genet. 1999 May;22(1):63-8 [10319863.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3601-9 [10339464.001]
  • [Cites] Annu Rev Immunol. 1999;17:89-108 [10358754.001]
  • [Cites] Curr Opin Immunol. 1999 Jun;11(3):265-9 [10375560.001]
  • [Cites] Bioessays. 1999 Nov;21(11):912-21 [10517864.001]
  • [Cites] Oncogene. 1999 Oct 14;18(42):5785-94 [10523859.001]
  • [Cites] J Exp Med. 2004 Nov 1;200(9):1167-77 [15520247.001]
  • [Cites] Cell Cycle. 2004 Dec;3(12):1520-3 [15611655.001]
  • [Cites] Science. 2005 Mar 4;307(5714):1465-8 [15746428.001]
  • [Cites] Science. 2005 Apr 1;308(5718):114-8 [15802604.001]
  • [Cites] Sci STKE. 2005 Apr 26;2005(281):re5 [15855411.001]
  • [Cites] Nat Immunol. 2005 Nov;6(11):1087-95 [16186825.001]
  • [Cites] Cancer. 2005 Nov 1;104(9):1885-93 [16177990.001]
  • [Cites] Genes Dev. 2005 Nov 15;19(22):2668-81 [16260493.001]
  • [Cites] J Exp Med. 2005 Nov 21;202(10):1423-31 [16301747.001]
  • [Cites] Immunity. 2005 Dec;23(6):561-74 [16356855.001]
  • [Cites] Immunity. 2005 Dec;23(6):575-85 [16356856.001]
  • [Cites] Cell. 2006 Feb 10;124(3):601-13 [16469705.001]
  • [Cites] Mol Cell Biol. 2006 Mar;26(6):2327-36 [16508008.001]
  • [Cites] Mol Biol Cell. 2006 May;17(5):2166-76 [16495340.001]
  • [Cites] Nature. 2006 May 4;441(7089):106-10 [16572121.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4500-7 [16484591.001]
  • [Cites] Mol Cell Biol. 2006 Jul;26(14):5497-508 [16809782.001]
  • [Cites] Mol Cell. 2006 Jul 7;23(1):13-23 [16818229.001]
  • [Cites] Nat Immunol. 2006 Aug;7(8):851-8 [16799562.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11677-82 [16857737.001]
  • [Cites] Nat Med. 2006 Sep;12(9):1088-92 [16921377.001]
  • [Cites] Int Immunol. 2006 Oct;18(10):1405-11 [16940043.001]
  • [Cites] Eur J Immunol. 2006 Nov;36(11):3033-43 [17048267.001]
  • [Cites] Immunity. 2006 Nov;25(5):701-15 [17098202.001]
  • [Cites] Mol Immunol. 2007 Mar;44(8):2095-100 [17052756.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):908-13 [17213322.001]
  • [Cites] Immunity. 2007 Jan;26(1):55-66 [17189706.001]
  • [Cites] EMBO J. 2007 Apr 4;26(7):1794-805 [17363905.001]
  • [Cites] J Exp Med. 2007 Dec 24;204(13):3285-93 [18086859.001]
  • [Cites] Nat Rev Cancer. 2008 Feb;8(2):83-93 [18094723.001]
  • [Cites] Cell. 2008 Feb 8;132(3):344-62 [18267068.001]
  • [Cites] Nat Immunol. 2008 Mar;9(3):263-71 [18223652.001]
  • [Cites] Nat Immunol. 2008 Mar;9(3):272-81 [18264101.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Feb 26;105(8):3023-8 [18287044.001]
  • [Cites] Mol Cell Biol. 2008 Apr;28(7):2470-80 [18227156.001]
  • [Cites] Science. 2008 Mar 21;319(5870):1676-9 [18323416.001]
  • [Cites] J Immunol. 2008 Jun 1;180(11):7107-11 [18490708.001]
  • [Cites] Mol Cell. 2008 Aug 8;31(3):415-21 [18691973.001]
  • [Cites] Mol Cell Biol. 2008 Sep;28(18):5668-86 [18625728.001]
  • (PMID = 19290929.001).
  • [ISSN] 1600-065X
  • [Journal-full-title] Immunological reviews
  • [ISO-abbreviation] Immunol. Rev.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM079451; United States / NIGMS NIH HHS / GM / R01GM065899; United States / NIGMS NIH HHS / GM / R56 GM065899; United States / NIGMS NIH HHS / GM / R01 GM065899-06; United States / NIGMS NIH HHS / GM / R01GM079451; United States / NIGMS NIH HHS / GM / R01 GM065899; United States / NIGMS NIH HHS / GM / GM065899-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CARD Signaling Adaptor Proteins; 0 / NF-kappa B; EC 2.7.12.2 / MAP Kinase Kinase 4
  • [Number-of-references] 119
  • [Other-IDs] NLM/ NIHMS100227; NLM/ PMC2878635
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63. Macor P, Secco E, Zorzet S, Tripodo C, Celeghini C, Tedesco F: An update on the xenograft and mouse models suitable for investigating new therapeutic compounds for the treatment of B-cell malignancies. Curr Pharm Des; 2008;14(21):2023-39
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  • [Title] An update on the xenograft and mouse models suitable for investigating new therapeutic compounds for the treatment of B-cell malignancies.
  • B-cell malignancies account for over the 90% of all lymphoid neoplasms.
  • Primary tumor samples are useful for examining the characteristics of a patient's own tumor, although both primary leukemic cells and cell lines provide an initial step for screening novel compounds for their activity in some hematological malignancies, they should be followed by models in intact animals.
  • In this review, we try to summarize the animal models generated to study B-cell malignancies, in particular, B-cell lymphoma, B-cell CLL and MM that represent the major part of B-cell malignancies.
  • Animals that spontaneously develop cancer are flawed to predict human disease.
  • [MeSH-minor] Animals. Drug Delivery Systems. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / metabolism. Mice. Multiple Myeloma / drug therapy. Multiple Myeloma / metabolism. Species Specificity

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  • (PMID = 18691113.001).
  • [ISSN] 1873-4286
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 195
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64. Bodzioch M, Dembinska-Kiec A, Hartwich J, Lapicka-Bodzioch K, Banas A, Polus A, Grzybowska J, Wybranska I, Dulinska J, Gil D, Laidler P, Placha W, Zawada M, Balana-Nowak A, Sacha T, Kiec-Wilk B, Skotnicki A, Moehle C, Langmann T, Schmitz G: The microarray expression analysis identifies BAX as a mediator of beta-carotene effects on apoptosis. Nutr Cancer; 2005;51(2):226-35
Hazardous Substances Data Bank. BETA-CAROTENE .

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  • We performed a microarray expression analysis in normal [human umbilical vein endothelial cells (HUVECs)] and neoplastic (melanoma A375 and myelomonocytic leukemia U937) actively proliferating cells and found evidence that beta-carotene stimulated vital cellular functions in the former and suppressed them in the latter.
  • These differential effects correlated with the expression of the proapoptotic BCL2-associated X protein (BAX), which was downregulated in HUVECs and upregulated in the two neoplastic cell lines.
  • The quantitative expression analysis using real-time polymerase chain reaction largely confirmed the inhibition of B-cell CLL/lymphoma 2 (BCL2) pathway-mediated apoptosis in HUVECs and its activation in melanoma and leukemic cells.
  • [MeSH-major] Antioxidants / pharmacology. Apoptosis / drug effects. Leukemia, Myelomonocytic, Acute / metabolism. Melanoma / metabolism. Protein Array Analysis. Proto-Oncogene Proteins c-bcl-2 / genetics. beta Carotene / pharmacology

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  • (PMID = 15860445.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / BAX protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 01YAE03M7J / beta Carotene
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65. Park HJ, Kim HJ, Park HK, Chung JH: Protective effect of histamine H2 receptor antagonist ranitidine against rotenone-induced apoptosis. Neurotoxicology; 2009 Nov;30(6):1114-9
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  • Histamine H(2) receptor antagonists have been reported to improve the motor symptoms of Parkinson's disease (PD) patients and to exert neuroprotective effects.
  • Ranitidine blocked the rotenone-induced phosphorylation of c-Jun NH(2)-terminal protein kinase (JNK) and P38 MAPK (P38), and promoted the phosphorylation of extracellular signal-regulated protein kinase (ERK).
  • Ranitidine also prevented the down-regulation of B-cell CLL/lymphoma 2 (BCL2) and the up-regulation of BCL2-associated X protein (BAX) by rotenone.
  • [MeSH-minor] Analysis of Variance. Caspase 3 / metabolism. Caspase 9 / metabolism. Cell Survival / drug effects. Dose-Response Relationship, Drug. Humans. In Situ Nick-End Labeling. Indoles. JNK Mitogen-Activated Protein Kinases / metabolism. Mitogen-Activated Protein Kinases / metabolism. Neuroblastoma / pathology. Phosphorylation / drug effects. Poly(ADP-ribose) Polymerases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Up-Regulation / drug effects. bcl-2-Associated X Protein / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism

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  • (PMID = 19723537.001).
  • [ISSN] 1872-9711
  • [Journal-full-title] Neurotoxicology
  • [ISO-abbreviation] Neurotoxicology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Histamine H2 Antagonists; 0 / Indoles; 0 / Insecticides; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 03L9OT429T / Rotenone; 47165-04-8 / DAPI; 884KT10YB7 / Ranitidine; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / CASP9 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspase 9
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66. Huang XX, McCaughan GW, Shackel NA, Gorrell MD: Up-regulation of proproliferative genes and the ligand/receptor pair placental growth factor and vascular endothelial growth factor receptor 1 in hepatitis C cirrhosis. Liver Int; 2007 Sep;27(7):960-8
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  • RESULTS: Real-time RT-PCR showed up-regulation of genes in HCV cirrhosis including the proliferation-associated genes bone morphogenetic protein 3 (BMP3), placental growth factor 3 (PGF3), vascular endothelial growth factor receptor 1 (VEGFR1) and soluble VEGFR1, the oncogene FYN, and the immune response-associated genes toll-like receptor 9 (TLR9) and natural killer cell transcript 4 (NK4).
  • Expressions of TLR2 and the oncogenes B-cell CLL/lymphoma 9 (BCL9) and PIM2 were decreased in HCV cirrhosis.
  • [MeSH-major] Carcinoma, Hepatocellular / genetics. Cell Proliferation. Hepatitis C / complications. Liver Cirrhosis / genetics. Liver Neoplasms / genetics. Pregnancy Proteins / analysis. Vascular Endothelial Growth Factor Receptor-1 / metabolism
  • [MeSH-minor] Adolescent. Adult. Bone Morphogenetic Proteins / analysis. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Cell Transformation, Neoplastic / pathology. Female. Gene Expression Regulation, Neoplastic. Hepatocyte Growth Factor / analysis. Humans. Liver / chemistry. Liver / pathology. Liver / virology. Male. Middle Aged. Neoplasm Proteins / analysis. Neovascularization, Pathologic / genetics. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / virology. Protein-Serine-Threonine Kinases / analysis. Proto-Oncogene Proteins / analysis. Proto-Oncogene Proteins c-fyn / analysis. RNA, Messenger / analysis. Toll-Like Receptors / analysis

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  • (PMID = 17696935.001).
  • [ISSN] 1478-3223
  • [Journal-full-title] Liver international : official journal of the International Association for the Study of the Liver
  • [ISO-abbreviation] Liver Int.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK56402
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BCL9 protein, human; 0 / Bone Morphogenetic Proteins; 0 / HGF protein, human; 0 / Neoplasm Proteins; 0 / PIM2 protein, human; 0 / Pregnancy Proteins; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; 0 / Toll-Like Receptors; 144589-93-5 / placenta growth factor; 67256-21-7 / Hepatocyte Growth Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1; EC 2.7.10.2 / FYN protein, human; EC 2.7.10.2 / Proto-Oncogene Proteins c-fyn; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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67. Kalac M, Suvic-Krizanic V, Ostojic S, Kardum-Skelin I, Barsic B, Jaksica B: Central nervous system involvement of previously undiagnosed chronic lymphocytic leukemia in a patient with neuroborreliosis. Int J Hematol; 2007 May;85(4):323-5
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  • [Title] Central nervous system involvement of previously undiagnosed chronic lymphocytic leukemia in a patient with neuroborreliosis.
  • Leukemic involvement of the central nervous system (CNS) in previously undiagnosed chronic lymphocytic leukemia (CLL) is very rare.
  • We report the case of a 62-year-old man with neuroborreliosis in which cytologic, immunocytochemical, and flow cytometry analyses revealed the presence of clonal B-lymphocytes in the cerebrospinal fluid (CSF).
  • Monoclonal lymphocytes were still detectable at the same percentage, however, despite systemic chlorambucil therapy.
  • The application of intrathecal dexamethasone therapy led to the disappearance of B-cell CLL (B-CLL) cells in the CSF.
  • We presumed that the neuroborreliosis enabled the transmigration of leukocytes, including B-CLL cells, across the blood-brain barrier via activation of matrix metalloproteinase 9, an enzyme known to open the blood-brain barrier.
  • [MeSH-major] Central Nervous System / pathology. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemic Infiltration / drug therapy. Leukemic Infiltration / pathology. Lyme Neuroborreliosis / drug therapy. Lyme Neuroborreliosis / pathology

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  • (PMID = 17483076.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Hormonal; 18D0SL7309 / Chlorambucil; 7S5I7G3JQL / Dexamethasone; EC 3.4.24.35 / Matrix Metalloproteinase 9
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68. Takeshita A, Shinjo K, Yamakage N, Ono T, Hirano I, Matsui H, Shigeno K, Nakamura S, Tobita T, Maekawa M, Ohnishi K, Sugimoto Y, Kiyoi H, Naoe T, Ohno R: CMC-544 (inotuzumab ozogamicin) shows less effect on multidrug resistant cells: analyses in cell lines and cells from patients with B-cell chronic lymphocytic leukaemia and lymphoma. Br J Haematol; 2009 Jun;146(1):34-43
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  • [Title] CMC-544 (inotuzumab ozogamicin) shows less effect on multidrug resistant cells: analyses in cell lines and cells from patients with B-cell chronic lymphocytic leukaemia and lymphoma.
  • The effect of CMC-544, a calicheamicin-conjugated anti-CD22 monoclonal antibody, was analysed in relation to CD22 and P-glycoprotein (P-gp) in B-cell chronic lymphocytic leukaemia (CLL) and non-Hodgkin lymphoma (NHL) in vitro.
  • The cell lines used were CD22-positive parental Daudi and Raji, and their P-gp positive sublines, Daudi/MDR and Raji/MDR.
  • Cells obtained from 19 patients with B-cell CLL or NHL were also used.
  • The effect of CMC-544 was analysed by viable cell count, morphology, annexin-V staining, and cell cycle distribution.
  • A dose-dependent, selective cytotoxic effect of CMC-544 was observed in cell lines that expressed CD22.
  • In clinical samples, the cytotoxic effect of CMC-544 was inversely related to the amount of P-gp (P = 0.003), and to intracellular rhodamine-123 accumulation (P < 0.001).
  • Our findings will help to predict the clinical effectiveness of this drug on these B-cell malignancies, suggesting a beneficial effect with combined use of CMC-544 and MDR modifiers.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Cell Count. Cell Line, Transformed. Cell Line, Tumor. Cyclosporins / therapeutic use. Dose-Response Relationship, Drug. Drug Resistance, Multiple / drug effects. Drug Resistance, Neoplasm. Flow Cytometry. Humans. Immunosuppressive Agents / therapeutic use. Jurkat Cells. P-Glycoprotein / analysis. P-Glycoprotein / antagonists & inhibitors. P-Glycoprotein / metabolism. Quinolines / therapeutic use. Sialic Acid Binding Ig-like Lectin 2 / analysis. Sialic Acid Binding Ig-like Lectin 2 / immunology. Treatment Outcome. Tumor Cells, Cultured

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  • (PMID = 19388933.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Cyclosporins; 0 / Immunosuppressive Agents; 0 / Inotuzumab Ozogamicin; 0 / P-Glycoprotein; 0 / Quinolines; 0 / Sialic Acid Binding Ig-like Lectin 2; 0BJK6B565B / dofequidar; 121584-18-7 / valspodar
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69. Campo S, Campo GM, Avenoso A, D'Ascola A, Musolino C, Calabrò L, Bellomo G, Quartarone E, Calatroni A: Lymphocytes from patients with early stage of B-cell chronic lymphocytic leukaemia and long survival synthesize decorin. Biochimie; 2006 Dec;88(12):1933-9
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  • [Title] Lymphocytes from patients with early stage of B-cell chronic lymphocytic leukaemia and long survival synthesize decorin.
  • mRNA/cDNA gene expression of both small leucine-rich proteoglycans decorin and biglycan was evaluated by PCR real time in lymphocytes collected from patients with chronic lymphocytic leukaemia (CLL) at different stages of disease and from healthy controls.
  • Lymphocytes obtained from healthy controls showed no or very low levels of mRNA expression of both decorin and biglycan.
  • Biglycan expression was very low in CLL patients, values being close to those of controls.
  • On the contrary, decorin mRNA was clearly expressed in patients with early B-cell CLL, while a low expression was found in advanced clinical stages.
  • Furthermore, a significant higher decorin expression was found in patients with non-progressive CLL type in comparison with patients with aggressive type of the disease.
  • Decorin expression resulted especially high in the low-progressive low-risk patients.
  • The peculiar occurrence of decorin in the non-aggressive type of CLL is consistent with its suggested anti-oncogenic role.
  • The measurement of galactosamine-containing proteoglycans concentration in plasma confirmed decorin expression results, with significant differences between CLL patients and controls.
  • Significant changes were also seen between groups of patients of Rai stage 0 with recent diagnosis (less than 5 years, from analysis), (low amount of decorin) and less recent diagnosis (more than 5 years), (high amount of decorin).
  • [MeSH-major] Extracellular Matrix Proteins / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Lymphocytes / metabolism. Proteoglycans / genetics

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  • (PMID = 16938379.001).
  • [ISSN] 0300-9084
  • [Journal-full-title] Biochimie
  • [ISO-abbreviation] Biochimie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / BGN protein, human; 0 / Biglycan; 0 / DCN protein, human; 0 / Decorin; 0 / Extracellular Matrix Proteins; 0 / Proteoglycans; 0 / RNA, Messenger
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70. Quintero-Rivera F, Nooraie F, Rao PN: Frequency of 5'IGH deletions in B-cell chronic lymphocytic leukemia. Cancer Genet Cytogenet; 2009 Apr 1;190(1):33-9
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  • [Title] Frequency of 5'IGH deletions in B-cell chronic lymphocytic leukemia.
  • In a retrospective analysis of a large group of cases (n=291) with B-cell CLL diagnosis, the various characteristics of IGH aberrations as identified by fluorescence in situ hybridization (FISH) probes were studied.
  • Among the IGH abnormalities detected, translocations with unknown partners (split signals) occurred in only a small group of patients (15%).
  • Instead, deletion of 5'IGH, corresponding to the variable IGH segment (IGH(V)) was the most recurrent aberration, observed in 82% (the second most common finding among our patients).
  • Although not exclusive to CLL, the deletion occurred in a high frequency, in contrast to its rarity in other B-cell lymphoproliferative disorders.
  • Longitudinal studies are warranted, to determine when in the disease progression this abnormality is acquired, as a potential early marker, and its impact on the natural history of CLL.
  • [MeSH-major] 5' Flanking Region / genetics. Gene Deletion. Immunoglobulin Heavy Chains / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics

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  • (PMID = 19264231.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 3.2.2.5 / Antigens, CD38
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71. Molica S, Digiesi G, Mirabelli R, Cutrona G, Antenucci A, Molica M, Giannarelli D, Sperduti I, Morabito F, Neri A, Baldini L, Ferrarini M: Serum level of CD26 predicts time to first treatment in early B-chronic lymphocytic leukemia. Eur J Haematol; 2009 Sep;83(3):208-14
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  • [Title] Serum level of CD26 predicts time to first treatment in early B-chronic lymphocytic leukemia.
  • We analyzed the correlation between well-established biological parameters of prognostic relevance in B-cell chronic lymphocytic leukemia (CLL) [i.e. mutational status of the immunoglobulin heavy chain variable region (IgV(H)), ZAP-70- and CD38-expression] and serum levels of CD26 (dipeptidyl peptidase IV, DPP IV) by evaluating the impact of these variables on the time to first treatment (TFT) in a series of 69 previously untreated Binet stage A B-cell CLL patients.
  • By using a commercial ELISA we found that with exception of a borderline significance for ZAP-70 (P = 0.07) and CD38 (P = 0.08), circulating levels of CD26 did not correlate with either Rai substages (P = 0.520) or other biomarker [beta2-microglobulin (P = 0.933), LDH (P = 0.101), mutational status of IgV(H) (P = 0.320)].
  • Along with higher serum levels of CD26, the univariate Cox proportional hazard model identified absence of mutation in IgV(H) (P < 0.0001) as predictor of shorter TFT.
  • As in multivariate analysis all these parameters maintained their discriminating power (mutational status of IgV(H,)P < 0.0001; soluble CD26, P = 0.02) their combined effect on clinical outcome was assessed.
  • (1) Low-risk group (n = 31), patients with concordant IgVH(mut) and low level of soluble CD26;.
  • (3) high-risk group (n = 12), patients with concordant IgVH(unmut) and high level of soluble CD26, differences in the TFT were statistically significant, with a TFT at 5 yr of respectively 88%, 51% and 43% (P < 0.0001).
  • Our results indicate that in early B-cell CLL biological profile including among other parameters soluble CD26 may provide a useful insight into the complex interrelationship of prognostic variables.
  • Furthermore, CD26 along with mutational status of IgV(H) can be adequately used to predict clinical behavior of patients with low risk disease.
  • [MeSH-major] Dipeptidyl Peptidase 4 / biosynthesis. Leukemia, Lymphocytic, Chronic, B-Cell / blood
  • [MeSH-minor] Aged. Antigens, CD38 / biosynthesis. Disease Progression. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Prognosis. Risk. Time Factors. Treatment Outcome. ZAP-70 Protein-Tyrosine Kinase / metabolism

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  • (PMID = 19459926.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 3.2.2.5 / Antigens, CD38; EC 3.4.14.5 / Dipeptidyl Peptidase 4
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72. Molica S, Vitelli G, Mirabelli R, Digiesu G, Giannarelli D, Cuneo A, Ribatti D, Vacca A: Serum levels of syndecan-1 in B-cell chronic lymphocytic leukemia: correlation with the extent of angiogenesis and disease-progression risk in early disease. Leuk Lymphoma; 2006 Jun;47(6):1034-40
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum levels of syndecan-1 in B-cell chronic lymphocytic leukemia: correlation with the extent of angiogenesis and disease-progression risk in early disease.
  • Syndecan-1 is a transmembrane proteoglycan generally not expressed in mature B-cell neoplasias like chronic lymphocytic leukemia (CLL).
  • Moreover, information dealing with the evaluation of soluble syndecan-1 in CLL are lacking.
  • We measured syndecan-1 concentrations in serum drawn at the time of diagnosis from 67 B-cell CLL patients (Binet stage A, 46; stage B, 7; stage C, 14).
  • Detectable levels of syndecan-1 were found in all patients, although serum concentrations were significantly lower in CLL patients in comparison to age- and sex-matched controls (P = 0.02; Mann-Whitney test).
  • Serum levels of syndecan-1 did not parallel those of several angiogenic cytokines such as vascular endothelial growth factor (VEGF) (P = 0.963), basic fibroblastic growth factor (FGF-2) (P = 0.216), angiogenin (P = 0.478), metalloproteinase-9 (MMP-9) (P = 0.125) as well as bone marrow (BM) microvessel density (P = 0.110).
  • In 46 Binet stage A patients, serum levels of syndecan-1 were further evaluated as a dichotomous variable with respect to progression-free survival (PFS), an end-point surrogate for overall survival in early B-cell CLL.
  • Median PFS was not reached in the patient group with low syndecan-1, compared to a median of 34 months observed in the remaining patients (P = 0.018; HR = 0.208; 95% CI = 0.115 - 0.816).
  • Despite the pro-angiogenic activity of syndecan-1 which mediates FGF-2 binding and activity, no correlation with either angiogenic cytokines or the extent of BM angiogenesis was found in CLL.
  • Finally, our results highlight the involvement of syndecan-1 in the mechanisms of disease-progression of early CLL.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Leukemia, Lymphocytic, Chronic, B-Cell / blood. Neovascularization, Pathologic. Syndecan-1 / blood
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Bone Marrow Cells / metabolism. Disease Progression. Disease-Free Survival. Female. Humans. Karyotyping. Male. Middle Aged


73. Cerezo M, Bandelt HJ, Martín-Guerrero I, Ardanaz M, Vega A, Carracedo A, García-Orad A, Salas A: High mitochondrial DNA stability in B-cell chronic lymphocytic leukemia. PLoS One; 2009;4(11):e7902
Genetic Alliance. consumer health - Leukemia, B-cell, chronic.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High mitochondrial DNA stability in B-cell chronic lymphocytic leukemia.
  • BACKGROUND: Chronic Lymphocytic Leukemia (CLL) leads to progressive accumulation of lymphocytes in the blood, bone marrow, and lymphatic tissues.
  • Previous findings have suggested that the mtDNA could play an important role in CLL.
  • METHODOLOGY/PRINCIPAL FINDINGS: The mitochondrial DNA (mtDNA) control-region was analyzed in lymphocyte cell DNA extracts and compared with their granulocyte counterpart extract of 146 patients suffering from B-Cell CLL; B-CLL (all recruited from the Basque country).
  • Only twenty instabilities were finally confirmed, most of them affecting the homopolymeric stretch located in the second hypervariable segment (HVS-II) around position 310, which is well known to constitute an extreme mutational hotspot of length polymorphism, as these mutations are frequently observed in the general human population.
  • A critical revision of the findings in previous studies indicates a lack of proper methodological standards, which eventually led to an overinterpretation of the role of the mtDNA in CLL tumorigenesis.
  • CONCLUSIONS/SIGNIFICANCE: Our results suggest that mtDNA instability is not the primary causal factor in B-CLL.
  • [MeSH-major] DNA, Mitochondrial / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism
  • [MeSH-minor] Base Sequence. DNA Primers / genetics. Databases, Genetic. Granulocytes / cytology. Haplotypes. Humans. Lymphocytes / cytology. Models, Statistical. Molecular Sequence Data. Mutation. Phylogeny. Sequence Analysis, DNA

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  • [Cites] BMC Cancer. 2009;9:113 [19371404.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Jul 22;333(1):122-30 [15958208.001]
  • [Cites] Forensic Sci Int. 2000 May 8;110(1):47-59 [10802200.001]
  • [Cites] Am J Hum Genet. 2000 Nov;67(5):1251-76 [11032788.001]
  • [Cites] Leukemia. 2001 Mar;15(3):445-51 [11237069.001]
  • [Cites] Int J Legal Med. 2001;114(3):186-90 [11296893.001]
  • [Cites] Leukemia. 2001 Sep;15(9):1317-25 [11516091.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Sep 30;335(3):891-9 [16102729.001]
  • [Cites] Electrophoresis. 2005 Sep;26(18):3414-29 [16167362.001]
  • [Cites] J Med Genet. 2005 Dec;42(12):957-60 [15923271.001]
  • [Cites] Leukemia. 2006 Feb;20(2):362-3 [16357835.001]
  • [Cites] Genetics. 2006 Jan;172(1):373-87 [16172508.001]
  • [Cites] PLoS Med. 2005 Nov;2(11):e296 [16187796.001]
  • [Cites] Hum Genet. 2006 Jun;119(5):505-15 [16528519.001]
  • [Cites] Blood. 2007 Jan 15;109(2):756-62 [16946307.001]
  • [Cites] Mol Biol Evol. 2007 Feb;24(2):436-48 [17099056.001]
  • [Cites] Mol Biol Evol. 2007 Mar;24(3):868-74 [17218641.001]
  • [Cites] Forensic Sci Int. 2007 May 3;168(1):1-13 [16814504.001]
  • [Cites] PLoS One. 2008;3(4):e2062 [18446216.001]
  • [Cites] J Med Genet. 2008 Dec;45(12):769-72 [18611982.001]
  • [Cites] PLoS One. 2009;4(4):e5112 [19340307.001]
  • [Cites] Am J Hum Genet. 2002 May;70(5):1152-71 [11938495.001]
  • [Cites] Blood. 2002 Jul 15;100(2):635-9 [12091358.001]
  • [Cites] Am J Hum Genet. 2002 Nov;71(5):1150-60 [12384858.001]
  • [Cites] Am J Phys Anthropol. 2003 Apr;120(4):391-404 [12627534.001]
  • [Cites] Blood. 2003 Apr 15;101(8):3118-25 [12446454.001]
  • [Cites] Electrophoresis. 2003 Apr;24(7-8):1159-65 [12707907.001]
  • [Cites] Int J Legal Med. 2003 Jun;117(3):180-4 [12799738.001]
  • [Cites] Leukemia. 2003 Aug;17(8):1437-47 [12886229.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2487-91 [14523470.001]
  • [Cites] Leukemia. 2004 Jan;18(1):18-22 [14614516.001]
  • [Cites] Oncogene. 2004 Feb 12;23(6):1314-20 [14647457.001]
  • [Cites] Forensic Sci Int. 2004 Feb 10;140(1):1-11 [15013160.001]
  • [Cites] Cancer Res. 2004 Mar 15;64(6):1966-71 [15026331.001]
  • [Cites] Forensic Sci Int. 2004 Mar 10;140(2-3):251-7 [15036446.001]
  • [Cites] Leukemia. 2004 Jul;18(7):1313-6 [15129223.001]
  • [Cites] Science. 2004 Sep 3;305(5689):1402-4 [15353782.001]
  • [Cites] Am J Hum Genet. 2004 Nov;75(5):910-8 [15382008.001]
  • [Cites] Ann Hum Genet. 1991 Jan;55(Pt 1):51-67 [2042936.001]
  • [Cites] Int J Legal Med. 1993;105(5):251-6 [8471542.001]
  • [Cites] N Engl J Med. 1995 Oct 19;333(16):1052-7 [7675049.001]
  • [Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]
  • [Cites] Int J Cancer. 1998 May 18;76(4):495-8 [9590124.001]
  • [Cites] Ann Intern Med. 1998 Oct 1;129(7):559-66 [9758577.001]
  • [Cites] Leukemia. 1998 Oct;12(10):1612-7 [9766507.001]
  • [Cites] Eur J Hum Genet. 1998 Jul-Aug;6(4):365-75 [9781045.001]
  • [Cites] Nat Genet. 1999 Oct;23(2):147 [10508508.001]
  • [Cites] Forensic Sci Int. 2005 Mar 10;148(2-3):191-8 [15639614.001]
  • [Cites] Int J Legal Med. 2004 Oct;118(5):267-73 [15257464.001]
  • [Cites] N Engl J Med. 2005 Feb 24;352(8):804-15 [15728813.001]
  • [Cites] Am J Hum Genet. 2005 May;76(5):883-6 [15791543.001]
  • [Cites] Electrophoresis. 2000 Feb;21(3):548-53 [10726758.001]
  • (PMID = 19924307.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / DNA, Mitochondrial
  • [Other-IDs] NLM/ PMC2775629
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74. Cvetković RS, Perry CM: Rituximab: a review of its use in non-Hodgkin's lymphoma and chronic lymphocytic leukaemia. Drugs; 2006;66(6):791-820
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  • [Title] Rituximab: a review of its use in non-Hodgkin's lymphoma and chronic lymphocytic leukaemia.
  • In phase III trials in patients with indolent or aggressive B-cell non-Hodgkin's lymphoma (NHL), intravenous rituximab in combination with chemotherapy was more effective as first- or second-line therapy than chemotherapy alone in providing tumour remission and patient survival.
  • Likewise, in patients with chronic lymphocytic leukaemia (CLL), rituximab in combination with chemotherapy appeared more effective than chemotherapy alone as either first- or second-line treatment.
  • In addition, rituximab maintenance therapy was shown to significantly prolong tumour remission and patient survival in patients with indolent B-cell NHL or CLL.
  • The combination of rituximab with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was cost effective as first-line therapy for advanced-stage diffuse large B-cell NHL compared with CHOP alone.
  • Rituximab, either alone or in combination with chemotherapy, was generally well tolerated in patients with NHL or CLL.
  • Overall, rituximab in combination with chemotherapy, is a valuable option for first- and second-line therapy in patients with advanced-stage indolent or aggressive B-cell NHL, and possibly those with B-cell CLL, and is included in current treatment guidelines for these indications.
  • The drug is also potentially useful as maintenance therapy in patients with indolent B-cell NHL or CLL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy

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  • (PMID = 16706552.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 108
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75. Tumilasci VF, Olière S, Nguyên TL, Shamy A, Bell J, Hiscott J: Targeting the apoptotic pathway with BCL-2 inhibitors sensitizes primary chronic lymphocytic leukemia cells to vesicular stomatitis virus-induced oncolysis. J Virol; 2008 Sep;82(17):8487-99
The Lens. Cited by Patents in .

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  • [Title] Targeting the apoptotic pathway with BCL-2 inhibitors sensitizes primary chronic lymphocytic leukemia cells to vesicular stomatitis virus-induced oncolysis.
  • Chronic lymphocytic leukemia (CLL) is characterized by clonal accumulation of CD5(+) CD19(+) B lymphocytes that are arrested in the G(0)/G(1) phase of the cell cycle and fail to undergo apoptosis because of overexpression of the antiapoptotic B-cell CLL/lymphoma 2 (BCL-2) protein.
  • Although primary CLL cells are largely resistant to VSV oncolysis, we postulated that targeting the apoptotic pathway via inhibition of BCL-2 may sensitize CLL cells to VSV oncolysis.
  • In the present study, we examined the capacity of EM20-25--a small-molecule antagonist of the BCL-2 protein--to overcome CLL resistance to VSV oncolysis.
  • We demonstrate a synergistic effect of the two agents in primary ex vivo CLL cells (combination index of 0.5; P < 0.0001).
  • In a direct comparison of peripheral blood mononuclear cells from healthy volunteers with primary CLL, the two agents combined showed a therapeutic index of 19-fold; furthermore, the combination of VSV and EM20-25 increased apoptotic cell death in Karpas-422 and Granta-519 B-lymphoma cell lines (P < 0.005) via the intrinsic mitochondrial pathway.
  • Mechanistically, EM20-25 blocked the ability of the BCL-2 protein to dimerize with proapoptotic BAX protein, thus sensitizing CLL to VSV oncolytic stress.
  • Together, these data indicate that the use of BCL-2 inhibitors may improve VSV oncolysis in treatment-resistant hematological malignancies, such as CLL, with characterized defects in the apoptotic response.
  • [MeSH-major] Apoptosis / drug effects. Barbiturates / pharmacology. Benzopyrans / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Oncolytic Virotherapy. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Vesicular stomatitis Indiana virus / physiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Case-Control Studies. Caspases / analysis. Cell Line, Tumor. Cell Survival / drug effects. Cells, Cultured. Drug Evaluation, Preclinical. Female. Formazans / metabolism. Humans. Jurkat Cells. Leukocytes, Mononuclear / drug effects. Male. Membrane Potential, Mitochondrial / drug effects. Middle Aged. Molecular Structure. Tetrazolium Salts / metabolism. Time Factors

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  • [Cites] J Biol Chem. 1997 May 23;272(21):13829-34 [9153240.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2589-96 [17105820.001]
  • [Cites] Mol Cell. 2005 Jan 7;17(1):93-102 [15629720.001]
  • [Cites] Br J Haematol. 2005 Feb;128(4):472-81 [15686454.001]
  • [Cites] J Virol. 2005 Apr;79(7):4170-9 [15767418.001]
  • [Cites] Immunology. 2005 Apr;114(4):441-9 [15804279.001]
  • [Cites] Virus Res. 2005 Apr;109(1):65-9 [15826914.001]
  • [Cites] Cancer Res. 2005 Jul 1;65(13):5554-60 [15994927.001]
  • [Cites] Leuk Res. 1999 Nov;23(11):1007-14 [10576505.001]
  • [Cites] Nat Med. 2000 Jul;6(7):821-5 [10888934.001]
  • [Cites] J Control Release. 2003 Feb 21;87(1-3):159-65 [12618032.001]
  • [Cites] J Clin Immunol. 2003 Mar;23(2):73-80 [12757259.001]
  • [Cites] Lancet Oncol. 2003 Aug;4(8):505-14 [12901966.001]
  • [Cites] Leukemia. 2003 Nov;17(11):2074-80 [12931228.001]
  • [Cites] Cancer Cell. 2003 Oct;4(4):263-75 [14585354.001]
  • [Cites] Cell. 2004 Jan 23;116(2):205-19 [14744432.001]
  • [Cites] J Immunol. 2004 Feb 15;172(4):2316-23 [14764700.001]
  • [Cites] Biochim Biophys Acta. 2004 Mar 1;1644(2-3):169-77 [14996501.001]
  • [Cites] Trends Mol Med. 2004 May;10(5):210-6 [15121047.001]
  • [Cites] Science. 2004 Jul 30;305(5684):626-9 [15286356.001]
  • [Cites] Cancer Cell. 2004 Sep;6(3):241-9 [15380515.001]
  • [Cites] Adv Enzyme Regul. 1984;22:27-55 [6382953.001]
  • [Cites] IUBMB Life. 2005 Feb;57(2):65-72 [16036565.001]
  • [Cites] J Cell Physiol. 2005 Dec;205(3):414-21 [15920759.001]
  • [Cites] Oncogene. 2005 Nov 21;24(52):7710-9 [16299531.001]
  • [Cites] Oncogene. 2005 Nov 21;24(52):7802-16 [16299539.001]
  • [Cites] Nat Rev Cancer. 2005 Dec;5(12):965-76 [16294217.001]
  • [Cites] Oncologist. 2006 Jan;11(1):21-30 [16401710.001]
  • [Cites] Oncogene. 2006 Jan 19;25(3):349-58 [16186807.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):981-8 [16424033.001]
  • [Cites] J Biol Chem. 2006 Apr 14;281(15):10066-72 [16481323.001]
  • [Cites] EMBO J. 2006 Jun 7;25(11):2287-96 [16642033.001]
  • [Cites] Cancer Invest. 2006 Apr-May;24(3):302-9 [16809159.001]
  • [Cites] Cell Death Differ. 2006 Aug;13(8):1419-21 [16645636.001]
  • [Cites] Cancer Res. 2007 Apr 15;67(8):3818-26 [17440096.001]
  • [Cites] J Clin Oncol. 2007 Apr 20;25(12):1512-8 [17442993.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 May;8(5):405-13 [17377525.001]
  • [Cites] Apoptosis. 2007 May;12(5):815-33 [17294078.001]
  • [Cites] Blood. 2007 May 15;109(10):4441-9 [17227835.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5430-8 [17332241.001]
  • [Cites] Virology. 2007 Aug 15;365(1):20-33 [17451770.001]
  • [Cites] Leukemia. 2007 Jul;21(7):1549-60 [17460700.001]
  • [Cites] Curr Opin Immunol. 2007 Oct;19(5):488-96 [17629468.001]
  • [Cites] Leuk Res. 2007 Dec;31(12):1687-700 [17428536.001]
  • [Cites] Nat Med. 2008 Jan;14(1):37-44 [18066076.001]
  • [Cites] Mol Ther. 2008 Jun;16(6):1041-7 [18388912.001]
  • [Cites] Cell Death Differ. 2006 Aug;13(8):1378-86 [16729025.001]
  • [Cites] Pharmacol Rev. 2006 Sep;58(3):621-81 [16968952.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2006;:273-8, 512 [17124072.001]
  • [Cites] Cancer Gene Ther. 2007 Jan;14(1):1-11 [17041564.001]
  • [Cites] J Virol. 2007 Feb;81(3):1479-91 [17108037.001]
  • [Cites] Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):621-9 [17255285.001]
  • [Cites] Oncogene. 2007 Feb 1;26(5):652-61 [16909121.001]
  • [Cites] Br J Cancer. 2007 Feb 26;96(4):600-8 [17311012.001]
  • [Cites] J Virol. 2007 Mar;81(6):2792-804 [17192316.001]
  • [Cites] Oncogene. 2007 Feb 26;26(9):1324-37 [17322918.001]
  • [Cites] Biochim Biophys Acta. 2004 Dec 10;1705(1):43-51 [15585172.001]
  • (PMID = 18579592.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 5-(6-chloro-2,4-dioxo-1,3,4,10-tetrahydro-2H-9-oxa-1,3-diazaanthracen-10-yl)pyrimidine-2,4,6-trione; 0 / Antineoplastic Agents; 0 / Barbiturates; 0 / Benzopyrans; 0 / Formazans; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tetrazolium Salts; 23305-68-2 / MTT formazan; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC2519628
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76. He JF, Zhang YM, Duan HJ, Cao JS, Zhang DL: [In silico identification, molecular cloning and verification of a novel pig gene homologous to human BCL10 of innate immunity and its preliminary expression profiles in pigs]. Yi Chuan; 2008 Jun;30(6):747-54

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [In silico identification, molecular cloning and verification of a novel pig gene homologous to human BCL10 of innate immunity and its preliminary expression profiles in pigs].
  • EU088132) which was homologous to human BCL10 (B-cell CLL/lymphoma 10) gene.
  • We found that, BCL10 expressed in high level in swine spleen, and with a modest level in thymus, brain and lymph node; low level mRNA was expressed in liver and not detectable level in kidney.
  • The swine BCL10 gene was cloned to the GFP-containing eukaryotic expression vector pEGFP-C1 and transfected to PK-15 cell line by lipofectin.

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  • (PMID = 18550498.001).
  • [ISSN] 0253-9772
  • [Journal-full-title] Yi chuan = Hereditas
  • [ISO-abbreviation] Yi Chuan
  • [Language] CHI
  • [Databank-accession-numbers] GENBANK/ EU088132
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / BCL10 protein, human
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77. Yang D, Zhang M, Huang X, Fang F, Chen B, Wang S, Cai J, Shi X, Qu J, Geng YJ: Protection of retinal vasculature by losartan against apoptosis and vasculopathy in rats with spontaneous hypertension. J Hypertens; 2010 Mar;28(3):510-9
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  • The present study was aimed at testing the role of losartan, a specific antagonist of angiotensin II receptor type 1 receptor in regulation of vascular apoptosis in retinal vasculature with hypertension.
  • Blood pressure was measured in SHR as well as normotensive Wistar-Kyoto rats (WKY).
  • The losartan-treated SHR showed marked improvement of retinal vascular morphology compared with untreated SHR.
  • TUNEL and transmission electron microscopy also revealed that losartan exerted its protective effects not only on endothelial cells but on pericytes as well.
  • The blood vessels of losartan-treated animals also showed decreased expression of bax with elevation of B-cell CLL/lymphoma 2.
  • CONCLUSION: Treatment with losartan, a medicine that lowers blood pressure by blocking angiotensin II receptor type 1 receptor, can protect the retinal vasculature against hypertensive vascular injury by inhibiting apoptosis of vascular cells and by preventing hypertensive retinopathy.
  • [MeSH-major] Angiotensin II Type 1 Receptor Blockers / pharmacology. Apoptosis / drug effects. Hypertension / drug therapy. Losartan / pharmacology. Retinal Vessels / drug effects. Vascular Diseases / prevention & control

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  • (PMID = 20051910.001).
  • [ISSN] 1473-5598
  • [Journal-full-title] Journal of hypertension
  • [ISO-abbreviation] J. Hypertens.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiotensin II Type 1 Receptor Blockers; JMS50MPO89 / Losartan
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78. Zagurovskaya M, Shareef MM, Das A, Reeves A, Gupta S, Sudol M, Bedford MT, Prichard J, Mohiuddin M, Ahmed MM: EGR-1 forms a complex with YAP-1 and upregulates Bax expression in irradiated prostate carcinoma cells. Oncogene; 2009 Feb 26;28(8):1121-31
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  • In this study, we investigated the functional role of early growth response-1 (Egr1 gene) in the regulation of radiation-induced clonogenic inhibition and apoptosis in p53 wild-type and mutant prostate cancer cells 22Rv1 and DU145, respectively.
  • Irradiation of PC3 cell xenografts that were treated with adenoviral EGR-1 showed significant regression in tumor volume.
  • These findings establish the radiation-induced pro-apoptotic action of EGR-1, in a p53-independent manner, by directly transactivating Bax, and prove that alters the B-cell CLL/lymphoma 2 (Bcl-2)/Bax ratio as one of the mechanisms resulting in significant activation of caspases, leading to cell death through the novel interaction of EGR-1 with YAP-1.

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  • (PMID = 19137013.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK62345; United States / NCI NIH HHS / CA / R01 CA78471
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / BAX protein, human; 0 / EGR1 protein, human; 0 / Early Growth Response Protein 1; 0 / NAB1 protein, human; 0 / Phosphoproteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / YAP1 (Yes-associated) protein, human; 0 / bcl-2-Associated X Protein; 9007-43-6 / Cytochromes c; EC 2.3.1.28 / Chloramphenicol O-Acetyltransferase; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 3
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79. Hunsberger JG, Austin DR, Chen G, Manji HK: Cellular mechanisms underlying affective resiliency: the role of glucocorticoid receptor- and mitochondrially-mediated plasticity. Brain Res; 2009 Oct 13;1293:76-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Bipolar disorder (BPD) is a devastating psychiatric illness marked by recurrent episodes of mania and depression.
  • Here, cellular resiliency is defined as the ability of a cell to adapt to an insult or stressor.
  • (1) B-cell CLL/lymphoma 2 (Bcl-2), (2) Bcl-2-associated athanogene (BAG-1), (3) glucocorticoid receptors (GRs), and (4) 51 kDa FK506-binding protein (FKBP5).
  • [MeSH-major] Adaptation, Physiological. Bipolar Disorder / physiopathology. Receptors, Glucocorticoid / physiology. Signal Transduction / physiology

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  • [Cites] J Neurosci. 2003 Aug 13;23(19):7311-6 [12917364.001]
  • [Cites] Biol Psychiatry. 2008 Jun 15;63(12):1103-10 [18191112.001]
  • [Cites] Brain Res. 2007 Dec 12;1184:270-6 [18028886.001]
  • [Cites] Cell Death Differ. 2002 Apr;9(4):405-13 [11965493.001]
  • [Cites] Biol Psychiatry. 2000 Jul 1;48(1):1-8 [10913502.001]
  • [Cites] Brain. 1986 Dec;109 ( Pt 6):1127-48 [3790971.001]
  • [Cites] CNS Spectr. 2008 Aug;13(8):663-81 [18704022.001]
  • [Cites] J Neurochem. 1999 Feb;72(2):879-82 [9930766.001]
  • [Cites] Neuropsychopharmacology. 1998 Apr;18(4):253-62 [9509493.001]
  • [Cites] Biol Psychiatry. 2001 May 1;49(9):741-52 [11331082.001]
  • [Cites] Curr Opin Neurobiol. 2001 Apr;11(2):240-9 [11301246.001]
  • [Cites] J Clin Psychiatry. 2000;61 Suppl 9:82-96 [10826666.001]
  • [Cites] Cell Stress Chaperones. 2003 Fall;8(3):225-31 [14984055.001]
  • [Cites] Biol Psychiatry. 2006 Apr 15;59(8):681-8 [16580345.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jan;88(1):277-84 [12519866.001]
  • [Cites] Psychopharmacology (Berl). 2001 Oct;158(1):100-6 [11685390.001]
  • [Cites] Neuropsychopharmacology. 2006 Mar;31(3):620-7 [16192984.001]
  • [Cites] Am J Psychiatry. 2004 Jan;161(1):169-71 [14702269.001]
  • [Cites] Cell. 1995 Jan 27;80(2):279-84 [7834747.001]
  • [Cites] IDrugs. 2004 Sep;7(9):846-50 [15470602.001]
  • [Cites] Metabolism. 2005 May;54(5 Suppl 1):20-3 [15877308.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3543-8 [19202080.001]
  • [Cites] J Neurosci. 1996 May 15;16(10):3534-40 [8627386.001]
  • [Cites] Psychiatry. 1999 Summer;62(2):138-72 [10420428.001]
  • [Cites] Am J Psychiatry. 2002 Nov;159(11):1841-7 [12411217.001]
  • [Cites] J Clin Endocrinol Metab. 1999 Feb;84(2):663-9 [10022435.001]
  • [Cites] Pharmacogenet Genomics. 2007 Aug;17(8):605-17 [17622937.001]
  • [Cites] J Psychiatr Res. 1999 Sep-Oct;33(5):363-70 [10504004.001]
  • [Cites] Bipolar Disord. 2002 Apr;4(2):89-104 [12071514.001]
  • [Cites] J Neurosci. 2007 Aug 15;27(33):8836-44 [17699665.001]
  • [Cites] Eur J Pharmacol. 2007 Aug 13;569(1-2):41-7 [17582397.001]
  • [Cites] Biol Psychiatry. 1999 Nov 1;46(9):1181-91 [10560024.001]
  • [Cites] Mol Psychiatry. 1998 May;3(3):220-6, 190-1 [9672897.001]
  • [Cites] J Clin Psychiatry. 2004 Feb;65(2):204-10 [15003074.001]
  • [Cites] Curr Opin Pharmacol. 2007 Feb;7(1):22-6 [17055337.001]
  • [Cites] J Clin Psychopharmacol. 2003 Aug;23(4):370-6 [12920413.001]
  • [Cites] Behav Brain Res. 2005 Dec 7;165(2):172-80 [16095731.001]
  • [Cites] Endocr Rev. 2000 Feb;21(1):55-89 [10696570.001]
  • [Cites] Biol Psychiatry. 1997 Jun 1;41(11):1131-6 [9146824.001]
  • [Cites] Biol Psychiatry. 2001 Mar 1;49(5):391-404 [11274650.001]
  • [Cites] J Neurosci. 2002 Apr 15;22(8):3251-61 [11943826.001]
  • [Cites] Mol Psychiatry. 2009 Mar;14(3):261-8 [18180755.001]
  • [Cites] Eur J Pharmacol. 2004 Jul 14;495(2-3):103-10 [15249158.001]
  • [Cites] Bipolar Disord. 2006 Feb;8(1):85-90 [16411985.001]
  • [Cites] Am J Psychiatry. 2008 Mar;165(3):385-9 [18245180.001]
  • [Cites] J Psychopharmacol. 2004 Dec;18(4):496-501 [15582915.001]
  • [Cites] Bipolar Disord. 2006 Jun;8(3):232-41 [16696824.001]
  • [Cites] J Clin Psychiatry. 1999 Apr;60(4):232-6 [10221283.001]
  • [Cites] Psychoneuroendocrinology. 1990;15(1):59-68 [2367616.001]
  • [Cites] Neuroendocrinology. 1995 Oct;62(4):340-7 [8544947.001]
  • [Cites] Bipolar Disord. 2003 Jun;5(3):217-25 [12780875.001]
  • [Cites] Bipolar Disord. 2002 Apr;4(2):117-28 [12071509.001]
  • [Cites] World Psychiatry. 2003 Oct;2(3):136-46 [16946919.001]
  • [Cites] J Cell Biol. 1999 Sep 6;146(5):929-40 [10477749.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 10;101(32):11851-6 [15280545.001]
  • [Cites] Nat Genet. 2004 Dec;36(12):1319-25 [15565110.001]
  • [Cites] Am J Psychiatry. 2006 Feb;163(2):257-64 [16449479.001]
  • [Cites] Bipolar Disord. 2003 Dec;5(6):396-406 [14636363.001]
  • [Cites] Cell Mol Biol (Noisy-le-grand). 2000 Feb;46(1):41-52 [10726970.001]
  • [Cites] Science. 1995 Mar 10;267(5203):1445-9 [7878463.001]
  • [Cites] Neuroreport. 1999 Jun 3;10(8):1741-6 [10501567.001]
  • [Cites] Eur J Pharmacol. 2006 Jun 6;539(1-2):18-26 [16678157.001]
  • [Cites] Adv Exp Med Biol. 1999;461:107-16 [10442170.001]
  • [Cites] J Clin Psychiatry. 2000 Jan;61(1):33-8 [10695644.001]
  • [Cites] J Affect Disord. 2001 Jun;65(1):85-93 [11426515.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Jun 24;105(25):8766-71 [18562287.001]
  • [Cites] J Neurosci. 2005 May 4;25(18):4493-502 [15872096.001]
  • [Cites] Am J Med Genet C Semin Med Genet. 2003 Nov 15;123C(1):48-58 [14601036.001]
  • (PMID = 19595676.001).
  • [ISSN] 1872-6240
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 MH999999; United States / Intramural NIH HHS / / ZIA MH002921-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antimanic Agents; 0 / Receptors, Glucocorticoid
  • [Number-of-references] 69
  • [Other-IDs] NLM/ NIHMS160379; NLM/ PMC2804877
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80. Cvetković RS, Perry CM: Spotlight on rituximab in non-Hodgkin lymphoma and chronic lymphocytic leukemia. BioDrugs; 2006;20(4):253-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spotlight on rituximab in non-Hodgkin lymphoma and chronic lymphocytic leukemia.
  • In phase III trials in patients with indolent or aggressive B-cell non-Hodgkin lymphoma (NHL), intravenous rituximab in combination with chemotherapy was more effective as first- or second-line therapy than chemotherapy alone in terms of tumor remission and patient survival.
  • Likewise, in patients with chronic lymphocytic leukemia (CLL), rituximab in combination with chemotherapy appeared more effective than chemotherapy alone as either first- or second-line treatment.
  • In addition, rituximab maintenance therapy was shown to significantly prolong tumor remission and patient survival in patients with indolent B-cell NHL or CLL.
  • The combination of rituximab with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was cost effective as first-line therapy for advanced-stage diffuse large B-cell NHL compared with CHOP alone.
  • Rituximab, either alone or in combination with chemotherapy, was generally well tolerated in patients with NHL or CLL.
  • Overall, rituximab in combination with chemotherapy, is a valuable option for first- and second-line therapy in patients with advanced-stage indolent or aggressive B-cell NHL, and possibly those with B-cell CLL, and is included in current treatment guidelines for these indications.
  • The drug is also potentially useful as maintenance therapy in patients with indolent B-cell NHL or CLL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma, Non-Hodgkin / drug therapy

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  • (PMID = 16831024.001).
  • [ISSN] 1173-8804
  • [Journal-full-title] BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy
  • [ISO-abbreviation] BioDrugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 45
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81. McWhirter JR, Kretz-Rommel A, Saven A, Maruyama T, Potter KN, Mockridge CI, Ravey EP, Qin F, Bowdish KS: Antibodies selected from combinatorial libraries block a tumor antigen that plays a key role in immunomodulation. Proc Natl Acad Sci U S A; 2006 Jan 24;103(4):1041-6
The Lens. Cited by Patents in .

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  • We searched for cell-surface-associated proteins overexpressed on B cell chronic lymphocytic leukemia (CLL) to use as therapeutic antibody targets.
  • Antibodies binding the immunosuppressive molecule CD200 were identified by cell panning of an antibody phage display library derived from rabbits immunized with primary CLL cells.
  • B cells from 87 CLL patients exhibited 1.6- to 5.4-fold cell-surface up-regulation of CD200 relative to normal B cells.
  • An effect of increased CD200 expression by CLL cells on the immune system was evaluated in mixed lymphocyte reactions.
  • Addition of primary CLL but not normal B cells to macrophages and T cells downregulated the Th1 response, as seen by a 50-95% reduction in secreted IL-2 and IFN-gamma.
  • Antibodies to CD200 prevented downregulation of the Th1 response in most B cell CLL samples evaluated, indicating abrogation of the CD200/CD200R interaction can be sufficient to restore the Th1 response.
  • A disease-progression-associated shift of the immune response from Th1 to Th2 has been observed in numerous cancers.
  • Because this cytokine shift is also believed to promote the induction of regulatory T cells, reverting the immune response to Th1 through direct targeting of the cancer cells may provide therapeutic benefits in CLL by encouraging a cytotoxic T cell response.
  • [MeSH-major] Antibodies / chemistry. Antigens, Neoplasm. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Peptide Library
  • [MeSH-minor] Antibodies, Monoclonal / chemistry. B-Lymphocytes / metabolism. Cell Line. Cell Line, Tumor. Cell Membrane / metabolism. Cell Separation. Cytokines / metabolism. Dendritic Cells / cytology. Down-Regulation. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Humans. Immunoglobulin Fragments / chemistry. Immunoprecipitation. Immunosuppressive Agents / pharmacology. Immunotherapy / methods. Interleukin-2 / metabolism. Leukocytes, Mononuclear / metabolism. Lymphocyte Culture Test, Mixed. Lymphocytes / immunology. Macrophages / metabolism. Mass Spectrometry. Monocytes / metabolism. T-Lymphocytes, Regulatory / cytology. Th1 Cells. Th2 Cells / immunology

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  • [Cites] Clin Cancer Res. 2000 May;6(5):1671-7 [10815885.001]
  • [Cites] Blood. 2005 Sep 15;106(6):2018-25 [15914560.001]
  • [Cites] Prostate. 2000 Sep 1;44(4):271-4 [10951490.001]
  • [Cites] Science. 2000 Dec 1;290(5497):1768-71 [11099416.001]
  • [Cites] Blood. 2001 Jan 1;97(1):256-63 [11133769.001]
  • [Cites] Br J Haematol. 2001 Mar;112(3):760-7 [11260081.001]
  • [Cites] Immunology. 2001 Feb;102(2):173-9 [11260322.001]
  • [Cites] Eur J Immunol. 2001 Aug;31(8):2331-7 [11477545.001]
  • [Cites] Blood. 2001 Nov 15;98(10):2999-3005 [11698283.001]
  • [Cites] Clin Exp Immunol. 2001 Nov;126(2):220-9 [11703364.001]
  • [Cites] Clin Immunol. 2001 Dec;101(3):328-34 [11726225.001]
  • [Cites] Cancer Immunol Immunother. 2002 Jan;50(11):588-96 [11807622.001]
  • [Cites] CA Cancer J Clin. 2002 Jan-Feb;52(1):23-47 [11814064.001]
  • [Cites] Leuk Res. 2002 Jul;26(7):657-60 [12008083.001]
  • [Cites] Neoplasma. 2002;49(3):159-66 [12098001.001]
  • [Cites] J Am Chem Soc. 2002 Oct 23;124(42):12439-46 [12381184.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2002;:193-213 [12446424.001]
  • [Cites] Br J Biomed Sci. 2002;59(4):235-8 [12572960.001]
  • [Cites] Cancer Res. 2003 Aug 1;63(15):4497-506 [12907623.001]
  • [Cites] Biol Pharm Bull. 2003 Sep;26(9):1336-41 [12951482.001]
  • [Cites] Cancer Res. 2004 Jan 15;64(2):704-10 [14744788.001]
  • [Cites] Blood. 2004 Feb 15;103(4):1202-10 [14576043.001]
  • [Cites] Leuk Lymphoma. 2004 Feb;45(2):205-19 [15101704.001]
  • [Cites] Transplantation. 2004 Apr 27;77(8):1138-44 [15114074.001]
  • [Cites] Blood. 2004 Jun 15;103(12):4389-95 [14962897.001]
  • [Cites] Nat Med. 2004 Sep;10(9):942-9 [15322536.001]
  • [Cites] J Immunol. 2004 Sep 15;173(6):3748-54 [15356121.001]
  • [Cites] Cancer Res. 1994 Aug 15;54(16):4430-5 [7913876.001]
  • [Cites] Cancer Immunol Immunother. 1997 Jan;43(6):375-81 [9067410.001]
  • [Cites] J Immunol Methods. 1997 Aug 7;206(1-2):73-85 [9328570.001]
  • [Cites] Blood. 1999 Mar 15;93(6):1992-2002 [10068672.001]
  • [Cites] Clin Cancer Res. 1999 Apr;5(4):925-31 [10213230.001]
  • [Cites] Am J Surg. 1999 Mar;177(3):203-8 [10219855.001]
  • [Cites] J Immunol. 1999 Aug 1;163(3):1654-60 [10415071.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2004;:163-83 [15561682.001]
  • [Cites] Transplantation. 2005 Feb 27;79(4):488-91 [15729177.001]
  • [Cites] Leukemia. 2005 May;19(5):759-66 [15759034.001]
  • [Cites] J Virol. 2005 May;79(10):6052-67 [15857991.001]
  • [Cites] Nat Med. 2000 Jun;6(6):667-72 [10835683.001]
  • (PMID = 16418292.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies; 0 / Antibodies, Monoclonal; 0 / Antigens, Neoplasm; 0 / Cytokines; 0 / Immunoglobulin Fragments; 0 / Immunosuppressive Agents; 0 / Interleukin-2; 0 / Peptide Library
  • [Other-IDs] NLM/ PMC1327729
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82. Molica S, Vitelli G, Cutrona G, Todoerti K, Mirabelli R, Digiesi G, Morabito F, Neri A, Ferrarini M: Serum thrombopoietin compared with ZAP-70 and immunoglobulin heavy-chain gene mutation status as a predictor of time to first treatment in early chronic lymphocytic leukemia. Leuk Lymphoma; 2008 Jan;49(1):62-7
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  • [Title] Serum thrombopoietin compared with ZAP-70 and immunoglobulin heavy-chain gene mutation status as a predictor of time to first treatment in early chronic lymphocytic leukemia.
  • In an effort to confirm previous reports we analyzed clinico-biological implications of increased serum levels of thrombopoietin (TPO) in a series of 71 previously untreated Binet stage A B-cell chronic lymphocytic leukemia (CLL) patients.
  • The risk of disease-progression according to known and putative prognostic parameters was also evaluated as time to first treatment (TFT).
  • Looking for cellular source of TPO we investigated the presence of TPO at gene expression level in 60 B-CLL patients belonging to an independent series.
  • Here we provide evidence for the presence of a low TPO gene expression transcript in B-CLL cells.
  • In conclusion, our results indicate that in early B-cell CLL circulating level of TPO does not provide a useful insight into the complex interrelationship of prognostic variables.
  • [MeSH-major] Genes, Immunoglobulin Heavy Chain / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Predictive Value of Tests. Thrombopoietin / blood. ZAP-70 Protein-Tyrosine Kinase / blood

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  • (PMID = 18203013.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 9014-42-0 / Thrombopoietin; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human
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83. Borovecki A, Korac P, Ventura RA, Perisa MM, Banham AH, Dominis M: MALT1, BCL10 and FOXP1 in salivary gland mucosa-associated lymphoid tissue lymphomas. Pathol Int; 2007 Jan;57(1):47-51
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  • [Title] MALT1, BCL10 and FOXP1 in salivary gland mucosa-associated lymphoid tissue lymphomas.
  • In view of the certain anatomic site-dependent frequency of chromosomal translocations involved in extranodal marginal zone B cell lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma) pathogenesis, 17 salivary gland MALT lymphoma cases were analyzed for MALT1 and FOXP1 translocations.
  • B cell CLL/lymphoma 10 (BCL10) and forkhead box PA (FOXP1) protein expression were studied by immunohistochemistry and translocations identified using fluorescence in situ hybridization (FISH)-specific probes FOXP1, t(11;18)(q21;q21)/API2-MALT1 and t(14;18)(q32;q21)/IgH-MALT1.
  • MALT1 translocations were mostly mutually exclusive except in a single case.
  • A case with strong FOXP1 protein expression indicates the possibility that the upregulation of FOXP1 expression is significant in a small subset of salivary gland MALT lymphomas.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / metabolism. Caspases / metabolism. Forkhead Transcription Factors / metabolism. Lymphoma, B-Cell, Marginal Zone / metabolism. Neoplasm Proteins / metabolism. Repressor Proteins / metabolism. Salivary Gland Neoplasms / metabolism

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  • (PMID = 17199743.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / BCL10 protein, human; 0 / FOXP1 protein, human; 0 / Forkhead Transcription Factors; 0 / Neoplasm Proteins; 0 / Repressor Proteins; EC 3.4.22.- / Caspases; EC 3.4.22.- / MALT1 protein, human
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84. Weiss DJ, Evanson OA, de Souza C, Abrahamsen MS: A critical role of interleukin-10 in the response of bovine macrophages to infection by Mycobacterium avium subsp paratuberculosis. Am J Vet Res; 2005 Apr;66(4):721-6
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  • PROCEDURE: Monocyte-derived macrophages were incubated with M avium subsp paratuberculosis for 2, 6, 24, 72, or 96 hours with or without addition of saturating concentrations of a goat anti-human IL-10 that has been documented to neutralize bovine IL-10 activity.
  • Variables assessed included ingestion and killing of M avium subsp paratuberculosis; expression of tumor necrosis factor (TNF)-alpha, IL-12, IL-8, major histocompatability (MHC) class II, vacuolar H+ ATPase, and B cell CLL/lymphoma 2 (BCL-2); production of nitric oxide; acidification of phagosomes; and apoptosis of macrophages.
  • RESULTS: Neutralization of IL-10 enabled macrophages to kill 57% of M avium subsp paratuberculosis organisms within 96 hours.
  • CONCLUSIONS AND CLINICAL RELEVANCE: The capacity of M avium subsp paratuberculosis to induce IL-10 expression may be a major determinant of virulence for this organism.

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  • (PMID = 15900955.001).
  • [ISSN] 0002-9645
  • [Journal-full-title] American journal of veterinary research
  • [ISO-abbreviation] Am. J. Vet. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class II; 0 / Interleukin-8; 0 / Nitrites; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 187348-17-0 / Interleukin-12; 63231-63-0 / RNA; EC 3.6.3.14 / Proton-Translocating ATPases
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85. Li L, Godfrey WR, Porter SB, Ge Y, June CH, Blazar BR, Boussiotis VA: CD4+CD25+ regulatory T-cell lines from human cord blood have functional and molecular properties of T-cell anergy. Blood; 2005 Nov 1;106(9):3068-73
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] CD4+CD25+ regulatory T-cell lines from human cord blood have functional and molecular properties of T-cell anergy.
  • Here, we examined the signaling properties of human Tregs, using CD4+CD25+ Treg and CD4+CD25- control (Tcont) cell lines generated from cord blood.
  • Treg cell lines were markedly hyporesponsive to stimulation with dendritic cells and with anti-CD3/CD28-coated beads.
  • T-cell receptor (TCR)-CD3/CD28-mediated activation of Rap1 and Akt was retained in Tregs, but activation of Ras, mitogenactivated protein kinase 1/2 (MEK1/2), and extracellular signal-regulated kinase 1/2 (Erk1/2) was impaired.
  • Tregs were blocked from cell cycle progression due to decrease of cyclin E and cyclin A and increase of p27kip1 (p27kip cyclin dependent kinase inhibitor).
  • Tregs had high susceptibility to apoptosis that was reversed by IL-2, which correlated with activation of Erk1/2, up-regulation of Bcl-x(L) (B-cell CLL/lymphoma 2-like nuclear gene encoding mitochondrial protein, transcript variant 2), and phosphorylation of Bad (Bcl2 antagonist of cell death) at Ser112.


91. Chanan-Khan A, Miller KC, Musial L, Lawrence D, Padmanabhan S, Takeshita K, Porter CW, Goodrich DW, Bernstein ZP, Wallace P, Spaner D, Mohr A, Byrne C, Hernandez-Ilizaliturri F, Chrystal C, Starostik P, Czuczman MS: Clinical efficacy of lenalidomide in patients with relapsed or refractory chronic lymphocytic leukemia: results of a phase II study. J Clin Oncol; 2006 Dec 1;24(34):5343-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical efficacy of lenalidomide in patients with relapsed or refractory chronic lymphocytic leukemia: results of a phase II study.
  • PURPOSE: Patients with relapsed or refractory chronic lymphocytic leukemia (CLL) have profound immune defects and limited treatment options.
  • Given the dramatic activity of lenalidomide in other B-cell malignancies and its pleotropic immunomodulatory effects, we conducted a phase II trial of this agent in CLL.
  • PATIENTS AND METHODS: Patients with relapsed or refractory B-cell CLL (B-CLL) were eligible if they required treatment as per the National Cancer Institute Working Group 1996 guidelines.
  • Lenalidomide was administered orally at 25 mg on days 1 through 21 of a 28-day cycle.
  • Patients were to continue treatment until disease progression, unacceptable toxicity, or complete remission.
  • Rituximab was added to lenalidomide on disease progression.
  • Sixty-four percent of the patients had Rai stage III or IV disease, and 51% were refractory to fludarabine.
  • CONCLUSION: Lenalidomide is clinically active in patients with relapsed or refractory B-CLL.
  • These findings are encouraging and warrant further investigation of this agent in the treatment of this disorder.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Immunologic Factors / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Thalidomide / analogs & derivatives


92. Robak T: Ofatumumab, a human monoclonal antibody for lymphoid malignancies and autoimmune disorders. Curr Opin Mol Ther; 2008 Jun;10(3):294-309
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

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  • [Title] Ofatumumab, a human monoclonal antibody for lymphoid malignancies and autoimmune disorders.
  • Genmab A/S and licensee GlaxoSmithKline plc are developing ofatumumab, an anti-CD20 human mAb, for the potential intravenous treatment of non-Hodgkin's lymphoma and autoimmune diseases, such as rheumatoid arthritis (RA) and multiple sclerosis (MS).
  • Phase I and II clinical trials have been completed in patients with chronic lymphocytic leukemia (CLL), rituximab-refractory follicular lymphoma (FL) and RA.
  • At the time of publication ofatumumab was undergoing a phase II clinical trial in patients with diffuse large B-cell lymphoma and phase III clinical trials in patients with B-cell CLL (B-CLL) in which fludarabine and alemtuzumab treatments have failed and in patients with rituximab-refractory FL.
  • Ofatumumab was also undergoing phase II clinical trials as a combination therapy for previously untreated patients with FL in combination with cyclophosphamide, adriamycin, vincristine, and prednisone and in combination with fludarabine and cyclophosphamide for the treatment of B-CLL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Autoimmune Diseases / drug therapy. Lymphatic Diseases / drug therapy

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  • (PMID = 18535937.001).
  • [ISSN] 1464-8431
  • [Journal-full-title] Current opinion in molecular therapeutics
  • [ISO-abbreviation] Curr. Opin. Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / ofatumumab
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93. Nakajima Y, Tsuge I, Kondo Y, Komatsubara R, Hirata N, Kakami M, Kato M, Kurahashi H, Urisu A, Asano Y: Up-regulated cytokine-inducible SH2-containing protein expression in allergen-stimulated T cells from hen's egg-allergic patients. Clin Exp Allergy; 2008 Sep;38(9):1499-506

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Among these, up-regulation of three genes, cytokine -inducible SH2-containing protein (CISH), nuclear factor of kappa light polypeptide gene enhancer in B-cell inhibitor Z (NFKBIZ) and B-cell CLL/lymphoma 2 (BCL2), was confirmed by real-time quantitative RT-PCR.
  • CISH, but not NFKBIZ or BCL2, showed a significantly higher ratio of antigen-stimulated cell transcription over unstimulated cells in HE-allergic than in non-HE-allergic children (P<0.01).
  • Flow-cytometric analysis revealed that the percentage of CD25(+)CISH(+) cells in CD4(+) cells from patients with HE allergy was significantly higher than that in controls (P<0.01).
  • [MeSH-major] Allergens / immunology. CD4-Positive T-Lymphocytes / metabolism. Egg Hypersensitivity / metabolism. Suppressor of Cytokine Signaling Proteins / metabolism. src Homology Domains

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  • (PMID = 18647318.001).
  • [ISSN] 1365-2222
  • [Journal-full-title] Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
  • [ISO-abbreviation] Clin. Exp. Allergy
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Allergens; 0 / I-kappa B Proteins; 0 / NFKBIZ protein, human; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Suppressor of Cytokine Signaling Proteins; 0 / cytokine inducible SH2-containing protein
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94. Thomadaki H, Scorilas A: BCL2 family of apoptosis-related genes: functions and clinical implications in cancer. Crit Rev Clin Lab Sci; 2006;43(1):1-67
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  • One of the most effective ways to combat different types of cancer is through early diagnosis and administration of effective treatment, followed by efficient monitoring that will allow physicians to detect relapsing disease and treat it at the earliest possible time.
  • Apoptosis, a normal physiological form of cell death, is critically involved in the regulation of cellular homeostasis.
  • Dysregulation of programmed cell death mechanisms plays an important role in the pathogenesis and progression of cancer as well as in the responses of tumours to therapeutic interventions.
  • Many members of the BCL2 (B-cell CLL/lymphoma 2; Bcl-2) family of apoptosis-related genes have been found to be differentially expressed in various malignancies, and some are useful prognostic cancer biomarkers.
  • Results have made it clear that a number of coordinating alterations in the BCL2 family of genes must occur to inhibit apoptosis and provoke carcinogenesis in a wide variety of cancers.
  • However, more research is required to increase our understanding of the extent to which and the mechanisms by which they are involved in cancer development, providing the basis for earlier and more accurate cancer diagnosis, prognosis and therapeutic intervention that targets the apoptosis pathways.
  • In the present review, we describe current knowledge of the function and molecular characteristics of a series of classic but also newly discovered genes of the BCL2 family as well as their implications in cancer development, prognosis and treatment.

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  • (PMID = 16531274.001).
  • [ISSN] 1040-8363
  • [Journal-full-title] Critical reviews in clinical laboratory sciences
  • [ISO-abbreviation] Crit Rev Clin Lab Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2
  • [Number-of-references] 484
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95. Bhattacharyya S, Gill R, Chen ML, Zhang F, Linhardt RJ, Dudeja PK, Tobacman JK: Toll-like receptor 4 mediates induction of the Bcl10-NFkappaB-interleukin-8 inflammatory pathway by carrageenan in human intestinal epithelial cells. J Biol Chem; 2008 Apr 18;283(16):10550-8
Hazardous Substances Data Bank. CARRAGEENAN GUM .

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  • The sulfated polysaccharide carrageenan (CGN) induces activation of NFkappaB and interleukin 8 (IL-8) in human colonic epithelial cells through a pathway of innate immunity mediated by Bcl10 (B-cell CLL/lymphoma 10).
  • Additional experiments with TLR4 blocking antibody and TLR4 small interfering RNAs showed 80% reductions in CGN-induced increases in Bcl10 and IL-8.

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  • [Cites] J Exp Med. 2003 Oct 20;198(8):1225-35 [14568981.001]
  • [Cites] Hepatology. 2003 May;37(5):1043-55 [12717385.001]
  • [Cites] J Biol Chem. 2004 Jan 23;279(4):2712-8 [14600154.001]
  • [Cites] Front Biosci. 1997 Apr 1;2:e1-11 [9159186.001]
  • [Cites] Anal Biochem. 1983 Apr 15;130(2):287-94 [6869815.001]
  • [Cites] In Vitro Cell Dev Biol Anim. 1996 Jun;32(6):315-7 [8842743.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Dec 23;94(26):14677-82 [9405672.001]
  • [Cites] Science. 1998 Dec 11;282(5396):2085-8 [9851930.001]
  • [Cites] Nat Genet. 1999 May;22(1):63-8 [10319863.001]
  • [Cites] J Biol Chem. 1999 Jun 18;274(25):17406-9 [10364168.001]
  • [Cites] Infect Immun. 2005 May;73(5):2940-50 [15845500.001]
  • [Cites] Shock. 2005 Sep;24(3):206-9 [16135957.001]
  • [Cites] Immunol Cell Biol. 2005 Dec;83(6):674-86 [16266320.001]
  • [Cites] Surg Today. 2006;36(3):287-90 [16493544.001]
  • [Cites] Bioorg Med Chem Lett. 2006 Jun 1;16(11):2842-5 [16563752.001]
  • [Cites] Liver Int. 2006 May;26(4):467-76 [16629651.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Aug 4;346(3):739-45 [16781673.001]
  • [Cites] J Biol Chem. 2006 Sep 8;281(36):26029-40 [16831874.001]
  • [Cites] J Clin Invest. 2006 Nov;116(11):3015-25 [17053832.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jan 2;104(1):134-8 [17095601.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2007 Mar;292(3):G829-38 [17095757.001]
  • [Cites] J Biol Chem. 2007 Jun 22;282(25):18265-75 [17400552.001]
  • [Cites] J Immunoassay Immunochem. 2007;28(3):173-88 [17613665.001]
  • [Cites] Diabetes. 2007 Aug;56(8):1986-98 [17519423.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2007 Aug;293(2):G429-37 [17540779.001]
  • [Cites] J Immunol. 2007 Oct 1;179(7):4808-20 [17878380.001]
  • [Cites] J Surg Res. 2001 Sep;100(1):127-34 [11516215.001]
  • [Cites] J Exp Med. 2002 Jan 7;195(1):99-111 [11781369.001]
  • [Cites] Am J Pathol. 2002 Jan;160(1):165-73 [11786410.001]
  • [Cites] J Exp Med. 2002 Mar 4;195(5):559-70 [11877479.001]
  • [Cites] J Biol Chem. 2002 Jun 7;277(23):20431-7 [11923281.001]
  • [Cites] Eur J Immunol. 2002 Jul;32(7):1958-68 [12115616.001]
  • [Cites] Infect Immun. 2002 Sep;70(9):4892-6 [12183533.001]
  • [Cites] Int J Colorectal Dis. 2003 Jan;18(1):25-32 [12458377.001]
  • [Cites] Curr Pharm Des. 2003;9(1):1-5 [12570669.001]
  • [Cites] Clin Exp Allergy. 2003 Feb;33(2):249-58 [12580919.001]
  • [Cites] J Clin Invest. 2000 Feb;105(3):301-10 [10675356.001]
  • [Cites] Nat Genet. 2000 Jun;25(2):187-91 [10835634.001]
  • [Cites] Biochemistry. 2000 Oct 3;39(39):11837-44 [11009595.001]
  • [Cites] Nature. 2001 May 31;411(6837):599-603 [11385576.001]
  • [Cites] Nature. 2001 May 31;411(6837):603-6 [11385577.001]
  • [Cites] J Pediatr Gastroenterol Nutr. 2001 Apr;32(4):449-53 [11396812.001]
  • [Cites] J Immunol. 2001 Aug 1;167(3):1609-16 [11466383.001]
  • [Cites] Nature. 2004 Jan 8;427(6970):167-71 [14695475.001]
  • (PMID = 18252714.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / P01 DK067887; United States / NHLBI NIH HHS / HL / R01 HL062244-05A1; United States / NIDDK NIH HHS / DK / R01 DK054016; United States / NHLBI NIH HHS / HL / R01 HL052622; United States / NHLBI NIH HHS / HL / R01 HL062244; United States / NHLBI NIH HHS / HL / HL052622-05; United States / NHLBI NIH HHS / HL / HL062244-05A1; United States / NIGMS NIH HHS / GM / GM038060-19; United States / NIGMS NIH HHS / GM / R01 GM038060; United States / NHLBI NIH HHS / HL / R01 HL052622-05; United States / NIDDK NIH HHS / DK / R01 DK068324; United States / NIGMS NIH HHS / GM / R01 GM038060-19; United States / NIDDK NIH HHS / DK / DK68324; United States / NIDDK NIH HHS / DK / DK54016
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / BCL10 protein, human; 0 / Interleukin-8; 0 / NF-kappa B; 0 / Toll-Like Receptor 4; 9000-07-1 / Carrageenan
  • [Other-IDs] NLM/ PMC2447641
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96. Satoh J, Nakanishi M, Koike F, Miyake S, Yamamoto T, Kawai M, Kikuchi S, Nomura K, Yokoyama K, Ota K, Kanda T, Fukazawa T, Yamamura T: Microarray analysis identifies an aberrant expression of apoptosis and DNA damage-regulatory genes in multiple sclerosis. Neurobiol Dis; 2005 Apr;18(3):537-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To clarify the molecular mechanisms underlying multiple sclerosis (MS)-promoting autoimmune process, we have investigated a comprehensive gene expression profile of T cell and non-T cell fractions of peripheral blood mononuclear cells (PBMC) isolated from 72 MS patients and 22 age- and sex-matched healthy control (CN) subjects by using a cDNA microarray.
  • They included upregulation in MS of orphan nuclear receptor Nurr1 (NR4A2), receptor-interacting serine/threonine kinase 2 (RIPK2), and silencer of death domains (SODD), and downregulation in MS of TNF-related apoptosis-inducing ligand (TRAIL), B-cell CLL/lymphoma 2 (BCL2), and death-associated protein 6 (DAXX).
  • These results suggest that MS lymphocytes show a complex pattern of gene regulation that represents a counterbalance between promoting and preventing apoptosis and DNA damage of lymphocytes.

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  • (PMID = 15755681.001).
  • [ISSN] 0969-9961
  • [Journal-full-title] Neurobiology of disease
  • [ISO-abbreviation] Neurobiol. Dis.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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97. Yan M, Hardin K, Ho E: Differential response to zinc-induced apoptosis in benign prostate hyperplasia and prostate cancer cells. J Nutr Biochem; 2010 Aug;21(8):687-94
Hazardous Substances Data Bank. ZINC, ELEMENTAL .

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  • PC-3 and BPH-1 cells were treated with zinc (0-250 microM) for 24 and 48 h, and cell growth and viability were examined.
  • Apoptosis was assessed by phosphatidylserine externalization, caspase activation and protein expression of B-cell CLL/lymphoma 2 (Bcl-2)-associated X protein (BAX):Bcl-2.
  • Additionally, different effects on the nuclear expression and activity of the p65 subunit of nuclear factor kappa B were observed in response to zinc between the two cell types.
  • The differential response to zinc in PC-3 and BPH-1 cells suggests that zinc may serve an important role in regulating cell growth and apoptosis in prostate cancer and hyperplasia cells.

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  • [Copyright] Published by Elsevier Inc.
  • [Cites] JAMA. 1996 Dec 25;276(24):1957-63 [8971064.001]
  • [Cites] Cell. 1997 Feb 7;88(3):323-31 [9039259.001]
  • [Cites] Int Urol Nephrol. 1996;28(5):687-94 [9061429.001]
  • [Cites] J Biol Chem. 1997 Nov 14;272(46):28875-81 [9360955.001]
  • [Cites] Int Urol Nephrol. 1997;29(5):565-74 [9413764.001]
  • [Cites] Prostate. 1998 Jun 1;35(4):285-96 [9609552.001]
  • [Cites] Nutrition. 1998 Jun;14(6):489-95 [9646288.001]
  • [Cites] Br J Urol. 1998 Sep;82(3):380-5 [9772874.001]
  • [Cites] J Am Coll Nutr. 1998 Oct;17(5):409-18 [9791836.001]
  • [Cites] Cancer Res. 1999 Mar 15;59(6):1225-30 [10096552.001]
  • [Cites] Prostate. 1999 Aug 1;40(3):200-7 [10398282.001]
  • [Cites] J Natl Cancer Inst. 2005 Feb 16;97(4):301-6 [15713965.001]
  • [Cites] Mitochondrion. 2005 Jun;5(3):143-53 [16050980.001]
  • [Cites] Cancer Causes Control. 2005 Oct;16(8):901-15 [16132800.001]
  • [Cites] Mol Cancer. 2005;4:32 [16153295.001]
  • [Cites] Urology. 2006 Oct;68(4):905-10 [17070390.001]
  • [Cites] Am J Clin Nutr. 2007 Feb;85(2):523-9 [17284753.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1999 Oct;8(10):887-92 [10548317.001]
  • [Cites] Mol Urol. 2000 Spring;4(1):31-6 [10851304.001]
  • [Cites] Prostate Suppl. 2000;9:4-14 [11056496.001]
  • [Cites] Prostate Suppl. 2000;9:25-8 [11056499.001]
  • [Cites] Urology. 2000 Nov 1;56(5 Suppl 1):3-6 [11074195.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Dec 20;279(2):607-14 [11118333.001]
  • [Cites] Prostate. 2001 Apr1;47(1):36-51 [11304728.001]
  • [Cites] Prostate. 2001 May 15;47(3):183-8 [11351347.001]
  • [Cites] Eur J Clin Nutr. 2001 Apr;55(4):293-7 [11360134.001]
  • [Cites] Leukemia. 2001 Apr;15(4):515-22 [11368354.001]
  • [Cites] Am J Physiol Cell Physiol. 2001 Sep;281(3):C751-7 [11502552.001]
  • [Cites] J Natl Cancer Inst. 2002 Mar 6;94(5):391-8 [11880478.001]
  • [Cites] Am J Physiol Cell Physiol. 2002 Aug;283(2):C631-8 [12107073.001]
  • [Cites] Prostate. 2002 Sep 1;52(4):311-8 [12210492.001]
  • [Cites] Oncogene. 2003 Sep 4;22(38):6005-12 [12955079.001]
  • [Cites] Cancer Lett. 2003 Oct 28;200(2):187-95 [14568174.001]
  • [Cites] Science. 2004 Feb 13;303(5660):1010-4 [14963330.001]
  • [Cites] Ann N Y Acad Sci. 2003 Dec;1010:316-20 [15033742.001]
  • [Cites] J Immunol Methods. 1983 Dec 16;65(1-2):55-63 [6606682.001]
  • [Cites] Prostate. 1993;23(2):123-34 [8104329.001]
  • [Cites] Semin Cancer Biol. 1993 Dec;4(6):327-32 [8142617.001]
  • [Cites] Cancer Res. 1994 Jun 15;54(12):3131-5 [8205530.001]
  • [Cites] In Vitro Cell Dev Biol Anim. 1995 Jan;31(1):14-24 [7535634.001]
  • [Cites] J Natl Cancer Inst. 1995 Dec 6;87(23):1767-76 [7473833.001]
  • [Cites] Oncogene. 2007 Feb 26;26(9):1324-37 [17322918.001]
  • [Cites] Clin Cancer Res. 2007 Jun 15;13(12):3435-8 [17575204.001]
  • [Cites] Clin Cancer Res. 2007 Jun 15;13(12):3585-90 [17575222.001]
  • [Cites] Nat Rev Mol Cell Biol. 2008 Jan;9(1):47-59 [18097445.001]
  • [Cites] Am J Epidemiol. 2008 Apr 15;167(8):925-34 [18263602.001]
  • [Cites] Mol Cancer. 2008;7:25 [18331646.001]
  • [Cites] Int J Cancer. 1997 Jan 27;70(3):341-8 [9033638.001]
  • (PMID = 19576751.001).
  • [ISSN] 1873-4847
  • [Journal-full-title] The Journal of nutritional biochemistry
  • [ISO-abbreviation] J. Nutr. Biochem.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P30 ES000210; United States / NIEHS NIH HHS / ES / P30 ES00210
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; J41CSQ7QDS / Zinc
  • [Other-IDs] NLM/ NIHMS617416; NLM/ PMC4125128
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98. Yuan HD, Quan HY, Zhang Y, Kim SH, Chung SH: 20(S)-Ginsenoside Rg3-induced apoptosis in HT-29 colon cancer cells is associated with AMPK signaling pathway. Mol Med Rep; 2010 Sep-Oct;3(5):825-31
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  • 20(S)-Rg3 down-regulated the expression of anti-apoptotic protein B-cell CLL/lymphoma 2 (Bcl2), up-regulated the expression of pro-apoptotic protein of p53 and Bcl-2-associated X protein (Bax), and caused the release of mitochondrial cytochrome c, PARP, caspase-9 and caspase-3.
  • However, 20(S)-Rg3-induced apoptosis was completely abolished in the presence of compound C (AMPK inhibitor) or small interfering RNA for AMPK (siAMPK).

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  • (PMID = 21472321.001).
  • [ISSN] 1791-3004
  • [Journal-full-title] Molecular medicine reports
  • [ISO-abbreviation] Mol Med Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
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99. Bhattacharyya S, Dudeja PK, Tobacman JK: Lipopolysaccharide activates NF-kappaB by TLR4-Bcl10-dependent and independent pathways in colonic epithelial cells. Am J Physiol Gastrointest Liver Physiol; 2008 Oct;295(4):G784-90
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  • In colonic epithelium, one of the pathways of lipopolysaccharide (LPS) activation of NF-kappaB and IL-8 is via Toll-like receptor (TLR)4, MyD88, IRAK1/4, and B-cell CLL/lymphoma 10 (Bcl10).
  • [MeSH-minor] Aged. Animals. Cell Line. Chemokine CXCL1 / secretion. Cyclic N-Oxides / pharmacology. HSP27 Heat-Shock Proteins / metabolism. Humans. I-kappa B Proteins / metabolism. Interleukin-8 / secretion. Male. Mice. Mice, Inbred C57BL. Phosphorylation. RNA, Small Interfering / pharmacology. Reactive Oxygen Species / metabolism. Spin Labels

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  • (PMID = 18718996.001).
  • [ISSN] 0193-1857
  • [Journal-full-title] American journal of physiology. Gastrointestinal and liver physiology
  • [ISO-abbreviation] Am. J. Physiol. Gastrointest. Liver Physiol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / BCL10 protein, human; 0 / Chemokine CXCL1; 0 / Cxcl1 protein, mouse; 0 / Cyclic N-Oxides; 0 / HSP27 Heat-Shock Proteins; 0 / HSPB1 protein, human; 0 / I-kappa B Proteins; 0 / Interleukin-8; 0 / Lipopolysaccharides; 0 / NF-kappa B; 0 / RNA, Small Interfering; 0 / Reactive Oxygen Species; 0 / Spin Labels; 0 / TLR4 protein, human; 0 / Toll-Like Receptor 4; U78ZX2F65X / tempol
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100. Burbach BJ, Srivastava R, Medeiros RB, O'Gorman WE, Peterson EJ, Shimizu Y: Distinct regulation of integrin-dependent T cell conjugate formation and NF-kappa B activation by the adapter protein ADAP. J Immunol; 2008 Oct 1;181(7):4840-51
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] Distinct regulation of integrin-dependent T cell conjugate formation and NF-kappa B activation by the adapter protein ADAP.
  • Naive DO11.10/ADAP(-/-) T cells show impaired adhesion to OVAp (OVA aa 323-339)-bearing APCs that is restored following reconstitution with wild-type ADAP.
  • Additionally, the ADAP proline-rich domain is required for optimal Ag-induced activation of CD69, CD25, and Bcl-x(L), but is not required for assembly of the CARMA1/Bcl10/Malt1 (caspase-recruitment domain (CARD) membrane-associated guanylate kinase (MAGUK) protein 1/B-cell CLL-lymphoma 10/mucosa-associated lymphoid tissue lymphoma translocation protein 1) signaling complex and subsequent TCR-dependent NF-kappaB activity.

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  • [Cites] J Immunol. 1999 Dec 1;163(11):5753-7 [10570256.001]
  • [Cites] Immunol Rev. 2007 Aug;218:82-91 [17624945.001]
  • [Cites] J Cell Biol. 2000 Apr 3;149(1):181-94 [10747096.001]
  • [Cites] EMBO J. 2000 Jun 15;19(12):2889-99 [10856234.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Dec 5;97(25):13784-9 [11095726.001]
  • [Cites] Nature. 2001 Jun 28;411(6841):1065-8 [11429608.001]
  • [Cites] Science. 2001 Sep 21;293(5538):2260-3 [11567140.001]
  • [Cites] Science. 2001 Sep 21;293(5538):2263-5 [11567141.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11527-32 [11553777.001]
  • [Cites] J Cell Sci. 2001 Dec;114(Pt 23):4307-18 [11739662.001]
  • [Cites] Mol Cell Biol. 2002 Feb;22(4):1001-15 [11809793.001]
  • [Cites] Annu Rev Immunol. 2002;20:371-94 [11861607.001]
  • [Cites] Immunol Res. 2002;26(1-3):131-41 [12403352.001]
  • [Cites] Nat Immunol. 2003 Feb;4(2):110-6 [12555096.001]
  • [Cites] Nat Immunol. 2003 Apr;4(4):366-74 [12652296.001]
  • [Cites] Immunol Rev. 2003 Apr;192:113-21 [12670399.001]
  • [Cites] Nat Immunol. 2003 Aug;4(8):741-8 [12845325.001]
  • [Cites] BMC Immunol. 2002 May 2;3:4 [12019030.001]
  • [Cites] Bioessays. 2004 Jan;26(1):61-7 [14696041.001]
  • [Cites] J Cell Biol. 2004 Feb 2;164(3):461-70 [14757755.001]
  • [Cites] Curr Opin Immunol. 2004 Jun;16(3):304-13 [15134779.001]
  • [Cites] Immunol Lett. 2004 Apr 30;93(1):1-5 [15134891.001]
  • [Cites] Dev Cell. 2004 Oct;7(4):585-95 [15469846.001]
  • [Cites] J Exp Med. 2004 Oct 18;200(8):1063-74 [15477347.001]
  • [Cites] Science. 1990 Dec 21;250(4988):1720-3 [2125367.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Feb 20;93(4):1540-4 [8643668.001]
  • [Cites] J Biol Chem. 1997 May 2;272(18):11674-7 [9115214.001]
  • [Cites] J Biol Chem. 1997 Jun 27;272(26):16077-80 [9195899.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7493-8 [9207119.001]
  • [Cites] Transplantation. 2007 Aug 15;84(3):400-6 [17700167.001]
  • [Cites] J Immunol. 2007 Sep 15;179(6):3559-69 [17785790.001]
  • [Cites] Mol Immunol. 2008 Jan;45(2):510-22 [17658605.001]
  • [Cites] Mol Cell Biol. 2007 Oct;27(19):6863-75 [17646386.001]
  • [Cites] Eur J Immunol. 2007 Oct;37(10):2961-72 [17823979.001]
  • [Cites] Eur J Immunol. 2007 Nov;37(11):3208-19 [17948263.001]
  • [Cites] Science. 1998 Jul 17;281(5375):416-9 [9665885.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 21;95(15):8779-84 [9671755.001]
  • [Cites] Cell. 1998 Jul 24;94(2):229-38 [9695951.001]
  • [Cites] J Biol Chem. 1998 Oct 2;273(40):25789-95 [9748251.001]
  • [Cites] Immunity. 1999 Mar;10(3):323-32 [10204488.001]
  • [Cites] J Biol Chem. 1999 Jul 23;274(30):21170-9 [10409671.001]
  • [Cites] J Mol Biol. 2005 May 13;348(4):1025-35 [15843031.001]
  • [Cites] FEBS Lett. 2005 Apr 25;579(11):2339-47 [15848169.001]
  • [Cites] J Exp Med. 2005 Jun 6;201(11):1733-9 [15939789.001]
  • [Cites] J Biol Chem. 2005 Jun 24;280(25):23576-83 [15849195.001]
  • [Cites] Immunity. 2005 Aug;23(2):213-26 [16111639.001]
  • [Cites] Mol Cell Biol. 2005 Sep;25(18):8052-63 [16135797.001]
  • [Cites] J Immunol Methods. 2006 Apr 20;311(1-2):117-29 [16563425.001]
  • [Cites] Methods Enzymol. 1997;283:205-19 [9251021.001]
  • [Cites] J Biol Chem. 2006 May 12;281(19):13743-50 [16461356.001]
  • [Cites] J Immunol. 2006 Jun 1;176(11):6681-9 [16709827.001]
  • [Cites] FEBS Lett. 2006 May 22;580(12):455-63 [16783873.001]
  • [Cites] Int Immunol. 2006 Aug;18(8):1305-14 [16775024.001]
  • [Cites] J Mol Biol. 2006 Aug 4;361(1):94-104 [16831444.001]
  • [Cites] Mol Cell Biol. 2006 Oct;26(19):7130-44 [16980616.001]
  • [Cites] Science. 2007 May 4;316(5825):754-8 [17478723.001]
  • [Cites] Mol Cell Biol. 2007 Jun;27(11):4070-81 [17403904.001]
  • [Cites] Biochemistry. 2007 Jun 12;46(23):6971-7 [17511475.001]
  • [Cites] Immunol Rev. 2007 Aug;218:65-81 [17624944.001]
  • [Cites] J Biol Chem. 2000 Feb 18;275(7):5143-52 [10671560.001]
  • (PMID = 18802088.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI056016; United States / NIAID NIH HHS / AI / R01AI031126; United States / NIAID NIH HHS / AI / AI031126-19; United States / NIAID NIH HHS / AI / R01 AI031126-19; United States / NIDCR NIH HHS / DE / T32 DE007288; United States / NIAID NIH HHS / AI / R01AI038474; United States / NIAID NIH HHS / AI / AI056016-05; United States / NIDCR NIH HHS / DE / T32DE007288; United States / NIAID NIH HHS / AI / R01 AI031126; United States / NIAID NIH HHS / AI / AI038474-14; United States / NIAID NIH HHS / AI / R01 AI056016-05; United States / NIAID NIH HHS / AI / R01 AI038474; United States / NIAID NIH HHS / AI / R01AI056016; United States / NIAID NIH HHS / AI / R01 AI038474-14
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Fyb protein, mouse; 0 / Integrins; 0 / Membrane Proteins; 0 / NF-kappa B; 0 / OVA 323-339; 0 / Peptide Fragments; 0 / Phosphoproteins; 0 / Receptors, Virus; 0 / SKAP55 protein, mouse; 0 / adenovirus receptor; 9006-59-1 / Ovalbumin
  • [Other-IDs] NLM/ NIHMS64388; NLM/ PMC2593878
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