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31. Grillo-López AJ: 90Y-ibritumomab tiuxetan: rationale for patient selection in the treatment of indolent non-Hodgkin's lymphoma. Semin Oncol; 2005 Feb;32(1 Suppl 1):S44-9
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  • [Title] 90Y-ibritumomab tiuxetan: rationale for patient selection in the treatment of indolent non-Hodgkin's lymphoma.
  • Radioimmunotherapy with 90Y-ibritumomab tiuxetan (Zevalin; Biogen Idec Inc, San Diego, CA, and Schering AG, Berlin, Germany) was approved in the United States in 2002 for patients with relapsed or refractory, low-grade, follicular, or transformed B-cell non-Hodgkin's lymphoma, including patients with rituximab-refractory disease, and in Europe in 2003.
  • This agent has yielded good results in the treatment of patients with relapsed or refractory non-Hodgkin's lymphoma, for whom limited treatment options are available.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Lymphoma, Non-Hodgkin / radiotherapy. Radioimmunotherapy. Radiopharmaceuticals / therapeutic use

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  • (PMID = 15786025.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD20; 0 / Radiopharmaceuticals; 0 / Yttrium Radioisotopes; 0 / ibritumomab tiuxetan
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32. Eissing T, Waldherr S, Allgöwer F, Scheurich P, Bullinger E: Response to bistability in apoptosis: roles of bax, bcl-2, and mitochondrial permeability transition pores. Biophys J; 2007 May 1;92(9):3332-4
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  • [Title] Response to bistability in apoptosis: roles of bax, bcl-2, and mitochondrial permeability transition pores.
  • [MeSH-major] Apoptosis / physiology. Cell Membrane Permeability / physiology. Ion Channels / metabolism. Mitochondria / physiology. Mitochondrial Membrane Transport Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. bcl-2-Associated X Protein / metabolism
  • [MeSH-minor] Animals. Cell Survival. Computer Simulation. Humans. Models, Biological

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  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13210-5 [15340155.001]
  • [Cites] J Biol Chem. 2004 Aug 27;279(35):36892-7 [15208304.001]
  • [Cites] Cell. 2004 Sep 17;118(6):675-85 [15369668.001]
  • [Cites] Clin Cancer Res. 2004 Oct 15;10(20):6807-20 [15501957.001]
  • [Cites] Nature. 1997 Jul 17;388(6639):300-4 [9230442.001]
  • [Cites] J Biol Chem. 1998 Oct 16;273(42):27084-90 [9765224.001]
  • [Cites] FEBS J. 2005 Aug;272(16):4071-9 [16098190.001]
  • [Cites] Biophys J. 2006 Mar 1;90(5):1546-59 [16339882.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jun 6;103(23):8697-702 [16735474.001]
  • [Cites] Cell Death Differ. 2006 Aug;13(8):1310-7 [16691212.001]
  • [Cites] Syst Biol (Stevenage). 2005 Dec;152(4):221-8 [16986264.001]
  • [Cites] EMBO J. 2006 Sep 20;25(18):4338-49 [16932741.001]
  • [Cites] Syst Biol (Stevenage). 2005 Mar;2(1):35-41 [17091581.001]
  • [Cites] PLoS Comput Biol. 2006 Sep 15;2(9):e120 [16978046.001]
  • [Cites] Biosystems. 2007 Nov-Dec;90(3):591-601 [17314003.001]
  • [Cites] Cell Death Differ. 1999 Nov;6(11):1054-9 [10578173.001]
  • [Cites] Cell Death Differ. 1999 Nov;6(11):1081-6 [10578177.001]
  • [Cites] J Biol Chem. 2002 Mar 29;277(13):11345-51 [11801595.001]
  • [Cites] BMC Bioinformatics. 2002 Dec 13;3:38 [12482327.001]
  • [Cites] Cell. 2004 Jan 23;116(2):205-19 [14744432.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 17;101(7):1822-7 [14766974.001]
  • [CommentOn] Biophys J. 2006 Mar 1;90(5):1546-59 [16339882.001]
  • (PMID = 17277182.001).
  • [ISSN] 0006-3495
  • [Journal-full-title] Biophysical journal
  • [ISO-abbreviation] Biophys. J.
  • [Language] eng
  • [Publication-type] Comment; Editorial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ion Channels; 0 / Mitochondrial Membrane Transport Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 0 / mitochondrial permeability transition pore
  • [Other-IDs] NLM/ PMC1852357
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33. Ke B, Shen XD, Gao F, Qiao B, Ji H, Busuttil RW, Volk HD, Kupiec-Weglinski JW: Small interfering RNA targeting heme oxygenase-1 (HO-1) reinforces liver apoptosis induced by ischemia-reperfusion injury in mice: HO-1 is necessary for cytoprotection. Hum Gene Ther; 2009 Oct;20(10):1133-42
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  • Administration of HO-1 siRNA significantly increased local neutrophil accumulation and the frequency of apoptotic cells.
  • Mice treated with HO-1 siRNA were characterized by increased caspase-3 activity and reduced HO-1 expression, whereas those given Ad-HO-1 showed decreased caspase-3 activity and increased HO-1/Bcl-2/Bcl-x(L), data confirmed by use of an in vitro cell culture system.

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  • [Cites] J Immunol. 2000 Jun 1;164(11):5739-45 [10820251.001]
  • [Cites] J Exp Med. 2000 Oct 2;192(7):1015-26 [11015442.001]
  • [Cites] Toxicol Sci. 2000 Nov;58(1):109-17 [11053547.001]
  • [Cites] Hepatology. 2001 Feb;33(2):397-405 [11172341.001]
  • [Cites] Cell. 2001 Mar 23;104(6):805-8 [11290317.001]
  • [Cites] Transplantation. 2002 Jan 27;73(2):287-92 [11821745.001]
  • [Cites] Hum Gene Ther. 2002 Jul 1;13(10):1189-99 [12133272.001]
  • [Cites] Transplantation. 2002 Jul 15;74(1):96-102 [12134106.001]
  • [Cites] Transplantation. 2002 Oct 15;74(7):905-12 [12394829.001]
  • [Cites] FEBS Lett. 2002 Dec 4;532(1-2):227-30 [12459495.001]
  • [Cites] Nat Genet. 2003 Mar;33(3):401-6 [12590264.001]
  • [Cites] Nat Med. 2003 Mar;9(3):347-51 [12579197.001]
  • [Cites] J Gastroenterol Hepatol. 2003 Aug;18(8):891-902 [12859717.001]
  • [Cites] Trends Immunol. 2003 Aug;24(8):449-55 [12909459.001]
  • [Cites] Am J Transplant. 2003 Sep;3(9):1076-82 [12919086.001]
  • [Cites] Gastroenterology. 2003 Oct;125(4):1246-57 [14517806.001]
  • [Cites] Nat Biotechnol. 2004 Mar;22(3):326-30 [14758366.001]
  • [Cites] J Biol Chem. 2004 Mar 12;279(11):10677-84 [14688267.001]
  • [Cites] Surgery. 2004 Aug;136(2):390-400 [15300206.001]
  • [Cites] Virology. 1973 Apr;52(2):456-67 [4705382.001]
  • [Cites] J Pharmacol Methods. 1985 Nov;14(3):157-67 [2997548.001]
  • [Cites] Proc Natl Acad Sci U S A. 1985 Dec;82(23):7865-9 [3865203.001]
  • [Cites] Transplantation. 1993 Jun;55(6):1265-72 [7685932.001]
  • [Cites] J Exp Med. 1996 Oct 1;184(4):1331-41 [8879205.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 1997;37:517-54 [9131263.001]
  • [Cites] EMBO J. 1997 Aug 1;16(15):4639-49 [9303308.001]
  • [Cites] Biochem J. 1997 Aug 15;326 ( Pt 1):1-16 [9337844.001]
  • [Cites] Hepatology. 1998 Jun;27(6):1652-60 [9620339.001]
  • [Cites] Nat Med. 1998 Sep;4(9):1073-7 [9734404.001]
  • [Cites] Nat Med. 1998 Dec;4(12):1392-6 [9846576.001]
  • [Cites] Oncogene. 1998 Dec 31;17(26):3401-15 [10030664.001]
  • [Cites] Transplant Proc. 1999 Feb-Mar;31(1-2):1012-5 [10083450.001]
  • [Cites] Nature. 2004 Nov 11;432(7014):173-8 [15538359.001]
  • [Cites] J Immunol. 2004 Dec 15;173(12):7115-9 [15585830.001]
  • [Cites] Biochem J. 2005 Jan 15;385(Pt 2):537-44 [15554901.001]
  • [Cites] Transplantation. 2005 Jan 27;79(2):240-3 [15665774.001]
  • [Cites] Gene Ther. 2005 Jun;12(12):965-73 [15729369.001]
  • [Cites] Clin Chim Acta. 2006 Mar;365(1-2):270-8 [16242122.001]
  • [Cites] Exp Mol Pathol. 2006 Aug;81(1):48-54 [16443218.001]
  • [Cites] J Gene Med. 2006 Jul;8(7):889-900 [16652398.001]
  • [Cites] Am J Transplant. 2006 Sep;6(9):2099-108 [16796725.001]
  • [Cites] Cardiovasc Res. 2007 Oct 1;76(1):132-40 [17601517.001]
  • [Cites] Liver Transpl. 2007 Oct;13(10):1435-43 [17902130.001]
  • [Cites] J Clin Invest. 1999 Dec;104(11):1631-9 [10587527.001]
  • [Cites] Mol Med. 2008 May-Jun;14(5-6):337-45 [18292799.001]
  • [Cites] Apoptosis. 2008 Aug;13(8):1013-21 [18561025.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2008 Aug;295(2):H801-6 [18567706.001]
  • (PMID = 19534599.001).
  • [ISSN] 1557-7422
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI23847; United States / NIAID NIH HHS / AI / AI42223; United States / NIDDK NIH HHS / DK / R01 DK062357
  • [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 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / bcl-X Protein; EC 1.14.99.3 / Heme Oxygenase-1; EC 2.6.1.1 / Aspartate Aminotransferases; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ PMC2829285
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4. Li YC, Lin HJ, Yang JH, Yang JS, Ho HC, Chang SJ, Hsai TC, Lu HF, Huang AC, Chung JG: Baicalein-induced apoptosis via endoplasmic reticulum stress through elevations of reactive oxygen species and mitochondria dependent pathway in mouse-rat hybrid retina ganglion cells (N18). Neurochem Res; 2009 Mar;34(3):418-29
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  • [Title] Baicalein-induced apoptosis via endoplasmic reticulum stress through elevations of reactive oxygen species and mitochondria dependent pathway in mouse-rat hybrid retina ganglion cells (N18).
  • Studies were designed to investigate the effects of baicalein on mouse-rat hybrid retina ganglion cells (N18) to better understand its effect on apoptosis and apoptosis-related genes in vitro.
  • Cell viability, reactive oxygen species (ROS), cytoplasmic Ca2+, mitochondrial membrane potential (MMP), apoptosis induction, and caspases-3 activity were examined by flow cytometric assay.
  • Apoptosis-associated proteins such as p53, Bax, Bcl-2, cytochrome c, and caspase-3 were examined by Western blot.
  • We demonstrated the increase in the levels of p53, Bax, and cytochrome c and decrease in the level of Bcl-2, which are associated with the induction of apoptotic cell death after 24 h treatment with baicalein in N18 cells.
  • We also demonstrated a release of the cytochrome c from mitochondria into cytosol and an activation of caspase-3, which led to the occurrence of apoptosis in N18 cells treated with baicalein by Western blot.
  • Pretreatment was conducted with BAPTA (intracellular calcium chelator) in baicalein-treated cells, the decline of MMP was recovered, and the increase in the level of cytoplasmic Ca2+ was suppressed, and the proportion of apoptosis was also markedly diminished.
  • In conclusion, our data suggests that oxidative stress and cellular Ca2+ modulates the baicalein-induced cell death via a Ca2+-dependent mitochondrial death pathway in N18 cells.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Apoptosis. Endoplasmic Reticulum / metabolism. Flavanones / pharmacology. Hybrid Cells / drug effects. Mitochondria / physiology. Reactive Oxygen Species / metabolism. Retinal Ganglion Cells / drug effects
  • [MeSH-minor] Animals. Cell Line. Mice. Rats. Signal Transduction

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  • [Cites] Biochem Biophys Res Commun. 2002 Aug 30;296(4):942-8 [12200139.001]
  • [Cites] Apoptosis. 2004 Nov;9(6):691-704 [15505412.001]
  • [Cites] Biotechniques. 1997 Sep;23(3):525-31 [9298227.001]
  • [Cites] Pharmacol Res. 2001 Feb;43(2):173-8 [11243719.001]
  • [Cites] J Ethnopharmacol. 2001 Oct;77(2-3):183-8 [11535362.001]
  • [Cites] Neuroreport. 2001 Jul 20;12(10):2199-202 [11447334.001]
  • [Cites] J Biol Chem. 1999 Oct 15;274(42):29831-7 [10514462.001]
  • [Cites] Planta Med. 2002 Mar;68(3):268-71 [11914968.001]
  • [Cites] Cardiovasc Res. 2000 Apr;46(1):126-38 [10727661.001]
  • [Cites] Am J Chin Med. 1996;24(1):31-6 [8739179.001]
  • [Cites] Biochim Biophys Acta. 2002 Jul 3;1571(3):201-10 [12090934.001]
  • [Cites] J Cell Biol. 1997 Dec 1;139(5):1317-24 [9382876.001]
  • [Cites] Cytometry. 2000 Feb 15;42(1):74-8 [10679746.001]
  • [Cites] Ann Allergy. 1988 Dec;61(6 Pt 2):53-7 [3061322.001]
  • [Cites] Arch Biochem Biophys. 1993 Oct;306(1):261-6 [8215413.001]
  • [Cites] Biochim Biophys Acta. 2002 Jul 18;1587(2-3):309-17 [12084473.001]
  • [Cites] Neurochem Res. 2006 Mar;31(3):383-93 [16733814.001]
  • [Cites] Carcinogenesis. 2000 Mar;21(3):485-95 [10688869.001]
  • [Cites] Biochim Biophys Acta. 1999 Nov 16;1472(3):643-50 [10564778.001]
  • [Cites] Eur J Pharmacol. 2007 Mar 15;559(1):14-20 [17223102.001]
  • [Cites] Neuron. 1997 Aug;19(2):453-63 [9292733.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1415-20 [8068938.001]
  • [Cites] Int J Mol Med. 2004 Oct;14(4):627-32 [15375593.001]
  • [Cites] Ann N Y Acad Sci. 2003 Dec;1010:331-4 [15033745.001]
  • [Cites] Planta Med. 2002 Apr;68(4):302-6 [11988851.001]
  • [Cites] Anticancer Res. 2000 Sep-Oct;20(5A):2861-5 [11062694.001]
  • [Cites] Exp Mol Med. 2006 Dec 31;38(6):616-24 [17202837.001]
  • [Cites] Oncogene. 1998 Dec 24;17(25):3225-36 [9916985.001]
  • [Cites] Biochem Pharmacol. 2001 Dec 15;62(12 ):1653-60 [11755119.001]
  • [Cites] Drug Metab Dispos. 2006 Feb;34(2):296-304 [16280456.001]
  • [Cites] Ann N Y Acad Sci. 2003 Dec;1010:648-58 [15033806.001]
  • [Cites] Toxicol Sci. 2000 Feb;53(2):340-51 [10696782.001]
  • [Cites] Toxicol Lett. 2000 Mar 15;112-113:41-8 [10720711.001]
  • [Cites] Nutr Cancer. 2000;38(2):200-8 [11525598.001]
  • [Cites] Cancer Res. 2002 May 1;62(9):2721-7 [11980674.001]
  • [Cites] Genes Dev. 1999 Aug 1;13(15):1899-911 [10444588.001]
  • [Cites] Carcinogenesis. 2001 Sep;22(9):1349-54 [11532854.001]
  • [Cites] Am J Chin Med. 1998;26(3-4):311-23 [9862019.001]
  • [Cites] Free Radic Biol Med. 2001 Feb 15;30(4):433-46 [11182299.001]
  • (PMID = 18661233.001).
  • [ISSN] 1573-6903
  • [Journal-full-title] Neurochemical research
  • [ISO-abbreviation] Neurochem. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Flavanones; 0 / Reactive Oxygen Species; 49QAH60606 / baicalein
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35. Chen CA, Tsai JC, Su PW, Lai YH, Chen HC: Signaling and regulatory mechanisms of integrinalpha3beta1 on the apoptosis of cultured rat podocytes. J Lab Clin Med; 2006 Jun;147(6):274-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Integrin is the major adhesion molecule for the attachment of podocytes to the glomerular basement membrane, and integrins have been shown to play a major role in the regulation of cell survival.
  • Cytochrome c was examined by immunohistochemical stain, and Fas, Fas ligand, Bax, Bcl-2, and ERK activation (p-ERK/ERK) were analyzed by Western blotting analysis.
  • The results demonstrated that the integrin antagonist, Gly-Arg-Gly-Asp (GRGD), increased the percentage of cells with apoptosis (from 0.9+/-0.5% to 27.2+/-9.9%, P < 0.01).
  • In GRGD-treated cells, cytochrome c was found released into cytoplasm by immunohistochemical study and the Bax expression was upregulated, whereas Bcl-2 expression was not changed.
  • Fas was not expressed in both control and GRGD-treated podocytes, although Fas ligand was upregulated in GRGD-treated cells.
  • ERK activation was also found to be increased in GRGD-treated cells.
  • The results indicated that alpha3beta1integrin is necessary for the prevention of the apoptosis of cultured rat podocytes, and that the signaling involves the Bax, Bcl-2, and cytochrome c pathways.
  • [MeSH-minor] Animals. Antigens, CD95 / metabolism. Cell Adhesion / physiology. Cells, Cultured. Cytochromes c / metabolism. Extracellular Signal-Regulated MAP Kinases / metabolism. Fas Ligand Protein. In Situ Nick-End Labeling. Membrane Glycoproteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factors / metabolism. bcl-2-Associated X Protein / metabolism

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  • (PMID = 16750664.001).
  • [ISSN] 0022-2143
  • [Journal-full-title] The Journal of laboratory and clinical medicine
  • [ISO-abbreviation] J. Lab. Clin. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Fas Ligand Protein; 0 / Integrin alpha3beta1; 0 / Membrane Glycoproteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tnfsf6 protein, rat; 0 / Tumor Necrosis Factors; 0 / bcl-2-Associated X Protein; 9007-43-6 / Cytochromes c; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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36. Fernández Y, Verhaegen M, Miller TP, Rush JL, Steiner P, Opipari AW Jr, Lowe SW, Soengas MS: Differential regulation of noxa in normal melanocytes and melanoma cells by proteasome inhibition: therapeutic implications. Cancer Res; 2005 Jul 15;65(14):6294-304
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  • [Title] Differential regulation of noxa in normal melanocytes and melanoma cells by proteasome inhibition: therapeutic implications.
  • Using bortezomib as a prototypic proteasome inhibitor, we have identified a novel and critical role of the proteasome in the maintenance of the malignant phenotype of melanoma cells that could have direct translational implications.
  • Thus, melanoma cells from early, intermediate, and late stages of the disease could not sustain proteasome inhibition and underwent an effective activation of caspase-dependent and -independent death programs.
  • This effect was tumor cell selective, because under similar conditions, normal melanocytes remained viable.
  • Intriguingly, and despite of interfering with a cellular machinery in charge of controlling the half-life of the vast majority of cellular proteins, bortezomib did not promote a generalized disruption of melanoma-associated survival factors (including NF-kappaB, Bcl-2, Bcl-x(L), XIAP, TRAF-2, or FLIP).
  • Instead, we identified a dramatic induction in vitro and in vivo of the BH3-only protein Noxa in melanoma cells (but not in normal melanocytes) in response to proteasome inhibition.
  • In summary, our results revealed Noxa as a new biomarker to gauge the efficacy of bortezomib specifically in tumor cells, and provide a new strategy to overcome tumor chemoresistance.

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  • (PMID = 16024631.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA008748; United States / NCI NIH HHS / CA / CA10456; United States / NCI NIH HHS / CA / CA13106; United States / NCI NIH HHS / CA / R01 CA107237
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / NF-kappa B; 0 / PMAIP1 protein, human; 0 / Pmaip1 protein, mouse; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 69G8BD63PP / Bortezomib; 80168379AG / Doxorubicin; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspases; Q20Q21Q62J / Cisplatin
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37. Guo F, Sigua C, Bali P, George P, Fiskus W, Scuto A, Annavarapu S, Mouttaki A, Sondarva G, Wei S, Wu J, Djeu J, Bhalla K: Mechanistic role of heat shock protein 70 in Bcr-Abl-mediated resistance to apoptosis in human acute leukemia cells. Blood; 2005 Feb 1;105(3):1246-55
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  • [Title] Mechanistic role of heat shock protein 70 in Bcr-Abl-mediated resistance to apoptosis in human acute leukemia cells.
  • Bcr-Abl-expressing primary or cultured leukemia cells display high levels of the antiapoptotic heat shock protein (hsp) 70 and are resistant to cytarabine (Ara-C), etoposide, or Apo-2L/TRAIL (TNF-related apoptosis-inducing ligand)-induced apoptosis.
  • Conversely, a stable expression of the cDNA of hsp70 in the reverse orientation attenuated not only hsp70 but also signal transducers and activators of transcription 5 (STAT5) and Bcl-x(L) levels.
  • Ectopic expression of hsp70 in HL-60 cells (HL-60/hsp70) inhibited Ara-C and etoposide-induced Bax conformation change and translocation to the mitochondria; attenuated the accumulation of cytochrome c, Smac, and Omi/HtrA2 in the cytosol; and inhibited the processing and activity of caspase-9 and caspase-3.
  • HL-60/hsp70 cells exhibited increased levels and DNA binding activity of STAT5, which was associated with high levels of Pim-2 and Bcl-x(L) and resistance to apoptosis.
  • Expression of the dominant negative (DN) STAT5 resensitized HL-60/hsp70 cells to cytarabine, etoposide, and Apo-2L/TRAIL-induced apoptosis.
  • Collectively, these findings suggest that hsp70 inhibits apoptosis upstream and downstream of the mitochondria and is a promising therapeutic target for reversing drug-resistance in chronic myeloid leukemia-blast crisis and acute myeloid leukemia cells.
  • [MeSH-minor] Cell Line, Tumor. DNA Primers. DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. HL-60 Cells. Humans. Jurkat Cells. Leukemia, Myeloid, Acute. Milk Proteins / genetics. Milk Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. STAT5 Transcription Factor. Trans-Activators / genetics. Trans-Activators / metabolism. bcl-2-Associated X Protein. bcl-X Protein

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  • (PMID = 15388581.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / BCL2L1 protein, human; 0 / DNA Primers; 0 / DNA-Binding Proteins; 0 / HSP70 Heat-Shock Proteins; 0 / Milk Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / STAT5 Transcription Factor; 0 / Trans-Activators; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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38. Linzmann H, Brunnberg L, Gruber AD, Klopfleisch R: A neurotropic lymphoma in the brachial plexus of a cat. J Feline Med Surg; 2009 Jun;11(6):522-4
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  • [Title] A neurotropic lymphoma in the brachial plexus of a cat.
  • A 7-year-old, intact male domestic shorthair cat was presented with a progressive, non-weight-bearing lameness of the right forelimb.
  • Further clinical, radiological and pathological findings lead to a diagnosis of a primary, neurotropic B-cell lymphoma in the brachial plexus.
  • [MeSH-major] Brachial Plexus. Cat Diseases / diagnosis. Lymphoma, B-Cell / veterinary. Peripheral Nervous System Neoplasms / veterinary

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  • (PMID = 19135398.001).
  • [ISSN] 1098-612X
  • [Journal-full-title] Journal of feline medicine and surgery
  • [ISO-abbreviation] J. Feline Med. Surg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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39. Kanthan R, Senger JL, Diudea D: Malignant mixed Mullerian tumors of the uterus: histopathological evaluation of cell cycle and apoptotic regulatory proteins. World J Surg Oncol; 2010;8:60
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  • [Title] Malignant mixed Mullerian tumors of the uterus: histopathological evaluation of cell cycle and apoptotic regulatory proteins.
  • AIM: The aim of our study was to evaluate survival outcomes in malignant mixed Mullerian tumors (MMMT) of the uterus with respect to the role of cell cycle and apoptotic regulatory proteins in the carcinomatous and sarcomatous components.
  • Immunohistochemical expression of Bad, Mcl-1, bcl-x, bak, mdm2, bax, p16, p21, p53, p27, EMA, Bcl-2, Ki67 and PCNA was correlated with clinico-pathological data including survival outcomes.
  • RESULTS: Histopathological examination confirmed malignant epithelial component with homologous (12 cases) and heterologous (11 cases) sarcomatous elements.
  • CONCLUSIONS: Our study supports that a) cell cycle and apoptotic regulatory protein dysregulation is an important pathway for tumorigenesis and b) p53 is an important immunoprognostic marker in MMMT of the uterus.
  • [MeSH-major] Apoptosis Regulatory Proteins / metabolism. Cell Cycle Proteins / metabolism. Mixed Tumor, Mullerian / metabolism. Uterine Cervical Neoplasms / metabolism
  • [MeSH-minor] Aged. Aged, 80 and over. Female. Humans. Immunoenzyme Techniques. Middle Aged. Neoplasm Metastasis. Prognosis


40. Wang G, Zhou D, Wang C, Gao Y, Zhou Q, Qian G, DeCoster MA: Hypoxic preconditioning suppresses group III secreted phospholipase A2-induced apoptosis via JAK2-STAT3 activation in cortical neurons. J Neurochem; 2010 Aug;114(4):1039-48
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  • In this report, we demonstrate that sPLA(2) III significantly decreased production of Bcl-xl and the ratio of Bcl-xl/Bax, and increased expression of Bax, cleaved caspase 3, and cleaved alpha-Fodrin in primary neuronal culture.
  • HPC prevented the sPLA(2) III-induced decreases in production of Bcl-xl and the ratio of Bcl-xl/Bax, and increases in expression of Bax, cleaved caspase 3, and alpha-Fodrin.
  • Our results suggest that sPLA(2) III-induced neuronal apoptosis is likely because of its alterations in expression and activity of Bcl-xl, Bax, caspase 3, and its target gene fodrin; and that HPC-produced neuroprotection against the sPLA(2) III toxicity is mediated via JAK-STAT signal pathways that regulate the expression of Bcl-xl, Bax, and cleaved caspase 3 in cultured cortical neurons.
  • [MeSH-minor] Animals. Apoptosis Regulatory Proteins / antagonists & inhibitors. Apoptosis Regulatory Proteins / metabolism. Cells, Cultured. Nerve Degeneration / enzymology. Nerve Degeneration / metabolism. Nerve Degeneration / pathology. Nerve Degeneration / prevention & control. Rats. Rats, Sprague-Dawley. Signal Transduction / physiology

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  • (PMID = 20492356.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / P20RR016456
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, rat; EC 2.7.10.2 / Jak2 protein, rat; EC 2.7.10.2 / Janus Kinase 2; EC 3.1.1.4 / Group III Phospholipases A2
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41. Lukyanova NY: Characteristics of homocysteine-induced multidrug resistance of human MCF-7 breast cancer cells and human A2780 ovarian cancer cells. Exp Oncol; 2010 Mar;32(1):10-4
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  • [Title] Characteristics of homocysteine-induced multidrug resistance of human MCF-7 breast cancer cells and human A2780 ovarian cancer cells.
  • METHODS: In current study human MCF-7 breast cancer cells and A2780 ovarian cancer cells sensitive to anticancer drugs were used.
  • To access the viability of cells, we applied 3-[4,5-dimethylthiazol-2-1]-2,5-diphenyltetrazolium bromide colorimetric assay (MTT-test).
  • Expression of Bcl-2, p-glycoprotein (P-gp), glutathione S-transferase (GST) and E-cadherin was studied by immunocytochemistry.
  • RESULTS: A2780 and MCF-7 cells were treated by homocysteine.
  • It was shown that every next treatment with homocysteine (up to 5th) decreased the sensitivity of A2780 and MCF-7 cells to cytotoxic drugs.
  • Immunocytochemical study of molecular profile of A2780 and MCF-7 cells after long-term cultivation with homocysteine has been carried out and has revealed that such treatment resulted in the induction of Bcl-2, P-gp, GST and E-cadherin expression.
  • This indicates that incubation of studied cells with homocysteine leads to simultaneous induction of expression of drug resistance markers to cisplatin and doxorubicin.
  • CONCLUSION: Cultivation of MCF-7 and A2780 cells with homocysteine leads to simultaneous development of resistance to doxorubicine and cisplatin.
  • The development of drug resistance is diverse for different drugs and varies among cell lines.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma / pathology. Drug Resistance, Multiple / drug effects. Drug Resistance, Neoplasm / drug effects. Homocysteine / pharmacology. Ovarian Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Cadherins / metabolism. Cell Line, Tumor. Cisplatin / therapeutic use. Doxorubicin / therapeutic use. Female. Humans. P-Glycoprotein / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism


42. Zhao J, Zhang X, Shi M, Xu H, Jin J, Ni H, Yang S, Dai J, Wu M, Guo Y: TIP30 inhibits growth of HCC cell lines and inhibits HCC xenografts in mice in combination with 5-FU. Hepatology; 2006 Jul;44(1):205-15
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  • [Title] TIP30 inhibits growth of HCC cell lines and inhibits HCC xenografts in mice in combination with 5-FU.
  • Previous works showed that loss of TIP30, also called CC3, a putative tumor suppressor, increased the incidence of hepatocellular carcinoma in mice, and some clinical samples of human HCC tissues had aberrant expression of TIP30.
  • Here, we report that the introduction of TIP30 by an adenovirus vector into HCC cell lines that had decreased expressions of TIP30 inhibited cell proliferation, decreased anchorage-dependent growth, suppressed invasion through the extracellular matrix, and inhibited tumorigenesis in nude mice.
  • Moreover, exogenous expression of Tip30 sensitized HCC cells to cytotoxic drugs and to apoptosis induced by tumor necrosis factor-related ligands in vitro.
  • Ectopic expression of TIP30 in HCC cells enhanced p53 expression and decreased Bcl-2/Bcl-xL expression.
  • [MeSH-major] Acetyltransferases / pharmacology. Antimetabolites, Antineoplastic / pharmacology. Carcinoma, Hepatocellular / pathology. Cell Proliferation / drug effects. Fluorouracil / pharmacology. Liver Neoplasms / pathology. Transcription Factors / pharmacology
  • [MeSH-minor] Adenoviridae. Animals. Apoptosis. Blotting, Western. Carcinogenicity Tests. Cell Line, Tumor. DNA, Neoplasm / genetics. Flow Cytometry. Gene Expression Regulation, Neoplastic. Genetic Vectors. Humans. Immunohistochemistry. In Vitro Techniques. Mice. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous. Treatment Outcome

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  • (PMID = 16799960.001).
  • [ISSN] 0270-9139
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / DNA, Neoplasm; 0 / Transcription Factors; EC 2.3.1.- / Acetyltransferases; EC 2.3.1.48 / HTATIP2 protein, human; U3P01618RT / Fluorouracil
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43. Sawatzky DA, Willoughby DA, Colville-Nash PR, Rossi AG: The involvement of the apoptosis-modulating proteins ERK 1/2, Bcl-xL and Bax in the resolution of acute inflammation in vivo. Am J Pathol; 2006 Jan;168(1):33-41
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  • [Title] The involvement of the apoptosis-modulating proteins ERK 1/2, Bcl-xL and Bax in the resolution of acute inflammation in vivo.
  • Inflammatory cell recruitment, activation, and apoptosis are highly regulated processes involving several checkpoints controlling the resolution of inflammation.
  • We investigated the role of the mitogen-activated protein kinase (MAPK) signaling pathway (ie, ERK1/2) and apoptosis-regulating Bcl-2 family members (ie, Bcl-x(L) and Bax) in the resolution of a rat carrageenan-induced pleurisy model.
  • In conclusion, this study shows that ERK1/2, Bax, and Bcl-x(L) play important functional roles in the resolution phase of the acute inflammatory response in vivo by influencing apoptosis.
  • [MeSH-major] Apoptosis / physiology. Extracellular Signal-Regulated MAP Kinases / metabolism. Inflammation / physiopathology. bcl-2-Associated X Protein / metabolism. bcl-X Protein / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Carrageenan / adverse effects. Disease Models, Animal. Enzyme Inhibitors / pharmacology. Flavonoids / pharmacology. Flow Cytometry. Macrophages / drug effects. Macrophages / immunology. Male. Neutrophils / drug effects. Neutrophils / immunology. Pleurisy / etiology. Pleurisy / immunology. Rats. Rats, Inbred Lew

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  • [Cites] Immunology. 2004 Sep;113(1):1-14 [15312130.001]
  • [Cites] Mol Pharmacol. 2004 Sep;66(3):683-93 [15322261.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Sep 3;321(4):961-6 [15358121.001]
  • [Cites] Br J Cancer. 1972 Aug;26(4):239-57 [4561027.001]
  • [Cites] Int Rev Cytol. 1980;68:251-306 [7014501.001]
  • [Cites] Carcinogenesis. 1990 May;11(5):847-53 [2139818.001]
  • [Cites] Agents Actions. 1991 Mar;32(3-4):283-8 [1650522.001]
  • [Cites] Transplantation. 1992 Apr;53(4):808-15 [1566346.001]
  • [Cites] Transplantation. 1994 Feb 27;57(4):563-8 [8116042.001]
  • [Cites] Br J Pharmacol. 1994 Nov;113(3):693-8 [7532080.001]
  • [Cites] N Engl J Med. 1995 Apr 6;332(14):962 [7877665.001]
  • [Cites] Lancet. 1995 Aug 19;346(8973):506 [7637500.001]
  • [Cites] Am J Pathol. 1995 Aug;147(2):278-92 [7543732.001]
  • [Cites] J Immunol. 1996 Sep 15;157(6):2577-85 [8805660.001]
  • [Cites] J Pharmacol Exp Ther. 1996 Dec;279(3):1453-61 [8968371.001]
  • [Cites] Nature. 1997 Jun 19;387(6635):773-6 [9194558.001]
  • [Cites] J Immunol. 1997 Nov 15;159(10):5070-8 [9366435.001]
  • [Cites] Nature. 1997 Nov 27;390(6658):350-1 [9389474.001]
  • [Cites] J Clin Invest. 1998 Feb 15;101(4):890-8 [9466984.001]
  • [Cites] Inflammation. 1998 Feb;22(1):67-82 [9484651.001]
  • [Cites] Gastroenterology. 1998 Jul;115(1):101-9 [9649464.001]
  • [Cites] J Biol Chem. 1998 Jul 17;273(29):18623-32 [9660836.001]
  • [Cites] J Leukoc Biol. 1998 Oct;64(4):537-45 [9766635.001]
  • [Cites] J Leukoc Biol. 1998 Oct;64(4):555-62 [9766637.001]
  • [Cites] Oncogene. 1998 Sep 17;17(11 Reviews):1475-82 [9779994.001]
  • [Cites] J Clin Invest. 1999 Mar;103(6):851-8 [10079106.001]
  • [Cites] J Biol Chem. 1999 Jun 18;274(25):18100-6 [10364264.001]
  • [Cites] Nat Med. 1999 Jun;5(6):698-701 [10371510.001]
  • [Cites] Proc Soc Exp Biol Med. 1962 Dec;111:544-7 [14001233.001]
  • [Cites] Clin Exp Allergy. 2004 Nov;34(11):1701-6 [15544593.001]
  • [Cites] J Cell Biol. 2004 Dec 20;167(6):1161-70 [15611337.001]
  • [Cites] FEBS Lett. 2002 Jun 5;520(1-3):145-52 [12044887.001]
  • [Cites] Immunol Rev. 2002 Aug;186:8-18 [12234358.001]
  • [Cites] Nat Rev Immunol. 2002 Oct;2(10):787-95 [12360216.001]
  • [Cites] Science. 2002 Dec 6;298(5600):1911-2 [12471242.001]
  • [Cites] Nature. 2002 Dec 19-26;420(6917):846-52 [12490957.001]
  • [Cites] Adv Exp Med Biol. 2002;507:33-40 [12664561.001]
  • [Cites] Nat Cell Biol. 2003 Apr;5(4):352-7 [12652309.001]
  • [Cites] Arthritis Rheum. 2000 Jan;43(1):175-83 [10643714.001]
  • [Cites] J Immunol. 2000 Apr 15;164(8):4286-91 [10754327.001]
  • [Cites] J Immunol. 2000 Aug 15;165(4):2198-204 [10925307.001]
  • [Cites] Endocr Rev. 2001 Apr;22(2):153-83 [11294822.001]
  • [Cites] Clin Exp Immunol. 2001 Apr;124(1):16-20 [11359438.001]
  • [Cites] Gut. 2001 Jul;49(1):35-41 [11413108.001]
  • [Cites] Am J Respir Crit Care Med. 2001 Aug 15;164(4):688-97 [11520738.001]
  • [Cites] J Leukoc Biol. 2001 Oct;70(4):649-58 [11590203.001]
  • [Cites] J Immunol. 2002 Feb 15;168(4):1861-8 [11823520.001]
  • [Cites] J Biol Chem. 2002 Apr 26;277(17):14884-93 [11842088.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Jul 11;306(4):1070-4 [12821152.001]
  • [Cites] Mol Cell Biochem. 2003 Apr;246(1-2):193-6 [12841362.001]
  • [Cites] Curr Opin Pharmacol. 2003 Aug;3(4):412-9 [12901951.001]
  • [Cites] Nat Rev Drug Discov. 2003 Sep;2(9):717-26 [12951578.001]
  • [Cites] J Immunol. 2003 Nov 1;171(9):4672-9 [14568942.001]
  • [Cites] FASEB J. 2003 Dec;17(15):2269-71 [14563690.001]
  • [Cites] Cell Signal. 2004 Jul;16(7):801-10 [15115659.001]
  • [Cites] Nat Rev Drug Discov. 2004 May;3(5):401-16 [15136788.001]
  • [Cites] J Immunol. 2004 Jun 1;172(11):7053-9 [15153527.001]
  • [Cites] Am J Pathol. 2004 Jul;165(1):115-26 [15215167.001]
  • [Cites] J Cell Physiol. 2005 Mar;202(3):642-53 [15316926.001]
  • [Cites] Transplantation. 2005 Apr 15;79(7):846-50 [15818329.001]
  • [CommentIn] Am J Pathol. 2006 May;168(5):1762; author reply 1762-3 [16651640.001]
  • (PMID = 16400007.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Enzyme Inhibitors; 0 / Flavonoids; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein; 9000-07-1 / Carrageenan; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ PMC1592663
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44. Yu YL, Chiang YJ, Chen YC, Papetti M, Juo CG, Skoultchi AI, Yen JJ: MAPK-mediated phosphorylation of GATA-1 promotes Bcl-XL expression and cell survival. J Biol Chem; 2005 Aug 19;280(33):29533-42
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  • [Title] MAPK-mediated phosphorylation of GATA-1 promotes Bcl-XL expression and cell survival.
  • In the interleukin 3-dependent hematopoietic cell line Ba/F3, inhibition of mitogen-activated protein kinase, a member of the MAPK/c-Jun N-terminal kinase/stress-activated protein kinase kinase family that plays an important role in cell growth and death control, rapidly leads to severe apoptosis.
  • Here we report that, upon interleukin-3 stimulation of Ba/F3 cells, the transcription factor GATA-1 is strongly phosphorylated at residue serine 26 by a MAPK-dependent pathway.
  • Further characterization of GATA-1 phosphorylation site mutants revealed that the antiapoptotic function of GATA-1 is strongly dependent upon its phosphorylation at the Ser-26 position and is probably mediated through its up-regulation of Bcl-X(L) expression.
  • Taken together, our data demonstrate that MAPK-dependent GATA-1 phosphorylation is important for its transactivation of the E4bp4 gene, Bcl-X(L) expression and cell survival.

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  • [Cites] Blood. 2000 Feb 15;95(4):1264-73 [10666199.001]
  • [Cites] J Biol Chem. 1994 Jun 17;269(24):16589-96 [8206977.001]
  • [Cites] Genes Dev. 2001 Oct 1;15(19):2503-8 [11581155.001]
  • [Cites] Mol Cell Biol. 2001 Nov;21(21):7460-9 [11585926.001]
  • [Cites] J Biol Chem. 2002 Jul 12;277(28):25446-56 [11948183.001]
  • [Cites] Curr Opin Cell Biol. 1994 Jun;6(3):415-24 [7917334.001]
  • [Cites] Protein Expr Purif. 1994 Dec;5(6):587-94 [7858429.001]
  • [Cites] Development. 1995 Jan;121(1):163-72 [7867497.001]
  • [Cites] J Biol Chem. 1995 Feb 24;270(8):4101-7 [7876160.001]
  • [Cites] J Biol Chem. 1995 Jun 23;270(25):15320-6 [7541039.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Oct 10;92(21):9623-7 [7568185.001]
  • [Cites] J Biol Chem. 1996 May 17;271(20):11684-8 [8662643.001]
  • [Cites] Oncogene. 1997 Jan 9;14(1):123-31 [9010239.001]
  • [Cites] J Immunol. 1997 May 15;158(10):4750-7 [9144489.001]
  • [Cites] EMBO J. 1997 Jul 1;16(13):3965-73 [9233806.001]
  • [Cites] Science. 1998 Aug 28;281(5381):1322-6 [9735050.001]
  • [Cites] Genes Dev. 1999 Jan 15;13(2):163-75 [9925641.001]
  • [Cites] Nucleic Acids Res. 1999 Feb 15;27(4):1168-75 [9927752.001]
  • [Cites] Blood. 1999 Apr 15;93(8):2569-77 [10194436.001]
  • [Cites] Blood. 1999 Jul 1;94(1):87-96 [10381501.001]
  • [Cites] Gene. 1999 Jul 8;234(2):297-305 [10395902.001]
  • [Cites] Mol Cell Biol. 1999 Sep;19(9):6195-206 [10454566.001]
  • [Cites] J Biol Chem. 1999 Sep 10;274(37):26563-71 [10473620.001]
  • [Cites] Mol Cell Biol. 1999 Nov;19(11):7399-409 [10523628.001]
  • [Cites] J Biol Chem. 2002 Jul 26;277(30):27144-53 [12023274.001]
  • [Cites] J Biol Chem. 2003 Feb 14;278(7):4705-12 [12468531.001]
  • [Cites] Mol Cell Biol. 2003 Mar;23(6):1896-909 [12612065.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6363-9 [14559825.001]
  • [Cites] Mol Cell Biol. 2003 Nov;23(21):7460-74 [14559995.001]
  • [Cites] Hematol J. 2004;5(3):262-72 [15167914.001]
  • [Cites] EMBO J. 2004 Jul 21;23(14):2841-52 [15215894.001]
  • [Cites] Nature. 1989 Jun 8;339(6224):446-51 [2725678.001]
  • [Cites] Cell. 1989 Sep 8;58(5):877-85 [2776214.001]
  • [Cites] EMBO J. 1990 Sep;9(9):2997-3002 [2118109.001]
  • [Cites] J Biol Chem. 1991 Aug 15;266(23):15180-4 [1907971.001]
  • [Cites] J Biol Chem. 1991 Nov 25;266(33):22159-63 [1939237.001]
  • [Cites] Annu Rev Cell Biol. 1991;7:663-98 [1809356.001]
  • [Cites] Blood. 1992 Aug 1;80(3):575-81 [1638017.001]
  • [Cites] Mol Cell Biol. 1993 Oct;13(10):6290-303 [8413228.001]
  • [Cites] J Immunol. 2000 Nov 15;165(10):5597-605 [11067915.001]
  • (PMID = 15967790.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA016368; United States / NHLBI NIH HHS / HL / HL077242-01; United States / NHLBI NIH HHS / HL / HL78381-30
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / Bcl2l1 protein, mouse; 0 / DNA-Binding Proteins; 0 / Erythroid-Specific DNA-Binding Factors; 0 / G-Box Binding Factors; 0 / GATA1 Transcription Factor; 0 / Gata1 protein, mouse; 0 / Interleukin-3; 0 / Nfil3 protein, mouse; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Transcription Factors; 0 / bcl-X Protein; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases
  • [Other-IDs] NLM/ NIHMS327442; NLM/ PMC3193074
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45. Cerchietti LC, Hatzi K, Caldas-Lopes E, Yang SN, Figueroa ME, Morin RD, Hirst M, Mendez L, Shaknovich R, Cole PA, Bhalla K, Gascoyne RD, Marra M, Chiosis G, Melnick A: BCL6 repression of EP300 in human diffuse large B cell lymphoma cells provides a basis for rational combinatorial therapy. J Clin Invest; 2010 Dec 1;120(12):4569-82
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  • [Title] BCL6 repression of EP300 in human diffuse large B cell lymphoma cells provides a basis for rational combinatorial therapy.
  • B cell lymphoma 6 (BCL6), which encodes a transcriptional repressor, is a critical oncogene in diffuse large B cell lymphomas (DLBCLs).
  • Although a retro-inverted BCL6 peptide inhibitor (RI-BPI) was recently shown to potently kill DLBCL cells, the underlying mechanisms remain unclear.
  • Here, we show that RI-BPI induces a particular gene expression signature in human DLBCL cell lines that included genes associated with the actions of histone deacetylase (HDAC) and Hsp90 inhibitors.
  • Induction of p300 and BAT3 was required for the antilymphoma effects of RI-BPI, since specific blockade of either protein rescued human DLBCL cell lines from the BCL6 inhibitor.
  • Furthermore, HDAC and Hsp90 inhibitors independently enhanced RI-BPI killing of primary human DLBCL cells in vitro.

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  • (PMID = 21041953.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA155226; United States / NIGMS NIH HHS / GM / R37 GM062437; United States / NCI NIH HHS / CA / R01-CA104348; United States / NCI NIH HHS / CA / K08 CA127353; United States / NIGMS NIH HHS / GM / GM62437; United States / NIGMS NIH HHS / GM / R01 GM062437; United States / NCI NIH HHS / CA / N01CO12400; United States / NCI NIH HHS / CA / R01 CA104348; United States / NCI NIH HHS / CO / N01-CO-12400; United States / NCI NIH HHS / CA / R01 CA143032
  • [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 / BAG6 protein, human; 0 / BCL6 protein, human; 0 / DNA-Binding Proteins; 0 / Histone Deacetylase Inhibitors; 0 / Molecular Chaperones; EC 2.3.1.48 / E1A-Associated p300 Protein; EC 2.3.1.48 / EP300 protein, human
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46. Yang N, Gong F, Sun L, Yang D, Han X, Ma C, Sun Y: Poly (ADP-ribose) polymerase-1 binds to BCL2 major breakpoint region and regulates BCL2 expression. J Cell Biochem; 2010 Aug 1;110(5):1208-18
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  • BCL2, originally identified as a proto-oncogene in B-cell lymphoma, is a key regulator of apoptosis.
  • Although it is more than 200 kb in length, at least 70% of the t(14;18) translocation in follicular lymphomas occurs at the BCL2 major breakpoint region (mbr), located in the 3'-untranslated region (3'-UTR).
  • In this study, we purified Poly(ADP-ribose) polymerase-1 (PARP-1) from the DNA-protein complexes formed by 37 mbr in Jurkat cells and demonstrated that PARP-1 participates in the 37 mbr-protein complex's formation in vitro and in vivo.
  • [MeSH-major] Chromosome Breakpoints. Gene Expression Regulation, Neoplastic. Poly(ADP-ribose) Polymerases / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] 3' Untranslated Regions / genetics. Blotting, Western. Cell Line. Cell Line, Tumor. Humans. Jurkat Cells. Protein Binding. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • [Copyright] Published 2010 Wiley-Liss, Inc.
  • (PMID = 20564216.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3' Untranslated Regions; 0 / Proto-Oncogene Proteins c-bcl-2; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
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47. Andréasson U, Ek S, Merz H, Rosenquist R, Andersen N, Jerkeman M, Dictor M, Borrebaeck CA: B cell lymphomas express CX3CR1 a non-B cell lineage adhesion molecule. Cancer Lett; 2008 Feb 8;259(2):138-45
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  • [Title] B cell lymphomas express CX3CR1 a non-B cell lineage adhesion molecule.
  • To study the differential expression of cell membrane-bound receptors and their potential role in growth and/or survival of the tumor cells, highly purified follicular lymphoma cells were analyzed, using gene expression analysis, and compared to non-malignant B cell populations.
  • Filtering the genome for overexpressed genes coding for cell membrane-bound proteins/receptors resulted in a hit list of 27 identified genes.
  • Among these, we have focused on the aberrant over expression of CX3CR1, in different types of B cell lymphoma, as compared to non-malignant B cells.
  • We show that CX3CR1, which normally is not expressed on B cells, is expressed both at the mRNA and protein level in several subtypes of lymphoma.
  • CX3CR1 has also shown to be involved in the homing to specific tissues that express the ligand, CX3CL1, in breast and prostate cancer and may thus be involved in dissemination of lymphoma.
  • [MeSH-major] B-Lymphocytes / immunology. Lymphoma, Follicular / immunology. Lymphoma, Mantle-Cell / immunology. Palatine Tonsil / immunology. Receptors, Chemokine / analysis
  • [MeSH-minor] Cell Separation. Flow Cytometry. Gene Expression Profiling / methods. Gene Expression Regulation, Neoplastic. Humans. Oligonucleotide Array Sequence Analysis. RNA, Messenger / analysis

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  • (PMID = 18060687.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / CX3CR1 protein, human; 0 / RNA, Messenger; 0 / Receptors, Chemokine
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48. Hara T, Omura-Minamisawa M, Chao C, Nakagami Y, Ito M, Inoue T: Bcl-2 inhibitors potentiate the cytotoxic effects of radiation in Bcl-2 overexpressing radioresistant tumor cells. Int J Radiat Oncol Biol Phys; 2005 Feb 1;61(2):517-28
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  • [Title] Bcl-2 inhibitors potentiate the cytotoxic effects of radiation in Bcl-2 overexpressing radioresistant tumor cells.
  • PURPOSE: Bcl-2, an inhibitor of apoptosis frequently shows elevated expression in human tumors, thus resulting in resistance to radiation therapy.
  • Therefore, inhibiting Bcl-2 function may enhance the radiosensitivity of tumor cells.
  • Tetrocarcin A (TC-A) and bcl-2 antisense oligonucleotides exhibit antitumor activity by inhibiting Bcl-2 function and transcription, respectively.
  • We investigated whether these antitumor agents would enhance the cytotoxic effects of radiation in tumor cells overexpressing Bcl-2.
  • METHODS AND MATERIALS: We used HeLa/bcl-2 cells, a stable Bcl-2-expressing cell line derived from wild-type HeLa (HeLa/wt) cells.
  • Cells were incubated with TC-A and bcl-2 antisense oligonucleotides for 24 h after irradiation, and cell viability was then determined.
  • Apoptotic cells were quantified by flow cytometric assay.
  • RESULTS: The HeLa/bcl-2 cells were more resistant to radiation than HeLa/wt cells.
  • At concentrations that are not inherently cytotoxic, both TC-A and bcl-2 antisense oligonucleotides increased the cytotoxic effects of radiation in HeLa/bcl-2 cells, but not in HeLa/wt cells.
  • However, in HeLa/bcl-2 cells, additional treatment with TC-A in combination with radiation did not significantly increase apoptosis.
  • CONCLUSIONS: The present results suggest that TC-A and bcl-2 antisense oligonucleotides reduce radioresistance of tumor cells overexpressing Bcl-2.
  • Therefore, a combination of radiotherapy and Bcl-2 inhibitors may prove to be a useful therapeutic approach for treating tumors that overexpress Bcl-2.
  • [MeSH-major] Aminoglycosides / pharmacology. Apoptosis. Oligonucleotides, Antisense / pharmacology. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Radiation Tolerance / drug effects. Radiation-Sensitizing Agents / pharmacology
  • [MeSH-minor] Analysis of Variance. Cell Survival / drug effects. Cell Survival / radiation effects. HeLa Cells / drug effects. HeLa Cells / metabolism. HeLa Cells / radiation effects. Humans. RNA, Messenger / antagonists & inhibitors. Tumor Stem Cell Assay

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  • (PMID = 15667975.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aminoglycosides; 0 / Oligonucleotides, Antisense; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Radiation-Sensitizing Agents; 73666-84-9 / tetrocarcin A
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49. Zubor P, Hatok J, Galo S, Dokus K, Klobusiakova D, Danko J, Racay P: Anti-apoptotic and pro-apoptotic gene expression evaluated from eutopic endometrium in the proliferative phase of the menstrual cycle among women with endometriosis and healthy controls. Eur J Obstet Gynecol Reprod Biol; 2009 Aug;145(2):172-6
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  • Hence, we investigated the expression of pro-apoptotic and anti-apoptotic genes in eutopic endometrium from women with endometriosis and healthy controls in relation to disease occurrence and severity.
  • The mRNA expression of apoptotic genes (p53, Bcl-x(L,S) and Bax) from eutopic endometrium was detected by RT-PCR.
  • RESULTS: A significant increase in expression of mRNA p53 (1.42 versus 1.02; p<0.05), and Bcl-x(S) (0.41 versus 0.19; p=0.0006) was found in women with endometriosis compared to healthy controls.
  • The expression of anti-apoptotic Bcl-x(L) was unchanged (1.08 versus 1.07).
  • The Bcl-x(L)/Bcl-x(S) ratio was twofold higher (5.63 versus 2.63) in controls.
  • By stratifying patients by disease stage we have revealed an increased mRNA expression of apoptotic genes in patients with grades III-IV endometriosis compared to those with grades I-II.
  • However, the difference was significant only for Bcl-x(S) expression (p<0.05).
  • CONCLUSIONS: Results suggest that an increased transcription of pro-apoptotic genes (p53 and Bcl-x(S)) in eutopic endometrium is significantly associated with endometriosis, which indicates dysregulation of apoptotic gene transcription associated with disease.
  • [MeSH-major] Apoptosis. Endometriosis / metabolism. Endometrium / metabolism. Follicular Phase / physiology. Infertility, Female / metabolism. Tumor Suppressor Protein p53 / biosynthesis. bcl-2-Associated X Protein / biosynthesis. bcl-X Protein / biosynthesis

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  • (PMID = 19467764.001).
  • [ISSN] 1872-7654
  • [Journal-full-title] European journal of obstetrics, gynecology, and reproductive biology
  • [ISO-abbreviation] Eur. J. Obstet. Gynecol. Reprod. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / BCL2L1 protein, human; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; 0 / bcl-X Protein
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50. Kvansakul M, Yang H, Fairlie WD, Czabotar PE, Fischer SF, Perugini MA, Huang DC, Colman PM: Vaccinia virus anti-apoptotic F1L is a novel Bcl-2-like domain-swapped dimer that binds a highly selective subset of BH3-containing death ligands. Cell Death Differ; 2008 Oct;15(10):1564-71
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  • [Title] Vaccinia virus anti-apoptotic F1L is a novel Bcl-2-like domain-swapped dimer that binds a highly selective subset of BH3-containing death ligands.
  • Some viruses express proteins homologous in sequence and function to mammalian pro-survival Bcl-2 proteins.
  • Anti-apoptotic F1L expressed by vaccinia virus is essential for survival of infected cells, but it bears no discernable sequence homology to proteins other than its immediate orthologues in related pox viruses.
  • Here we report that the crystal structure of F1L reveals a Bcl-2-like fold with an unusual N-terminal extension.
  • Structural comparison of F1L with other Bcl-2 family members reveals a novel sequence signature that redefines the BH4 domain as a structural motif present in both pro- and anti-apoptotic Bcl-2 members, including viral Bcl-2-like proteins.
  • [MeSH-major] Protein Structure, Quaternary. Protein Structure, Tertiary. Proto-Oncogene Proteins c-bcl-2 / chemistry. Viral Proteins / chemistry. Viral Proteins / metabolism


51. Paoluzzi L, Gonen M, Bhagat G, Furman RR, Gardner JR, Scotto L, Gueorguiev VD, Heaney ML, Manova K, O'Connor OA: The BH3-only mimetic ABT-737 synergizes the antineoplastic activity of proteasome inhibitors in lymphoid malignancies. Blood; 2008 Oct 1;112(7):2906-16
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  • Overexpression of antiapoptotic members of the Bcl-2 family is observed in approximately 80% of B-cell lymphomas, contributing to intrinsic and acquired drug resistance.
  • ABT-737 is a BH3-only mimetic and potent inhibitor of the antiapoptotic Bcl-2 family members Bcl-2, Bcl-X(L), and Bcl-w.
  • In vitro, ABT-737 exhibited concentration-dependent cytotoxicity against a broad panel of lymphoma cell lines including mantle cell lymphoma (MCL) and diffuse large B-cell lymphoma (DLBCL).
  • ABT-737 showed synergism when combined with the proteasome inhibitors bortezomib or carfilzomib in select lymphoma cell lines and induced potent mitochondrial membrane depolarization and apoptosis when combined with either.
  • ABT-737 plus bortezomib also induced significant apoptosis in primary samples of MCL, DLBCL, and chronic lymphocytic leukemia (CLL) but no significant cytotoxic effect was observed in peripheral blood mononuclear cells from healthy donors.
  • Collectively, these data suggest that ABT-737 alone or in combination with a proteasome inhibitor represents a novel and potentially important platform for the treatment of B-cell malignancies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Biphenyl Compounds / pharmacology. Enzyme Inhibitors / pharmacology. Lymphoma / enzymology. Lymphoma / pathology. Molecular Mimicry / drug effects. Nitrophenols / pharmacology. Proteasome Inhibitors. Sulfonamides / pharmacology
  • [MeSH-minor] Animals. Boronic Acids / pharmacology. Bortezomib. Cell Death / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm / drug effects. Drug Synergism. Health. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukocytes, Mononuclear / drug effects. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Mantle-Cell / pathology. Membrane Potential, Mitochondrial / drug effects. Mice. Microscopy, Confocal. Piperazines / pharmacology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Pyrazines / pharmacology. Tissue Donors. Xenograft Model Antitumor Assays

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  • (PMID = 18591385.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABT-737; 0 / Antineoplastic Agents; 0 / Biphenyl Compounds; 0 / Boronic Acids; 0 / Enzyme Inhibitors; 0 / Nitrophenols; 0 / Piperazines; 0 / Proteasome Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / Sulfonamides; 69G8BD63PP / Bortezomib
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52. Bolisetty MT, Dy G, Tam W, Beemon KL: Reticuloendotheliosis virus strain T induces miR-155, which targets JARID2 and promotes cell survival. J Virol; 2009 Dec;83(23):12009-17
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  • [Title] Reticuloendotheliosis virus strain T induces miR-155, which targets JARID2 and promotes cell survival.
  • The precursor of miR-155, termed bic, was first observed to cooperate with myc in chicken B-cell lymphomas induced by avian leukosis proviral integrations.
  • We also observed very high levels of miR-155 in REV-T-induced B-cell lymphomas.
  • To study the role of miR-155 in these tumors, we identified JARID2/Jumonji, a cell cycle regulator and part of a histone methyltransferase complex, as a target of miR-155.
  • Further, the overexpression of a sponge complementary to miR-155 in a tumor cell line increased endogenous JARID2 mRNA levels.
  • The overexpression of JARID2 in chicken fibroblasts led to decreased cell numbers and an increase in apoptotic cells.
  • The overexpression of miR-155 rescued cells undergoing cytopathic effect caused by infection with subgroup B avian retroviruses.
  • [MeSH-minor] Animals. Cell Line. Cell Survival. Chickens. Fibroblasts / virology. Humans

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  • [Cites] Oncogene. 1999 Nov 22;18(49):6925-37 [10602467.001]
  • [Cites] J Immunol. 2007 Oct 15;179(8):5082-9 [17911593.001]
  • [Cites] J Virol. 2000 Dec;74(24):11490-4 [11090145.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1381-7 [11830490.001]
  • [Cites] J Virol. 2002 May;76(9):4275-86 [11932393.001]
  • [Cites] J Virol. 2002 Jun;76(11):5581-7 [11991986.001]
  • [Cites] J Virol. 2003 Sep;77(17):9378-87 [12915553.001]
  • [Cites] J Virol. 2003 Dec;77(23):12552-61 [14610178.001]
  • [Cites] Lancet Oncol. 2004 Jan;5(1):11-8 [14700604.001]
  • [Cites] Oncogene. 2004 Mar 25;23(13):2275-86 [14755244.001]
  • [Cites] J Virol. 2004 May;78(10):5139-46 [15113896.001]
  • [Cites] RNA. 2004 Oct;10(10):1507-17 [15383676.001]
  • [Cites] Virology. 1979 Feb;93(1):20-30 [219596.001]
  • [Cites] Cell. 1981 Aug;25(2):421-31 [6269747.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Oct 9;104(41):16170-5 [17911264.001]
  • [Cites] J Virol. 2007 Dec;81(23):12836-45 [17881434.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Nov 27;104(48):18952-7 [18024587.001]
  • [Cites] Nature. 2007 Dec 13;450(7172):1096-9 [18075594.001]
  • [Cites] Immunity. 2007 Dec;27(6):847-59 [18055230.001]
  • [Cites] J Biol Chem. 2008 Feb 1;283(5):2654-62 [18048365.001]
  • [Cites] RNA Biol. 2007 Nov;4(3):131-7 [18347435.001]
  • [Cites] J Virol. 2008 Jun;82(11):5295-306 [18367535.001]
  • [Cites] Immunity. 2008 May;28(5):621-9 [18450484.001]
  • [Cites] Immunity. 2008 May;28(5):630-8 [18455451.001]
  • [Cites] J Virol. 2008 Nov;82(21):10436-43 [18753206.001]
  • [Cites] Br J Haematol. 2008 Nov;143(4):570-80 [18950466.001]
  • [Cites] J Virol. 2008 Dec;82(24):12213-20 [18842708.001]
  • [Cites] J Virol. 2009 Jan;83(1):489-92 [18945769.001]
  • [Cites] J Biol Chem. 2009 Jan 9;284(2):733-9 [19010785.001]
  • [Cites] Immunity. 2009 Jan 16;30(1):80-91 [19144316.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2735-40 [19193853.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Apr 28;106(17):7113-8 [19359473.001]
  • [Cites] Blood. 2009 Aug 13;114(7):1374-82 [19520806.001]
  • [Cites] J Virol. 1981 Sep;39(3):713-21 [6270346.001]
  • [Cites] Nature. 1984 Feb 23-29;307(5953):702-8 [6321996.001]
  • [Cites] J Virol. 1984 Oct;52(1):172-82 [6090694.001]
  • [Cites] Science. 1985 Dec 6;230(4730):1126-32 [2999973.001]
  • [Cites] J Biol Chem. 1987 Mar 5;262(7):3422-7 [3029112.001]
  • [Cites] J Virol. 1987 Oct;61(10):3004-12 [3041020.001]
  • [Cites] Mol Cell Biol. 1989 Jun;9(6):2657-64 [2548084.001]
  • [Cites] Cell. 1992 Apr 3;69(1):119-28 [1555236.001]
  • [Cites] Avian Dis. 1992 Apr-Jun;36(2):432-9 [1320872.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Nov 8;91(23):10962-6 [7971992.001]
  • [Cites] Mol Cell Biol. 1997 Mar;17(3):1490-502 [9032277.001]
  • [Cites] Mol Cell Biol. 1998 May;18(5):2997-3009 [9566919.001]
  • [Cites] Trends Cell Biol. 1998 May;8(5):202-6 [9695840.001]
  • [Cites] Anal Biochem. 1999 May 15;270(1):41-9 [10328763.001]
  • [Cites] Mol Cell Biol. 1999 Jul;19(7):4672-83 [10373516.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 8;102(10):3627-32 [15738415.001]
  • [Cites] RNA. 2005 Apr;11(4):459-69 [15703439.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7065-70 [16103053.001]
  • [Cites] Cell. 2005 Aug 26;122(4):553-63 [16122423.001]
  • [Cites] J Biol Chem. 2005 Sep 2;280(35):30916-23 [15870077.001]
  • [Cites] J Pathol. 2005 Oct;207(2):243-9 [16041695.001]
  • [Cites] Nucleic Acids Res. 2006 Jan 1;34(Database issue):D140-4 [16381832.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 [16461460.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 2;103(18):7024-9 [16641092.001]
  • [Cites] Dev Biol. 2007 Mar 15;303(2):549-60 [17189626.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Feb 20;104(8):2750-5 [17293455.001]
  • [Cites] Science. 2007 Apr 27;316(5824):608-11 [17463290.001]
  • [Cites] RNA. 2007 Jun;13(6):930-6 [17456563.001]
  • [Cites] Blood. 2007 Jun 1;109(11):4944-51 [17327404.001]
  • [Cites] Nat Methods. 2007 Sep;4(9):721-6 [17694064.001]
  • [Cites] Cancer Res. 2000 Oct 15;60(20):5640-3 [11059754.001]
  • (PMID = 19759154.001).
  • [ISSN] 1098-5514
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA124596; United States / NCI NIH HHS / CA / R01 CA124596
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / Nerve Tissue Proteins
  • [Other-IDs] NLM/ PMC2786729
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53. Chen AI, Advani RH: Beyond the guidelines in the treatment of peripheral T-cell lymphoma: new drug development. J Natl Compr Canc Netw; 2008 Apr;6(4):428-35
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  • [Title] Beyond the guidelines in the treatment of peripheral T-cell lymphoma: new drug development.
  • Peripheral T-cell lymphomas (PTCLs) are a rare and diverse group of neoplasms with a poor prognosis.
  • Management of these disorders has been largely extrapolated from the treatment of aggressive B-cell lymphomas; however, therapeutic responses to this approach are neither adequate nor durable for most patients with PTCL.
  • These emerging therapies include new uses of existing agents and the development of novel agents specifically targeted against T-cell lymphoma.
  • These novel therapies are being tested as single agents and in combination with conventional lymphoma regimens in the frontline and salvage settings.
  • Because of the rarity and heterogeneity of PTCL, national and international cooperation is needed to conduct the clinical studies required for the development of more effective treatment paradigms.
  • [MeSH-major] Lymphoma, T-Cell, Peripheral / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Diphtheria Toxin / therapeutic use. Histone Deacetylase Inhibitors. Humans. Immunosuppressive Agents / therapeutic use. Interleukin-2 / therapeutic use. Practice Guidelines as Topic. Protease Inhibitors / therapeutic use. Purine Nucleosides / therapeutic use. Purine-Nucleoside Phosphorylase / antagonists & inhibitors. Pyrimidinones / therapeutic use. Recombinant Fusion Proteins / therapeutic use. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • (PMID = 18433608.001).
  • [ISSN] 1540-1405
  • [Journal-full-title] Journal of the National Comprehensive Cancer Network : JNCCN
  • [ISO-abbreviation] J Natl Compr Canc Netw
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 0 / Diphtheria Toxin; 0 / Histone Deacetylase Inhibitors; 0 / Immunosuppressive Agents; 0 / Interleukin-2; 0 / Protease Inhibitors; 0 / Purine Nucleosides; 0 / Pyrimidinones; 0 / Recombinant Fusion Proteins; 0 / Vascular Endothelial Growth Factor A; 0 / zanolimumab; 0W860991D6 / Deoxycytidine; 25E79B5CTM / denileukin diftitox; 3A189DH42V / alemtuzumab; 426X066ELK / forodesine; 60158CV180 / nelarabine; B76N6SBZ8R / gemcitabine; EC 2.4.2.1 / Purine-Nucleoside Phosphorylase
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54. Woroniecka R, Grygalewicz B, Pienkowska-Grela B, Rymkiewicz G, Konecki R, Swoboda P, Janik P: Variant t(2;11)(p11.2;q13) without IGK involvement in a case of mantle cell lymphoma. Cancer Genet Cytogenet; 2007 Jun;175(2):154-8
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  • [Title] Variant t(2;11)(p11.2;q13) without IGK involvement in a case of mantle cell lymphoma.
  • Mantle cell lymphoma (MCL) is characterized by the t(11;14)(q13;q32) translocation, which leads to overexpression of the cyclin D1 (CCND1) gene.
  • Translocations affecting IGH loci are mostly prevalent in B-cell lymphomas, but variant translocations involving immunoglobulin kappa (IGK) or lambda (IGL) light chain loci have been observed in a minority of B-lymphoid malignancies.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 2 / genetics. Genetic Variation. Immunoglobulin kappa-Chains. Lymphoma, Mantle-Cell / genetics. Translocation, Genetic


55. Utkan G, Tek I, Kocer M, Muallaoglu S, Durnal AG, Arslan UY, Celenkoglu G, Tokluoglu S, Alkis N: Blood viscosity in patients with diffuse large B cell non-Hodgkin's lymphoma. Exp Oncol; 2006 Dec;28(4):326-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Blood viscosity in patients with diffuse large B cell non-Hodgkin's lymphoma.
  • The aim of the study was to evaluate blood viscosity as possible marker of disease progression in patients with newly diagnosed non-Hodgkin's lymphoma (NHL).
  • [MeSH-major] Blood Viscosity. Lymphoma, B-Cell / blood. Lymphoma, Large B-Cell, Diffuse / blood

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  • (PMID = 17285120.001).
  • [ISSN] 1812-9269
  • [Journal-full-title] Experimental oncology
  • [ISO-abbreviation] Exp. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ukraine
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56. Hirose A, Yamane T, Nakajima Y, Manabe M, Kanashima H, Hagihara K, Sakamoto E, Nakamae M, Terada Y, Kosaka S, Aoyama Y, Sakamoto C, Kumura T, Koh KR, Hirai M, Ohta K, Nakao Y, Mugitani A, Teshima H, Hino M: [Autologous hematopoietic stem cell transplantation for aggressive B-cell non-Hodgkin's lymphoma]. Gan To Kagaku Ryoho; 2005 Dec;32(13):2059-64
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  • [Title] [Autologous hematopoietic stem cell transplantation for aggressive B-cell non-Hodgkin's lymphoma].
  • To evaluate the results of high-dose chemotherapy (HDT) and autologous hematopoietic stem cell transplantation (ASCT) in patients with diffuse B-cell aggressive non-Hodgkin's lymphoma(NHL).
  • The 5-year probability of disease-free survival for patients in the low-risk group and in the high-risk group was 68.8% and 60.0%,respectively (p = 0.9 6).
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Lymphoma, B-Cell / therapy. Lymphoma, Large B-Cell, Diffuse / therapy. Transplantation, Autologous
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Cytarabine / administration & dosage. Disease-Free Survival. Drug Administration Schedule. Etoposide / administration & dosage. Female. Humans. Male. Middle Aged. Nitrosourea Compounds / administration & dosage. Remission Induction. Treatment Outcome

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  • (PMID = 16352929.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Nitrosourea Compounds; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; Q20Q21Q62J / Cisplatin; RYH2T97J77 / ranimustine
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57. Lin P, Jetly R, Lennon PA, Abruzzo LV, Prajapati S, Medeiros LJ: Translocation (18;22)(q21;q11) in B-cell lymphomas: a report of 4 cases and review of the literature. Hum Pathol; 2008 Nov;39(11):1664-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translocation (18;22)(q21;q11) in B-cell lymphomas: a report of 4 cases and review of the literature.
  • Follicular lymphomas characteristically carry t(14;18)(q32;q21) which results in IGH-BCL-2 fusion.
  • Variant translocations that juxtapose the BCL-2 gene with the immunoglobulin kappa (2p11) and lambda (22q11) light chain genes are rare.
  • We report 4 cases of B-cell lymphoma/leukemia associated with t(18;22)(q21;q11).
  • Three cases were classified as chronic lymphocytic leukemia, and one as follicular lymphoma based on morphology and immunophenotype.
  • Fluorescence in situ hybridization analysis was performed on all 4 cases using a BCL-2 breakapart probe.
  • The BCL-2 gene was rearranged in all cases.
  • These cases illustrate that t(18;22)(q21;q11) is more commonly observed in chronic lymphocytic leukemia and may represent either an initial or secondary genetic event.
  • [MeSH-major] Chromosomes, Human, Pair 18. Chromosomes, Human, Pair 22. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lymphoma, B-Cell / genetics
  • [MeSH-minor] Aged. Fatal Outcome. Female. Gene Rearrangement, B-Lymphocyte. Genes, bcl-2. Humans. Male. Middle Aged. Translocation, Genetic

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  • (PMID = 18656237.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 25
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58. Joseph LD, Panicker VK, Prathiba D, Damodharan J: Subcutaneous panniculitis-like T cell lymphoma in a HIV positive patient. J Assoc Physicians India; 2005 Apr;53:314-6
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  • [Title] Subcutaneous panniculitis-like T cell lymphoma in a HIV positive patient.
  • Immunocompromised patients are at increased risk for developing certain malignant tumors, particularly aggressive B cell lymphomas and extranodal lymphomas like primary central nervous system lymphoma and primary effusion lymphoma.
  • T cell lymphomas are uncommon in these patients.
  • We report a rare case of subcutaneous panniculitis-like T cell lymphoma in a HIV positive patient who presented with multiple subcutaneous nodules.
  • [MeSH-major] CD8-Positive T-Lymphocytes / pathology. HIV Infections / complications. Lymphoma, T-Cell / diagnosis. Panniculitis / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Adipocytes / pathology. Adult. Cytoplasm / pathology. Diagnosis, Differential. Humans. Male. Risk Factors


59. Meyer J, Delay J, Bienzle D: Clinical, laboratory, and histopathologic features of equine lymphoma. Vet Pathol; 2006 Nov;43(6):914-24
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  • [Title] Clinical, laboratory, and histopathologic features of equine lymphoma.
  • Clinical, laboratory and tissue findings from 37 horses with lymphoma were investigated.
  • Tumor cell morphology was heterogeneous in 17 tumors, and 8 tumors had marked histiocytic and multinucleated giant cell infiltrates.
  • Extensive necrosis or focal fibrosis was present in 22 and 4 lymphomas, respectively.
  • Staining of tumor sections with antibodies against CD3 and CD79alpha molecules resulted in classification of T-cell (n = 26) or B-cell (n = 7) origin.
  • Most T-cell tumors comprised small to medium CD3(+) lymphocytes, whereas 5 of 7 B-cell tumors were infiltrated by numerous small T lymphocytes and classified as T-cell-rich B-cell lymphoma.
  • Fresh tumor cells from 6 horses bound antibodies reactive with equine CD4, CD5, CD8, CD21, or major histocompatibility class II molecules, confirming T-cell (n = 5) or B-cell origin (n = 1).
  • These findings suggest that T-cell lymphoma is more common than B-cell lymphoma in horses and that inflammation, possibly from tumor cytokine production, is frequent.
  • [MeSH-major] Horse Diseases / pathology. Lymphoma / veterinary

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  • (PMID = 17099148.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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60. Haddadin WJ: Malignant lymphoma in Jordan: a retrospective analysis of 347 cases according to the World Health Organization classification. Ann Saudi Med; 2005 Sep-Oct;25(5):398-403
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  • [Title] Malignant lymphoma in Jordan: a retrospective analysis of 347 cases according to the World Health Organization classification.
  • BACKGROUND: Most studies describing the subtypes of lymphoma in Jordan were carried out in the 1980s at a time when immunohistochemical facilities were unavailable.
  • Using a database established after immunohistochemical studies were introduced, we determined the frequency of the various types of nodal and extranodal lymphomas in the adult and paediatric Jordanian population.
  • We also assessed the incidence of bone marrow involvement at the initial presentation for each lymphoma type.
  • METHODS: A retrospective analysis of the histopathological subtypes of various lymphomas was conducted on all primary lymphoma cases diagnosed during a 3-year period between January 2001 and December 2003.
  • RESULTS: Of 347 patients included in the study, 78.4% had non-Hodgkin's lymphoma (NHL) and 21.6% had Hodgkin's lymphoma (HL).
  • In the NHL group, diffuse large B-cell lymphoma was the most common (28.2%) followed by follicular lymphoma (15.6%).
  • In the HL group, the nodular sclerosis variant was the most frequent (7.8%) followed by the mixed cellularity type (5.5%).
  • Of all the lymphoma cases, the highest incidence of marrow involvement was seen in patients with lymphoplasmacytic lymphoma.
  • Forty-nine patients were children (age <15 years) in whom Burkitt's lymphoma (15 cases) and HL (14 cases) were the commonest subtypes.
  • One-hundred six patients with primary extranodal lymphomas (ENL) accounted for 30.5% of all lymphomas.
  • Among the various lymphomas, diffuse large B-cell lymphoma is the most commonly encountered lymphoma in adults.
  • Burkitt's lymphoma and Hodgkin's disease are the most frequent childhood lymphomas, followed closely by lymphoblastic lymphoma.
  • [MeSH-major] Hodgkin Disease / epidemiology. Hodgkin Disease / pathology. Lymphoma, Non-Hodgkin / epidemiology. Lymphoma, Non-Hodgkin / pathology

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  • (PMID = 16270763.001).
  • [ISSN] 0256-4947
  • [Journal-full-title] Annals of Saudi medicine
  • [ISO-abbreviation] Ann Saudi Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Saudi Arabia
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61. Westphal D, Ledgerwood EC, Hibma MH, Fleming SB, Whelan EM, Mercer AA: A novel Bcl-2-like inhibitor of apoptosis is encoded by the parapoxvirus ORF virus. J Virol; 2007 Jul;81(13):7178-88
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  • [Title] A novel Bcl-2-like inhibitor of apoptosis is encoded by the parapoxvirus ORF virus.
  • Apoptotic cell death forms part of the host defense against virus infection.
  • We tested orf virus, a member of the poxvirus family, for the ability to inhibit apoptosis and found that orf virus-infected cells were fully resistant to UV-induced changes in cell morphology, caspase activation, and DNA fragmentation.
  • These features are comparable to the antiapoptotic properties of the mitochondrial regulator Bcl-2.
  • Furthermore, bioinformatic analyses revealed sequence and secondary-structure similarities to Bcl-2 family members, including characteristic residues of all four Bcl-2 homology domains.
  • Consistent with this, the viral protein inhibited the UV-induced activation of the proapoptotic Bcl-2 family members Bax and Bak.
  • ORFV125 is the first parapoxvirus apoptosis inhibitor to be identified, and we propose that it is a new antiapoptotic member of the Bcl-2 family.
  • [MeSH-minor] Apoptosis. Caspases / metabolism. DNA Fragmentation / radiation effects. Enzyme Activation / genetics. Enzyme Activation / radiation effects. HeLa Cells. Humans. JNK Mitogen-Activated Protein Kinases / metabolism. Mitochondria / metabolism. Protein Structure, Secondary. Protein Structure, Tertiary. Ultraviolet Rays. bcl-2 Homologous Antagonist-Killer Protein / genetics. bcl-2 Homologous Antagonist-Killer Protein / metabolism. bcl-2-Associated X Protein / genetics. bcl-2-Associated X Protein / metabolism

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  • [Cites] Cancer Res. 2000 May 15;60(10):2666-72 [10825139.001]
  • [Cites] J Virol. 2004 Jan;78(1):353-66 [14671117.001]
  • [Cites] J Gen Virol. 2000 Nov;81(Pt 11):2803-11 [11038395.001]
  • [Cites] Protein Sci. 2000 Dec;9(12):2528-34 [11206074.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Mar 13;98(6):3012-7 [11248023.001]
  • [Cites] Mol Biol Cell. 2002 May;13(5):1615-25 [12006657.001]
  • [Cites] Curr Opin Microbiol. 2002 Aug;5(4):395-402 [12160859.001]
  • [Cites] Genes Dev. 2002 Oct 1;16(19):2465-78 [12368257.001]
  • [Cites] J Gen Virol. 2000 Apr;81(Pt 4):1087-97 [10725436.001]
  • [Cites] J Virol. 2000 Apr;74(8):3815-31 [10729156.001]
  • [Cites] J Exp Med. 2000 May 1;191(9):1487-98 [10790424.001]
  • [Cites] Biochim Biophys Acta. 2004 Mar 1;1644(2-3):83-94 [14996493.001]
  • [Cites] Biochim Biophys Acta. 2004 Mar 1;1644(2-3):95-105 [14996494.001]
  • [Cites] J Virol. 2004 Jul;78(13):7097-111 [15194786.001]
  • [Cites] Science. 2004 Jul 30;305(5684):626-9 [15286356.001]
  • [Cites] Arch Virol. 1982;71(1):43-55 [6279055.001]
  • [Cites] Nucleic Acids Res. 1987 Sep 11;15(17):7192 [2821498.001]
  • [Cites] Arch Virol. 1988;101(3-4):255-9 [3178493.001]
  • [Cites] J Virol. 1994 Dec;68(12):7728-37 [7966562.001]
  • [Cites] Nature. 1996 May 23;381(6580):335-41 [8692274.001]
  • [Cites] Cell. 1996 Jul 12;86(1):147-57 [8689682.001]
  • [Cites] Science. 1997 Feb 14;275(5302):983-6 [9020082.001]
  • [Cites] Oncogene. 1997 Jan 30;14(4):405-14 [9053837.001]
  • [Cites] Virology. 1997 Mar 3;229(1):193-200 [9123861.001]
  • [Cites] Biochem J. 1998 Jan 1;329 ( Pt 1):95-9 [9405280.001]
  • [Cites] Virology. 1998 May 10;244(2):365-96 [9601507.001]
  • [Cites] Virus Genes. 1998;17(2):107-15 [9857983.001]
  • [Cites] Trends Microbiol. 1999 Apr;7(4):160-5 [10217831.001]
  • [Cites] Curr Opin Cell Biol. 2004 Dec;16(6):647-52 [15530776.001]
  • [Cites] J Virol. 2005 Jan;79(2):1084-98 [15613337.001]
  • [Cites] Bioinformatics. 2005 Apr 1;21(7):951-60 [15531603.001]
  • [Cites] Cancer Biol Ther. 2005 Feb;4(2):139-63 [15725726.001]
  • [Cites] Biochem J. 2005 Jul 1;389(Pt 1):83-9 [15727562.001]
  • [Cites] FEBS Lett. 2005 Jul 4;579(17):3503-7 [15949801.001]
  • [Cites] J Virol. 2005 Nov;79(22):14031-43 [16254338.001]
  • [Cites] Curr Opin Cell Biol. 2005 Dec;17(6):617-25 [16243507.001]
  • [Cites] J Virol. 2006 Feb;80(3):1140-51 [16414991.001]
  • [Cites] Virus Res. 2006 Mar;116(1-2):146-58 [16274827.001]
  • [Cites] Cell Death Differ. 2006 Sep;13(9):1423-33 [16676004.001]
  • [Cites] Cell Death Differ. 2006 Oct;13(10):1651-62 [16439990.001]
  • [Cites] J Biol Chem. 2006 Dec 22;281(51):39728-39 [17074758.001]
  • [Cites] Mol Cell. 2007 Mar 23;25(6):933-42 [17386268.001]
  • [Cites] Oncogene. 2000 May 4;19(19):2286-95 [10822379.001]
  • [Cites] J Cell Biol. 2003 Jan 6;160(1):53-64 [12515824.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Mar 4;100(5):2432-7 [12591950.001]
  • [Cites] Cell Death Differ. 2003 Jan;10 Suppl 1:S68-76 [12655348.001]
  • [Cites] EMBO J. 2003 Apr 1;22(7):1497-507 [12660157.001]
  • [Cites] Bioessays. 2003 Sep;25(9):888-96 [12938178.001]
  • [Cites] J Cell Biol. 2003 Sep 1;162(5):877-87 [12952938.001]
  • [Cites] Immunity. 2003 Sep;19(3):341-52 [14499110.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14345-50 [14610284.001]
  • [Cites] J Virol. 2004 Jan;78(1):168-77 [14671098.001]
  • [Cites] Trends Cell Biol. 2000 Sep;10(9):369-77 [10932094.001]
  • (PMID = 17475653.001).
  • [ISSN] 0022-538X
  • [Journal-full-title] Journal of virology
  • [ISO-abbreviation] J. Virol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Inhibitor of Apoptosis Proteins; 0 / Viral Proteins; 0 / bcl-2 Homologous Antagonist-Killer Protein; 0 / bcl-2-Associated X Protein; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC1933275
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62. Horning SJ, Younes A, Jain V, Kroll S, Lucas J, Podoloff D, Goris M: Efficacy and safety of tositumomab and iodine-131 tositumomab (Bexxar) in B-cell lymphoma, progressive after rituximab. J Clin Oncol; 2005 Feb 1;23(4):712-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy and safety of tositumomab and iodine-131 tositumomab (Bexxar) in B-cell lymphoma, progressive after rituximab.
  • PURPOSE: To determine overall response (OR) and complete response (CR) rates, response duration, progression-free (PFS) and overall survival and safety with the tositumomab and iodine-131 tositumomab ((131)I tositumomab) therapeutic regimen in patients with indolent, follicular large-cell, or transformed B-cell lymphoma, progressive after rituximab.
  • CONCLUSION: (131)I tositumomab is effective in CD20-positive lymphoma progressive after rituximab, with a 65% OR rate and median PFS of 24.5 months for responders.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Lymphoma, B-Cell / radiotherapy. Radioimmunotherapy

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  • (PMID = 15613695.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / iodine-131 anti-B1 antibody; 4F4X42SYQ6 / Rituximab
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63. Libra M, Gloghini A, Malaponte G, Gangemi P, De Re V, Cacopardo B, Spandidos DA, Nicoletti F, Stivala F, Zignego AL, Carbone A: Association of t(14;18) translocation with HCV infection in gastrointestinal MALT lymphomas. J Hepatol; 2008 Aug;49(2):170-4
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  • [Title] Association of t(14;18) translocation with HCV infection in gastrointestinal MALT lymphomas.
  • BACKGROUND/AIMS: The gastrointestinal tract is the most common site of mucosa-associated lymphoid tissue (MALT) lymphoma development.
  • Among the several genetic abnormalities involved in MALT development, the impact of t(14;18)-(IgH;Bcl-2) translocation has only been marginally analyzed.
  • To this end, a consecutive series of gastrointestinal MALT lymphomas were analyzed.
  • METHODS: t(14;18)-(IgH;Bcl-2) translocation, at the major break point region (MBR) and minor cluster region (mcr), were assessed by the polymerase chain reaction (PCR) in tumour DNA obtained from 40 consecutive gastrointestinal MALT lymphoma patients.
  • Interestingly, both lymphomas bearing t(14;18) translocation derived from patients with chronic HCV infection.
  • Nucleotide sequence analysis confirmed that Bcl-2 was joined to JH6 in both MALT lymphomas.
  • Moreover, the heavy chain gene combinations detected in both MALT lymphomas were those usually found in the HCV-associated lymphomas.
  • CONCLUSIONS: Our data support the notion that among gastrointestinal MALT lymphomas, t(14;18)-(IgH;Bcl-2) translocation clusters in HCV-positive patients sustaining the role of HCV infection in the lymphoma development.
  • [MeSH-major] Gastrointestinal Neoplasms / genetics. Genes, bcl-2 / genetics. Hepatitis C / complications. Immunoglobulin Heavy Chains / genetics. Lymphoma, B-Cell, Marginal Zone / genetics. Translocation, Genetic

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  • (PMID = 18538438.001).
  • [ISSN] 0168-8278
  • [Journal-full-title] Journal of hepatology
  • [ISO-abbreviation] J. Hepatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Immunoglobulin Heavy Chains
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64. Boffetta P, van der Hel O, Kricker A, Nieters A, de Sanjosé S, Maynadié M, Cocco PL, Staines A, Becker N, Font R, Mannetje A', Goumas C, Brennan P: Exposure to ultraviolet radiation and risk of malignant lymphoma and multiple myeloma--a multicentre European case-control study. Int J Epidemiol; 2008 Oct;37(5):1080-94
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  • [Title] Exposure to ultraviolet radiation and risk of malignant lymphoma and multiple myeloma--a multicentre European case-control study.
  • BACKGROUND: Three recent studies have reported a decreased risk of non-Hodgkin lymphoma (NHL) for high ultraviolet (UV) radiation exposure.
  • METHODS: We conducted a multicentre case-control study during 1998-2004 in France, Germany, Ireland, Italy and Spain, comprising 1518 cases of NHL, 268 cases of Hodgkin lymphoma, 242 cases of multiple myeloma and 2124 population or hospital controls.
  • RESULTS: The risk of Hodgkin and NHL was increased for increasing skin sensitivity to the sun [odds ratio (OR) for no suntan vs very brown 2.35, 95% CI 0.94-5.87 and 1.39, 95% CI 1.03-1.87, respectively].
  • The risk of diffuse large B-cell lymphoma was reduced for increasing adult personal (OR for highest vs lowest quartile of exposure in free days 0.62, 95% CI 0.44-0.87) and for occupational exposure to UV radiation (OR for highest vs lowest exposure tertile 0.63, 95% CI 0.37-1.04).
  • A protective effect was observed for use of sun lamps for diffuse large B-cell lymphoma (OR for 25+ times vs never 0.63, 95% CI 0.38-1.03).
  • CONCLUSIONS: The hypothesis of a protective effect of UV radiation on lymphoma is supported by our results.
  • [MeSH-major] Lymphoma / etiology. Multiple Myeloma / etiology. Neoplasms, Radiation-Induced. Ultraviolet Rays / adverse effects
  • [MeSH-minor] Adult. Case-Control Studies. Europe. European Continental Ancestry Group. Hodgkin Disease / etiology. Humans. Lymphoma, Large B-Cell, Diffuse / prevention & control. Lymphoma, Non-Hodgkin / etiology. Occupational Exposure. Odds Ratio. Risk. Skin Pigmentation. Sunburn / complications

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  • (PMID = 18511490.001).
  • [ISSN] 1464-3685
  • [Journal-full-title] International journal of epidemiology
  • [ISO-abbreviation] Int J Epidemiol
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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65. Chen L, Willis SN, Wei A, Smith BJ, Fletcher JI, Hinds MG, Colman PM, Day CL, Adams JM, Huang DC: Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function. Mol Cell; 2005 Feb 04;17(3):393-403
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  • [Title] Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function.
  • Apoptosis is initiated when Bcl-2 and its prosurvival relatives are engaged by proapoptotic BH3-only proteins via interaction of its BH3 domain with a groove on the Bcl-2-like proteins.
  • These interactions have been considered promiscuous, but our analysis of the affinity of eight BH3 peptides for five Bcl-2-like proteins has revealed that the interactions vary over 10,000-fold in affinity, and accordingly, only certain protein pairs associate inside cells.
  • Bad, however, bound tightly to Bcl-2, Bcl-xL, and Bcl-w but only weakly to A1 and not to Mcl-1.
  • [MeSH-major] Apoptosis / physiology. Cell Survival / physiology. Peptide Fragments / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] Amino Acid Sequence. Animals. Apoptosis Regulatory Proteins. Bcl-2-Like Protein 11. Binding, Competitive. Biosensing Techniques. Carrier Proteins / chemistry. Carrier Proteins / genetics. Carrier Proteins / metabolism. Genetic Complementation Test. Humans. In Vitro Techniques. Ligands. Membrane Proteins / chemistry. Membrane Proteins / genetics. Membrane Proteins / metabolism. Mice. Models, Biological. Models, Molecular. Molecular Sequence Data. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Protein Structure, Tertiary. Proteins / chemistry. Proteins / genetics. Proteins / metabolism. Recombinant Proteins / chemistry. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Sequence Homology, Amino Acid. bcl-X Protein


66. Sansonno D, Tucci FA, Lauletta G, De Re V, Montrone M, Troiani L, Sansonno L, Dammacco F: Hepatitis C virus productive infection in mononuclear cells from patients with cryoglobulinaemia. Clin Exp Immunol; 2007 Feb;147(2):241-8
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  • [Title] Hepatitis C virus productive infection in mononuclear cells from patients with cryoglobulinaemia.
  • HCV minus strand RNA, the viral replicative intermediate, was searched for by a polyA(+) tract strand-specific Tth-based reverse transcriptase-polymerase chain reaction (RT-PCR) in lymphoid cells of 46 patients with acute and chronic infection.
  • The HCV replicating form in lymphoid cells was associated strictly with mixed cryoglobulinaemia (MCG), in that it was found in six of 13 (46%) MCG patients, including two with B cell non-Hodgkin's lymphoma (NHL).
  • These results emphasize the direct role of the virus in the pathogenesis of MCG and support the contention that HCV is not specifically lymphotropic, its entry and replication in lymphoid cells being determined largely by selective interactions.
  • [MeSH-minor] Acute Disease. Adult. Aged. Bone Marrow Cells / virology. Female. Hepatitis C, Chronic / complications. Humans. Lymphoma, B-Cell / virology. Male. Middle Aged. RNA, Viral / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Virus Replication

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  • [Cites] J Viral Hepat. 2004 Jul;11(4):310-8 [15230853.001]
  • [Cites] Curr Top Microbiol Immunol. 2000;242:55-84 [10592656.001]
  • [Cites] Arch Virol. 1994;134(3-4):293-302 [7510473.001]
  • [Cites] Virology. 1994 Aug 1;202(2):606-14 [8030225.001]
  • [Cites] Blood. 1995 Sep 1;86(5):1887-92 [7655017.001]
  • [Cites] J Hepatol. 1995 Jun;22(6):696-9 [7560864.001]
  • [Cites] J Virol. 1995 Dec;69(12):8079-83 [7494326.001]
  • [Cites] Clin Exp Immunol. 1996 Mar;103(3):414-21 [8608640.001]
  • [Cites] J Clin Invest. 1996 Feb 1;97(3):845-51 [8609243.001]
  • [Cites] Blood. 1996 Dec 15;88(12):4638-45 [8977256.001]
  • [Cites] Blood. 1998 Nov 1;92(9):3328-37 [9787170.001]
  • [Cites] J Hepatol. 2005 Apr;42(4):491-8 [15763335.001]
  • [Cites] Science. 2005 Jul 22;309(5734):623-6 [15947137.001]
  • [Cites] J Virol. 2000 May;74(10):4824-30 [10775621.001]
  • [Cites] Hepatology. 2000 Aug;32(2):382-7 [10915746.001]
  • [Cites] Adv Virus Res. 2000;55:231-69 [11050944.001]
  • [Cites] Eur J Clin Invest. 2001 Jul;31(7):628-38 [11454019.001]
  • [Cites] Cell. 2002 Mar 8;108(5):717-25 [11893341.001]
  • [Cites] EMBO J. 2002 Oct 1;21(19):5017-25 [12356718.001]
  • [Cites] Blood. 2003 Jan 1;101(1):52-7 [12393733.001]
  • [Cites] J Virol. 2003 Mar;77(5):3007-19 [12584326.001]
  • [Cites] J Exp Med. 2003 Mar 3;197(5):633-42 [12615904.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 10;100(12):7271-6 [12761383.001]
  • [Cites] J Virol. 2003 Oct;77(19):10432-6 [12970428.001]
  • [Cites] Eur J Immunol. 2004 Jan;34(1):126-36 [14971038.001]
  • [Cites] Hepatology. 2005 Nov;42(5):1019-27 [16231354.001]
  • [Cites] J Hepatol. 2006 Feb;44(2):436-9 [16360233.001]
  • [Cites] J Virol. 2006 Feb;80(4):1734-41 [16439530.001]
  • [Cites] Gastroenterology. 2006 Apr;130(4):1107-16 [16618405.001]
  • [Cites] Clin Exp Immunol. 2006 Feb;143(2):288-96 [16412053.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12766-71 [10535997.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Mar 15;88(6):2451-5 [1848704.001]
  • (PMID = 17223964.001).
  • [ISSN] 0009-9104
  • [Journal-full-title] Clinical and experimental immunology
  • [ISO-abbreviation] Clin. Exp. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Viral
  • [Other-IDs] NLM/ PMC1810461
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67. Li B, Shi S, Qian W, Zhao L, Zhang D, Hou S, Zheng L, Dai J, Zhao J, Wang H, Guo Y: Development of novel tetravalent anti-CD20 antibodies with potent antitumor activity. Cancer Res; 2008 Apr 1;68(7):2400-8
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  • Despite the effectiveness of the anti-CD20 monoclonal antibody (mAb) Rituximab (C2B8) in the treatment of B-cell lymphoma, its efficacy remains variable and often modest.
  • Unfortunately, all the current anti-CD20 mAbs effective in CDC are relatively inactive in signaling cell death and vice versa.
  • TetraMcAbs, with a molecular mass only 25 kDa higher than native divalent antibodies (DiMcAb), were shown not only to be as effective in mediating CDC and antibody-dependent cellular cytotoxicity against B-lymphoma cells as DiMcAbs but also to have antiproliferative and apoptosis-inducing activity markedly superior to that of DiMcAbs.
  • Interestingly, whereas 2F2 and C2B8 were equally effective in inducing cell growth arrest and apoptosis, the functions of their tetravalent versions, 2F2(ScFvHL)(4)-Fc and C2B8(ScFvHL)(4)-Fc, were significantly different.
  • Immunotherapeutic studies further showed that 2F2(ScFvHL)(4)-Fc was far more effective in prolonging the survival of severe combined immunodeficient mice bearing systemic Daudi or Raji tumors than C2B8, 2F2, and C2B8(ScFvHL)(4)-Fc, suggesting that it might be a promising therapeutic agent for B-cell lymphoma.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD30 / immunology. Antineoplastic Agents / pharmacology. Burkitt Lymphoma / therapy. Lymphoma, B-Cell / therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Murine-Derived. CHO Cells. Cell Line, Tumor. Cricetinae. Cricetulus. Female. Humans. Lymphoma, T-Cell / immunology. Lymphoma, T-Cell / therapy. Mice. Mice, Inbred BALB C. Mice, Inbred ICR. Mice, SCID. Rituximab. Xenograft Model Antitumor Assays

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  • (PMID = 18381448.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD30; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
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68. Ci W, Polo JM, Melnick A: B-cell lymphoma 6 and the molecular pathogenesis of diffuse large B-cell lymphoma. Curr Opin Hematol; 2008 Jul;15(4):381-90
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  • [Title] B-cell lymphoma 6 and the molecular pathogenesis of diffuse large B-cell lymphoma.
  • PURPOSE OF REVIEW: The B-cell lymphoma 6 transcriptional repressor is the most commonly involved oncogene in B-cell lymphomas.
  • Sustained expression of B-cell lymphoma 6 causes malignant transformation of germinal center B cells.
  • Understanding the mechanism of action of B-cell lymphoma 6 is crucial for the study of how aberrant transcriptional programming leads to lymphomagenesis and development of targeted antilymphoma therapy.
  • RECENT FINDINGS: Identification of B-cell lymphoma 6 target genes indicates a critical role for B-cell lymphoma 6 in facilitating a state of physiological genomic instability required for germinal center B cells to undergo affinity maturation, and suggests its contribution to several additional cellular functions.
  • The discovery of several layers of counterregulatory mechanisms reveals how B cells can control and fine-tune the potentially lymphomagenic actions of B-cell lymphoma 6.
  • From the biochemical standpoint, B-cell lymphoma 6 can regulate distinct biological pathways through different cofactors.
  • This observation explains how the biological actions of B-cell lymphoma 6 can be physiologically controlled through separate mechanisms and affords the means for improved therapeutic targeting.
  • The fact that patients with B-cell lymphoma 6-dependent lymphoma can be identified on the basis of gene signatures suggests that therapeutic trials of B-cell lymphoma 6 inhibitors could be personalized to these individuals.
  • SUMMARY: B-cell lymphoma 6 plays a fundamental role in lymphomagenesis and is an excellent therapeutic target for development of improved antilymphoma therapeutic regimens.

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  • [Cites] Nature. 2004 Dec 2;432(7017):635-9 [15577913.001]
  • [Cites] Blood Cells Mol Dis. 2008 Jul-Aug;41(1):95-9 [18346918.001]
  • [Cites] Nat Med. 2004 Dec;10(12):1329-35 [15531890.001]
  • [Cites] J Immunol. 2005 Jan 1;174(1):205-14 [15611242.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):28-40 [15671525.001]
  • [Cites] Blood. 2005 Mar 1;105(5):1851-61 [15550490.001]
  • [Cites] Cancer Cell. 2005 May;7(5):445-55 [15894265.001]
  • [Cites] Nat Immunol. 2005 Oct;6(10):1054-60 [16142238.001]
  • [Cites] Mol Immunol. 2006 May;43(12):1965-71 [16423395.001]
  • [Cites] Oncogene. 2006 Apr 6;25(15):2223-33 [16331266.001]
  • [Cites] Mol Cell Biol. 2006 Sep;26(18):6880-9 [16943429.001]
  • [Cites] Oncogene. 2007 Jan 11;26(2):224-33 [16819511.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Cancer Invest. 2000;18(4):356-65 [10808372.001]
  • [Cites] Genes Dev. 2000 Jul 15;14(14):1810-23 [10898795.001]
  • [Cites] J Exp Med. 2000 Dec 18;192(12):1841-8 [11120780.001]
  • [Cites] Nat Immunol. 2000 Sep;1(3):214-20 [10973278.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):341-6 [11460166.001]
  • [Cites] Science. 2007 Jan 26;315(5811):528-31 [17185562.001]
  • [Cites] Mol Cell. 2003 Dec;12(6):1551-64 [14690607.001]
  • [Cites] Blood. 2004 Feb 15;103(4):1454-63 [14551142.001]
  • [Cites] J Immunol. 2004 Jul 15;173(2):1158-65 [15240705.001]
  • [Cites] Cell. 2004 Oct 1;119(1):75-86 [15454082.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 28;101(39):14198-203 [15375218.001]
  • [Cites] Blood. 1996 Jun 15;87(12):5257-68 [8652841.001]
  • [Cites] Science. 1997 Apr 25;276(5312):589-92 [9110977.001]
  • [Cites] Nat Genet. 1997 Jun;16(2):161-70 [9171827.001]
  • [Cites] Nature. 2007 Mar 1;446(7131):83-7 [17268470.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Feb 27;104(9):3207-12 [17360630.001]
  • [Cites] J Exp Med. 2007 Apr 16;204(4):819-30 [17403935.001]
  • [Cites] Mol Cell Proteomics. 2007 May;6(5):820-34 [17296600.001]
  • [Cites] Nat Immunol. 2007 Jul;8(7):705-14 [17558410.001]
  • [Cites] Oncogene. 2007 Aug 13;26(37):5439-49 [17694085.001]
  • [Cites] J Pathol. 2007 Sep;213(1):106-15 [17573669.001]
  • [Cites] Blood. 2007 Sep 15;110(6):2067-74 [17545502.001]
  • [Cites] Cancer Cell. 2007 Sep;12(3):280-92 [17785208.001]
  • [Cites] Nat Immunol. 2007 Oct;8(10):1132-9 [17828269.001]
  • [Cites] Eur J Cell Biol. 2007 Oct;86(10):581-9 [17651861.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2332-43 [17625604.001]
  • [Cites] Nat Genet. 2008 Jan;40(1):108-12 [18066064.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1515-23 [17951530.001]
  • [Cites] J Pathol. 2008 Mar;214(4):498-507 [18189332.001]
  • [Cites] Nature. 2008 Feb 14;451(7180):841-5 [18273020.001]
  • [Cites] Mol Cell. 2008 Feb 15;29(3):384-91 [18280243.001]
  • [Cites] Mol Cell Biol. 2008 Apr;28(7):2175-86 [18212045.001]
  • [Cites] Blood. 2008 Apr 1;111(7):3701-13 [18160665.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3361-9 [18451163.001]
  • [Cites] Leuk Lymphoma. 2008 May;49(5):874-82 [18452090.001]
  • [Cites] Blood. 2004 Dec 15;104(13):4088-96 [15331443.001]
  • (PMID = 18536578.001).
  • [ISSN] 1531-7048
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA104348-05; United States / NCI NIH HHS / CA / R01 CA104348; United States / NCI NIH HHS / CA / R01 CA104348-05
  • [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 / Proto-Oncogene Proteins c-bcl-6
  • [Number-of-references] 51
  • [Other-IDs] NLM/ NIHMS126312; NLM/ PMC2748732
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69. Sandrini S, Valerio F, Insalaco M: [Kidney transplantation and lymphomas]. G Ital Nefrol; 2010 Sep-Oct;27 Suppl 50:S46-50
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  • [Title] [Kidney transplantation and lymphomas].
  • [Transliterated title] Linfomi nel trapianto renale.
  • Post-transplant lymphoproliferative disease (PTLD) accounts for 30% of nonskin cancers after kidney transplants.
  • Diffuse large B-cell lymphoma is the most frequent form of PTLD.
  • Moreover, not only is it more frequent but also more serious than the early type because of the lower responsiveness to therapy.
  • Epstein-Barr virus (EVB) infection is one of the most important risk factors for this disease, along with the use of antilymphocyte agents, which should be avoided in EVB-negative patients.
  • During the first year after transplant, EBV-PCR monitoring can be helpful for the early diagnosis of EBV-associated PTLD, especially in children.
  • Chemotherapy becomes essential in relapsed or refractory disease, but it significantly increases the risk of life-threatening infections.
  • The mortality rate is around 50% 12 months after diagnosis, often due to the side effects of chemotherapy.
  • [MeSH-major] Kidney Transplantation / adverse effects. Lymphoma / etiology

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  • (PMID = 20922695.001).
  • [ISSN] 0393-5590
  • [Journal-full-title] Giornale italiano di nefrologia : organo ufficiale della Società italiana di nefrologia
  • [ISO-abbreviation] G Ital Nefrol
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Italy
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70. Dyer MJ, Akasaka T, Capasso M, Dusanjh P, Lee YF, Karran EL, Nagel I, Vater I, Cario G, Siebert R: Immunoglobulin heavy chain locus chromosomal translocations in B-cell precursor acute lymphoblastic leukemia: rare clinical curios or potent genetic drivers? Blood; 2010 Feb 25;115(8):1490-9
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  • [Title] Immunoglobulin heavy chain locus chromosomal translocations in B-cell precursor acute lymphoblastic leukemia: rare clinical curios or potent genetic drivers?
  • Chromosomal translocations involving the immunoglobulin heavy chain (IGH) locus define common subgroups of B-cell lymphoma but are rare in B-cell precursor acute lymphoblastic leukemia (BCP-ALL).
  • Recent fluorescent in situ hybridization and molecular cloning studies have identified several novel IGH translocations involving genes that play important roles in normal hemopoiesis, including the cytokine receptor genes CRLF2 and EPOR, all members of the CCAAT enhancer-binding protein gene family, as well as genes not normally expressed in hemopoietic cells including inhibitor of DNA binding 4.
  • The possible clinical importance of many of the various IGH translocations in BCP-ALL remains to be determined from prospective studies, but CRLF2 expression is associated with a poor prognosis.
  • Despite their rarity, IGH chromosomal translocations in BCP-ALL therefore define not only new mechanisms of B-cell transformation but also clinically important subgroups of disease and suggest new targeted therapeutic approaches.
  • [MeSH-major] B-Lymphocytes / metabolism. Cell Transformation, Neoplastic / metabolism. Immunoglobulin Heavy Chains / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Quantitative Trait Loci. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Animals. Core Binding Factor Alpha 2 Subunit / biosynthesis. Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Leukemic / genetics. Hematopoiesis / genetics. Humans. Inhibitor of Differentiation Proteins / biosynthesis. Inhibitor of Differentiation Proteins / genetics. Oncogene Proteins, Fusion / biosynthesis. Oncogene Proteins, Fusion / genetics. Prognosis. Receptors, Cytokine / biosynthesis. Receptors, Cytokine / genetics. Receptors, Erythropoietin / biosynthesis. Receptors, Erythropoietin / genetics

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  • (PMID = 20042721.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670597
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CRLF2 protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / ID4 protein, human; 0 / Immunoglobulin Heavy Chains; 0 / Inhibitor of Differentiation Proteins; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Cytokine; 0 / Receptors, Erythropoietin; 0 / TEL-AML1 fusion protein
  • [Number-of-references] 87
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71. Hatzimichael E, Dasoula A, Shah R, Syed N, Papoudou-Bai A, Coley HM, Dranitsaris G, Bourantas KL, Stebbing J, Crook T: The prolyl-hydroxylase EGLN3 and not EGLN1 is inactivated by methylation in plasma cell neoplasia. Eur J Haematol; 2010 Jan 1;84(1):47-51
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  • [Title] The prolyl-hydroxylase EGLN3 and not EGLN1 is inactivated by methylation in plasma cell neoplasia.
  • EGLN3 also has pro-apoptotic activity in some cell types.
  • Analyses of a well-characterised series of cases of plasma cell dyscrasias, including multiple myeloma (MM), Waldenström's macroglobulinaemia (WM) and monoclonal gammopathy of undetermined significance (MGUS) surprisingly demonstrated that the CpG island of EGLN3, and not EGLN1, is frequently methylated in these disorders.
  • Multiple myeloma patients with a methylated EGLN3 promoter showed trends towards an increased risk of death, bone lytic lesions, anaemia, advanced stage of disease and the presence of extramedullary disease.
  • These data suggest that the prolyl-hydroxylases may be a novel class of potential tumour suppressors in plasma cell neoplasia that warrant further investigation with regard to their potential utility as biomarkers.
  • Moreover, we observed that EGLN3 is also methylated at high frequency in B-cell lymphoma subtypes, implying that loss of EGLN3 is an important epigenetic event not only in plasma cell neoplasias but also in B-cell neoplasias.
  • [MeSH-minor] Aged. Cell Line, Tumor / enzymology. DNA, Neoplasm / genetics. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Hypoxia-Inducible Factor-Proline Dioxygenases. Lymphoma, B-Cell / classification. Lymphoma, B-Cell / enzymology. Lymphoma, B-Cell / genetics. Male. Middle Aged. Monoclonal Gammopathy of Undetermined Significance / enzymology. Monoclonal Gammopathy of Undetermined Significance / genetics. Multiple Myeloma / complications. Multiple Myeloma / enzymology. Multiple Myeloma / genetics. Multiple Myeloma / mortality. Waldenstrom Macroglobulinemia / enzymology. Waldenstrom Macroglobulinemia / genetics

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  • (PMID = 19737309.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; EC 1.13.11.- / Dioxygenases; EC 1.14.11.2 / EGLN1 protein, human; EC 1.14.11.2 / Procollagen-Proline Dioxygenase; EC 1.14.11.29 / EGLN3 protein, human; EC 1.14.11.29 / Hypoxia-Inducible Factor-Proline Dioxygenases
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72. Maddocks-Christianson K, Slager SL, Zent CS, Reinalda M, Call TG, Habermann TM, Bowen DA, Hoyer JD, Schwager S, Jelinek DF, Kay NE, Shanafelt TD: Risk factors for development of a second lymphoid malignancy in patients with chronic lymphocytic leukaemia. Br J Haematol; 2007 Nov;139(3):398-404
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  • [Title] Risk factors for development of a second lymphoid malignancy in patients with chronic lymphocytic leukaemia.
  • Previous studies suggested that patients with chronic lymphocytic leukaemia (CLL) are at a three- to fivefold increased risk of developing a second lymphoproliferative disorder (LPD).
  • Diffuse large B-cell lymphoma was the most common subtype of secondary LPD (12 of 26 cases).
  • Physicians should strictly adhere to established criteria to initiate treatment for CLL patients who are not participating in clinical trials.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Lymphoma / etiology. Neoplasms, Second Primary / etiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / adverse effects. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Purine Nucleotides / adverse effects. Risk Factors. Vidarabine / adverse effects. Vidarabine / analogs & derivatives

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  • (PMID = 17910629.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 113408; United States / NCI NIH HHS / CA / CA 94919; United States / NCI NIH HHS / CA / CA 97274
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Purine Nucleotides; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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73. McCaw DL, Chan AS, Stegner AL, Mooney B, Bryan JN, Turnquist SE, Henry CJ, Alexander H, Alexander S: Proteomics of canine lymphoma identifies potential cancer-specific protein markers. Clin Cancer Res; 2007 Apr 15;13(8):2496-503
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  • [Title] Proteomics of canine lymphoma identifies potential cancer-specific protein markers.
  • PURPOSE: Early diagnosis of cancer is crucial for the success of treatment of the disease, and there is a need for markers whose differential expression between disease and normal tissue could be used as a diagnostic tool.
  • Lymphoma, one of the most common neoplasms in dogs, is similar to human non-Hodgkin's lymphoma and could serve as an experimental model system.
  • EXPERIMENTAL DESIGN: Thirteen lymph nodes from normal dogs and 11 lymph nodes from dogs with B-cell lymphoma were subjected to proteomic analysis using two-dimensional PAGE separation and matrix-assisted laser desorption/ionization time-of-flight analysis.
  • Of these, prolidase (proline dipeptidase), triosephosphate isomerase, and glutathione S-transferase were down-regulated in lymphoma samples, whereas macrophage capping protein was up-regulated in the lymphoma samples.
  • CONCLUSIONS: These proteins represent potential markers for the diagnosis of lymphoma and should be further investigated in human samples for validation of their utility as diagnostic markers.
  • [MeSH-major] Biomarkers, Tumor / analysis. Dog Diseases / pathology. Lymphoma / veterinary. Neoplasm Proteins / analysis. Proteomics

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  • (PMID = 17438110.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / GM53929
  • [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 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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74. Kurkus J, Nilsson R, Lindén O, Schönström N, Sandberg BE, Tennvall J: Biocompatibility of a novel avidin-agarose adsorbent for extracorporeal removal of redundant radiopharmaceutical from the blood. Artif Organs; 2007 Mar;31(3):208-14
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  • The use of monoclonal antibodies (MAbs) in cytotoxic conjugates (radionuclides, toxins, or drugs) for targeting tumor cells is restricted due to toxicity in vital organs.
  • Through improved tumor targeting, it is possible to administer larger amounts of such labeled MAbs, thus improving the ability to eradicate tumor cells without increased normal organ toxicity.
  • During ECAT, excess radioimmunoconjugates, not bound to the tumor cells, can be removed improving tumor targeting.
  • Seven patients with B-cell lymphoma not responding to conventional treatment were studied.
  • The AA adsorbent had no effect on the blood cells, immunological status or P-bradykinin level.
  • [MeSH-major] Avidin / therapeutic use. Extracorporeal Circulation / instrumentation. Hemoperfusion / methods. Lymphoma, B-Cell / radiotherapy. Radioimmunotherapy / methods. Sepharose / therapeutic use

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  • (PMID = 17343696.001).
  • [ISSN] 0160-564X
  • [Journal-full-title] Artificial organs
  • [ISO-abbreviation] Artif Organs
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Radioisotopes; 0 / avidin-agarose; 1405-69-2 / Avidin; 9012-36-6 / Sepharose
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75. Stathis A, Chini C, Bertoni F, Proserpio I, Capella C, Mazzucchelli L, Pedrinis E, Cavalli F, Pinotti G, Zucca E: Long-term outcome following Helicobacter pylori eradication in a retrospective study of 105 patients with localized gastric marginal zone B-cell lymphoma of MALT type. Ann Oncol; 2009 Jun;20(6):1086-93
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  • [Title] Long-term outcome following Helicobacter pylori eradication in a retrospective study of 105 patients with localized gastric marginal zone B-cell lymphoma of MALT type.
  • BACKGROUND: Treatment aimed at eradicating Helicobacter pylori infection results in lymphoma remission in most localized gastric mucosa-associated lymphoid tissue (MALT) lymphomas.
  • METHODS: One hundred and five patients with localized gastric MALT lymphoma were initially treated only with H. pylori eradication regimens.
  • Lymphoma responses were graded using the Wotherspoon score.
  • Histological regression of the lymphoma was achieved in 78 of 102 assessable patients [76%, 95% confidence interval (CI): 67% to 84%] with complete remission (score 0-2) in 66 and partial remission (score 3) in 12.
  • At a median follow-up time of 6.3 years, histological remission was consistently confirmed in 33 of 74 assessable patients, while 25 had score fluctuations (from 0 to 4) and 13 presented a lymphoma relapse (score 5).
  • Transformation to a large-cell lymphoma was seen in two cases.
  • Only one patient died of lymphoma after transformation to a high-grade lymphoma.
  • CONCLUSIONS: Helicobacter pylori eradication resulted in complete lymphoma remission in the majority of cases.
  • Long-term clinical disease control was achieved in most patients.
  • A watch and wait policy appears to be safe in patients with minimal residual disease or histological-only local relapse.


76. Nemet AY, Deckel Y, Kourt G: Orbital invasion of frontal sinus lymphoma. Orbit; 2006 Jun;25(2):149-51
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  • [Title] Orbital invasion of frontal sinus lymphoma.
  • Paranasal sinus lymphoma is an uncommon malignancy and is often difficult to diagnose.
  • Early diagnosis is essential for effective treatment.
  • Ophthalmological symptoms and signs occur early in the disease process due to the close proximity of the orbit to the paranasal sinuses.
  • We report a case of frontal sinus lymphoma that presented as a superior-nasal orbital mass in an 84 year old man.
  • Histology revealed diffuse large B cell non Hodgkin's lymphoma.
  • [MeSH-major] Frontal Sinus / pathology. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Orbit / pathology. Paranasal Sinus Neoplasms / pathology
  • [MeSH-minor] Aged, 80 and over. Humans. Male. Neoplasm Invasiveness

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  • (PMID = 16754228.001).
  • [ISSN] 0167-6830
  • [Journal-full-title] Orbit (Amsterdam, Netherlands)
  • [ISO-abbreviation] Orbit
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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77. Kim SK, Chan CC, Wallace DJ: Management of primary intraocular lymphoma. Curr Oncol Rep; 2005 Jan;7(1):74-9
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  • [Title] Management of primary intraocular lymphoma.
  • Primary intraocular lymphoma (PIOL) is a subset of primary central nervous system lymphoma (PCNSL) in which malignant lymphoid cells invade the retina, vitreous body, or optic nerve head.
  • It is usually a large B-cell non-Hodgkin's lymphoma.
  • Diagnosis of PIOL requires pathologic confirmation of malignant cells in specimens of the cerebrospinal fluid, vitreous, or chorioretinal biopsies.
  • However, several new developments for PIOL with central nervous system involvement have been reported, including intrathecal therapy and autologous stem-cell transplantation.
  • In addition, intravitreal methotrexate has been successful in the treatment of isolated recurrent ocular disease.
  • [MeSH-major] Eye Neoplasms / diagnosis. Eye Neoplasms / therapy. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / therapy. Medical Oncology / methods
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Clinical Trials as Topic. Combined Modality Therapy / methods. Humans. Methotrexate / therapeutic use. Radiotherapy / methods. Recurrence. Retina / pathology. Stem Cell Transplantation. Treatment Outcome

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  • [Cites] Surv Ophthalmol. 2001 May-Jun;45(6):463-71 [11425352.001]
  • [Cites] Br J Haematol. 2004 Jul;126(2):202-8 [15238140.001]
  • [Cites] Ophthalmology. 2001 Mar;108(3):426-7 [11237883.001]
  • [Cites] Oncology (Williston Park). 2000 Feb;14(2):228-34; discussion 237-42, 244 [10736810.001]
  • [Cites] Cancer. 1993 Aug 1;72(3):843-9 [8334638.001]
  • [Cites] Cancer Control. 2004 Sep-Oct;11(5):285-95 [15377987.001]
  • [Cites] Ophthalmology. 1988 May;95(5):625-30 [3050698.001]
  • [Cites] J Neurooncol. 1999 Jul;43(3):199-201 [10563423.001]
  • [Cites] N Engl J Med. 2001 Jan 11;344(2):114-23 [11150363.001]
  • [Cites] Ocul Immunol Inflamm. 2000 Dec;8(4):243-50 [11262654.001]
  • [Cites] J Clin Oncol. 1992 Apr;10(4):635-43 [1548527.001]
  • [Cites] Ophthalmology. 2003 Aug;110(8):1671-2 [12917196.001]
  • [Cites] Am J Ophthalmol. 1995 Nov;120(5):671-3 [7485372.001]
  • [Cites] Haematologica. 2004 Jun;89(6):753-4 [15194546.001]
  • [Cites] Cancer. 1989 May 15;63(10):1918-21 [2702565.001]
  • [Cites] Onkologie. 2003 Aug;26(4):351-4 [12972702.001]
  • [Cites] J Neurooncol. 1999 Jul;43(3):249-57 [10563431.001]
  • [Cites] J Clin Oncol. 1999 Apr;17(4):1329 [10561199.001]
  • [Cites] Retina. 2002 Feb;22(1):37-43 [11884876.001]
  • [Cites] Trans Am Ophthalmol Soc. 2003;101:275-92 [14971583.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1992;23(1):9-17 [1572835.001]
  • [Cites] Surv Ophthalmol. 1979 Mar-Apr;23(5):279-96 [380030.001]
  • [Cites] Ophthalmology. 1987 Dec;94(12):1631-9 [3323986.001]
  • [Cites] J Clin Oncol. 1998 Mar;16(3):864-71 [9508167.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):711-5 [12576439.001]
  • [Cites] Arch Ophthalmol. 2001 Oct;119(10):1518-24 [11594954.001]
  • [Cites] Eye (Lond). 2003 May;17(4):513-21 [12802353.001]
  • [Cites] Ophthalmology. 2002 Sep;109(9):1709-16 [12208721.001]
  • [Cites] Br J Ophthalmol. 1999 Apr;83(4):448-51 [10434868.001]
  • [Cites] J Clin Oncol. 2002 Dec 15;20(24):4643-8 [12488408.001]
  • [Cites] J Clin Oncol. 2001 Feb 1;19(3):742-9 [11157026.001]
  • [Cites] Arch Ophthalmol. 1997 Sep;115(9):1157-60 [9298057.001]
  • [Cites] Retina. 1995;15(2):125-9 [7624599.001]
  • [Cites] Cancer. 1980 Feb 15;45(4):688-92 [6766795.001]
  • [Cites] Ann Oncol. 2004 Jan;15(1):129-33 [14679132.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1995 Oct 15;33(3):663-73 [7558957.001]
  • [Cites] J Clin Oncol. 2003 Mar 15;21(6):1044-9 [12637469.001]
  • [Cites] Curr Opin Ophthalmol. 2002 Dec;13(6):411-8 [12441846.001]
  • [Cites] Curr Opin Oncol. 2001 May;13(3):137-42 [11307054.001]
  • [Cites] Clin Lymphoma. 2003 Jun;4(1):22-9 [12837150.001]
  • [Cites] Blood. 2003 Jan 15;101(2):466-8 [12393404.001]
  • [Cites] Am J Ophthalmol. 1996 Apr;121(4):442-4 [8604740.001]
  • [Cites] Cancer. 1986 Apr 1;57(7):1273-5 [2418934.001]
  • [Cites] Ophthalmology. 1993 Sep;100(9):1399-406 [8371930.001]
  • [Cites] J Clin Oncol. 1998 Mar;16(3):859-63 [9508166.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Jun 1;41(3):615-20 [9635710.001]
  • [Cites] Ann Oncol. 2002 Apr;13(4):531-8 [12056702.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Dec;44(12):5235-41 [14638722.001]
  • [Cites] Ophthalmology. 2003 Jun;110(6):1241-4 [12799254.001]
  • [Cites] Arch Ophthalmol. 1997 Sep;115(9):1152-6 [9298056.001]
  • [Cites] J Clin Oncol. 2003 Nov 15;21(22):4151-6 [14615443.001]
  • (PMID = 15610690.001).
  • [ISSN] 1534-6269
  • [Journal-full-title] Current oncology reports
  • [ISO-abbreviation] Curr Oncol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; YL5FZ2Y5U1 / Methotrexate
  • [Number-of-references] 51
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78. Walls KC, Ghosh AP, Ballestas ME, Klocke BJ, Roth KA: bcl-2/Adenovirus E1B 19-kd interacting protein 3 (BNIP3) regulates hypoxia-induced neural precursor cell death. J Neuropathol Exp Neurol; 2009 Dec;68(12):1326-38
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  • [Title] bcl-2/Adenovirus E1B 19-kd interacting protein 3 (BNIP3) regulates hypoxia-induced neural precursor cell death.
  • In addition to producing neuron death, HI causes death of neural precursor cells (NPCs) in the developing brain.
  • To characterize the molecular pathways that regulate hypoxia-induced death of NPCs, we treated a mouse neural stem cell line (C17.2 cells) and fibroblastic growth factor II-expanded primary NPCs derived from wild-type or gene-disrupted mice, with oxygen glucose deprivation or the hypoxia mimetics desferrioxamine or cobalt chloride.
  • Neural precursor cells undergoing hypoxia exhibited time- and concentration-dependent caspase-3 activation and cell death, which was significantly reduced by treatment with a broad caspase inhibitor or protein synthesis inhibition.
  • Oxygen glucose deprivation or hypoxia-mimetic exposure also resulted in increased hypoxia-inducible factor alpha and bcl-2/adenovirus E1B 19-kd interacting protein 3 (BNIP3) expression.
  • BNIP3 shRNA treatment failed to affect hypoxia-induced caspase-3 activation but inhibited cell death and nuclear translocation of apoptosis-inducing factor, indicating that BNIP3 is an important regulator of caspase-independent NPC death after hypoxia.
  • These studies demonstrate that hypoxia activates both caspase-dependent and -independent NPC death pathways that are critically regulated by multiple Bcl-2 family members.

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  • [Cites] J Biol Chem. 1999 Nov 12;274(46):32631-7 [10551817.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2008 Nov;295(5):H2025-31 [18790835.001]
  • [Cites] Mol Cell Biol. 2000 Aug;20(15):5454-68 [10891486.001]
  • [Cites] FEBS Lett. 2001 Feb 23;491(1-2):85-90 [11226425.001]
  • [Cites] Science. 2001 Apr 20;292(5516):464-8 [11292862.001]
  • [Cites] Science. 2001 Apr 20;292(5516):468-72 [11292861.001]
  • [Cites] EMBO Rep. 2001 Jul;2(7):615-20 [11454738.001]
  • [Cites] Cell. 2001 Oct 5;107(1):43-54 [11595184.001]
  • [Cites] Science. 2004 Feb 13;303(5660):1010-4 [14963330.001]
  • [Cites] Biochim Biophys Acta. 2004 Mar 1;1644(2-3):189-203 [14996503.001]
  • [Cites] Cancer Res. 2004 Jun 15;64(12):4286-93 [15205343.001]
  • [Cites] Anat Embryol (Berl). 1990;181(3):195-213 [2186664.001]
  • [Cites] Cell. 1992 Jan 10;68(1):33-51 [1732063.001]
  • [Cites] Science. 1995 Oct 6;270(5233):96-9 [7569956.001]
  • [Cites] Nature. 1998 Mar 26;392(6674):405-8 [9537326.001]
  • [Cites] J Biol Chem. 1999 Jan 1;274(1):7-10 [9867803.001]
  • [Cites] Cancer Cell. 2004 Dec;6(6):597-609 [15607964.001]
  • [Cites] Neuroscience. 2005;131(1):55-65 [15680691.001]
  • [Cites] Oncogene. 2005 Feb 3;24(6):980-91 [15592527.001]
  • [Cites] FASEB J. 2005 Aug;19(10):1308-10 [15941769.001]
  • [Cites] Cell. 2005 Sep 23;122(6):927-39 [16179260.001]
  • [Cites] Apoptosis. 2006 Jan;11(1):67-77 [16374551.001]
  • [Cites] Cell Death Differ. 2006 Oct;13(10):1727-39 [16514420.001]
  • [Cites] J Neuropathol Exp Neurol. 2007 Jan;66(1):66-74 [17204938.001]
  • [Cites] Cell Death Differ. 2007 Apr;14(4):775-84 [17039248.001]
  • [Cites] Cell Biochem Biophys. 2007;47(1):11-20 [17406056.001]
  • [Cites] Stroke. 2007 May;38(5):1606-13 [17379825.001]
  • [Cites] Free Radic Biol Med. 2007 Jul 1;43(1):117-27 [17561100.001]
  • [Cites] Biochem J. 2007 Aug 1;405(3):407-15 [17447897.001]
  • [Cites] J Exp Med. 2007 Aug 6;204(8):1741-8 [17635954.001]
  • [Cites] Mol Cell Biol. 2007 Sep;27(17):6229-42 [17576813.001]
  • [Cites] J Clin Invest. 2007 Oct;117(10):2825-33 [17909626.001]
  • [Cites] Autophagy. 2007 Nov-Dec;3(6):616-9 [17786027.001]
  • [Cites] J Neurochem. 2007 Nov;103(3):1121-31 [17711427.001]
  • [Cites] Autophagy. 2008 Feb;4(2):195-204 [18059169.001]
  • [Cites] J Biol Chem. 2008 Apr 18;283(16):10892-903 [18281291.001]
  • [Cites] FASEB J. 2008 Aug;22(8):2662-75 [18375543.001]
  • [Cites] J Biol Chem. 2000 Jan 14;275(2):1439-48 [10625696.001]
  • (PMID = 19915483.001).
  • [ISSN] 1554-6578
  • [Journal-full-title] Journal of neuropathology and experimental neurology
  • [ISO-abbreviation] J. Neuropathol. Exp. Neurol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / P30 NS047466; United States / NINDS NIH HHS / NS / NS047466-05; United States / NINDS NIH HHS / NS / R01 NS035107-11; United States / NINDS NIH HHS / NS / R01 NS041962; United States / NINDS NIH HHS / NS / P30 NS057098; United States / NINDS NIH HHS / NS / P30 NS047466-05; United States / NINDS NIH HHS / NS / R01 NS041962-06; United States / NINDS NIH HHS / NS / NS57098; United States / NINDS NIH HHS / NS / R01 NS035107; United States / NINDS NIH HHS / NS / NS057098-04; United States / NINDS NIH HHS / NS / NS35107; United States / NINDS NIH HHS / NS / NS035107-11; United States / NINDS NIH HHS / NS / NS47466; United States / NINDS NIH HHS / NS / NS41962; United States / NINDS NIH HHS / NS / NS041962-06; United States / NINDS NIH HHS / NS / P30 NS057098-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BNip3 protein, mouse; 0 / Enzyme Inhibitors; 0 / Membrane Proteins; 0 / Mitochondrial Proteins; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ NIHMS161285; NLM/ PMC2791349
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79. Henrich M, Hecht W, Weiss AT, Reinacher M: A new subgroup of immunoglobulin heavy chain variable region genes for the assessment of clonality in feline B-cell lymphomas. Vet Immunol Immunopathol; 2009 Jul 15;130(1-2):59-69
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  • [Title] A new subgroup of immunoglobulin heavy chain variable region genes for the assessment of clonality in feline B-cell lymphomas.
  • In human medicine, PCR-amplification of the complementarity determining region 3 of the immunoglobulin heavy chain genes followed by polyacrylamide gel electrophoresis (PAGE) is an accepted method to assess clonality in B-cell lymphomas and thereby facilitates the differentiation of neoplasias from benign hyperplasias or reactive infiltrates.
  • To generate a basis for the development of a PCR-based assay for the assessment of clonality in feline B-cell lymphomas we analyzed 28 transcripts (cDNA) of the feline immunoglobulin heavy chain variable region genes (IGHV).
  • With these four sets of primers, the assay was able to detect monoclonality in 7/10 (70%) cats with histologically and immunohistochemically diagnosed B-cell lymphomas.
  • The use of a PCR-based assay in combination with standard techniques for the diagnosis of feline lymphoma is helpful and the characterization of the additional subgroup of feline variable regions genes puts this assay on a broader basis.
  • [MeSH-major] Cat Diseases / immunology. Cat Diseases / pathology. Immunoglobulin Heavy Chains / genetics. Immunoglobulin Variable Region / genetics. Lymphoma, B-Cell / veterinary
  • [MeSH-minor] Amino Acid Sequence. Animals. Cats. Clone Cells. Molecular Sequence Data. Plasmids / genetics. RNA, Neoplasm / chemistry. RNA, Neoplasm / genetics. Random Amplified Polymorphic DNA Technique / veterinary. Sequence Alignment. Sequence Analysis, DNA

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  • (PMID = 19243841.001).
  • [ISSN] 1873-2534
  • [Journal-full-title] Veterinary immunology and immunopathology
  • [ISO-abbreviation] Vet. Immunol. Immunopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / RNA, Neoplasm
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80. Ye BS, Sunwoo IN, Suh BC, Park JP, Shim DS, Kim SM: Diffuse large B-cell lymphoma presenting as piriformis syndrome. Muscle Nerve; 2010 Mar;41(3):419-22
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  • [Title] Diffuse large B-cell lymphoma presenting as piriformis syndrome.
  • A diagnosis of diffuse large B-cell lymphoma with neurolymphomatosis (NL) was made.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Large B-Cell, Diffuse / complications. Lymphoma, Large B-Cell, Diffuse / diagnosis. Piriformis Muscle Syndrome / etiology. Sciatica / etiology
  • [MeSH-minor] Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Cyclophosphamide / administration & dosage. Disease-Free Survival. Doxorubicin / administration & dosage. Humans. Magnetic Resonance Imaging. Male. Neural Conduction / physiology. Rituximab. Treatment Outcome. Vincristine / administration & dosage

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  • (PMID = 19918770.001).
  • [ISSN] 1097-4598
  • [Journal-full-title] Muscle & nerve
  • [ISO-abbreviation] Muscle Nerve
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide
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81. García JF, Mollejo M, Fraga M, Forteza J, Muniesa JA, Pérez-Guillermo M, Pérez-Seoane C, Rivera T, Ortega P, Piris MA: Large B-cell lymphoma with Hodgkin's features. Histopathology; 2005 Jul;47(1):101-10
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  • [Title] Large B-cell lymphoma with Hodgkin's features.
  • AIMS: To describe the features of a series of nine cases of diffuse large B-cell lymphoma (DLBCL) showing morphological and immunophenotypic features that are intermediate with Hodgkin's lymphoma (HL).
  • Histopathologically, tumours showed diffuse large cell areas in a polymorphous background, with pleomorphic cytology and the common presence of Hodgkin's and Reed-Sternberg cells.
  • Immunophenotypically, tumours shared features of DLBCL and classical HL, with expression of CD30, CD15 (6/9), and a full B-cell profile including CD45RB, CD20, CD79a and OCT2.
  • CONCLUSIONS: These findings suggest that DLBCLs with HL features constitute a distinctive subgroup of aggressive lymphomas whose neoplastic growth and peculiar characteristics could be facilitated by a particular microenvironment found in the mediastinum.
  • [MeSH-major] Hodgkin Disease / pathology. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Adult. Aged. Antigens, CD / analysis. DNA-Binding Proteins / analysis. DNA-Binding Proteins / genetics. Diagnosis, Differential. Female. Gene Rearrangement. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Ki-67 Antigen / analysis. Male. Middle Aged. Mutation. Neoplasm Staging. Proto-Oncogene Proteins / analysis. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins c-bcl-2 / analysis. Proto-Oncogene Proteins c-bcl-6. Transcription Factors / analysis. Transcription Factors / genetics. Tumor Suppressor Protein p53 / analysis. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 15982329.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-bcl-6; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53
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82. Tsukahara S, Yamamoto S, Tin-Tin-Win-Shwe, Ahmed S, Kunugita N, Arashidani K, Fujimaki H: Inhalation of low-level formaldehyde increases the Bcl-2/Bax expression ratio in the hippocampus of immunologically sensitized mice. Neuroimmunomodulation; 2006;13(2):63-8
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  • [Title] Inhalation of low-level formaldehyde increases the Bcl-2/Bax expression ratio in the hippocampus of immunologically sensitized mice.
  • In the present study, we examined the effects of FA on apoptotic mechanisms regulating survival and death of cells and on N-methyl-D-aspartate (NMDA) receptors related to hippocampal functions in the mouse hippocampus.
  • METHODS: Western blot analyses were performed for Bcl-2, Bax and NMDA receptor subtypes 2A and 2B of the hippocampus taken from C3H mice exposed to 0 or 400 ppb of FA with or without ovalbumin (OVA) immunization.
  • RESULTS: The ratio of Bcl-2 to Bax expression levels significantly increased with 400-ppb FA exposure in OVA-immunized mice but not in mice without OVA immunization, although differences in each protein level were not significant among groups.
  • Active caspase- 3-immunoreactive cells were found in the hippocampus.
  • NMDA receptor type 2A and 2B expression levels of FA-exposed mice were sustained at comparative levels with those for the control mice with or without OVA immunization.
  • CONCLUSIONS: These results indicate that changes in the Bcl-2/Bax expression ratio, which occurs with low-level FA exposure and immunization and may follow enhancement of nerve growth factor production, exerts a protective effect against cell death by apoptosis.
  • [MeSH-minor] Animals. Caspase 3 / drug effects. Caspase 3 / metabolism. Cell Survival / drug effects. Cell Survival / immunology. Female. Immunization. Mice. Mice, Inbred C3H. Neurotoxins / toxicity. Ovalbumin / immunology. Proto-Oncogene Proteins c-bcl-2 / drug effects. Proto-Oncogene Proteins c-bcl-2 / metabolism. Receptors, N-Methyl-D-Aspartate / drug effects. Receptors, N-Methyl-D-Aspartate / metabolism. Up-Regulation / drug effects. Up-Regulation / immunology. bcl-2-Associated X Protein / drug effects. bcl-2-Associated X Protein / metabolism

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  • (PMID = 16888403.001).
  • [ISSN] 1021-7401
  • [Journal-full-title] Neuroimmunomodulation
  • [ISO-abbreviation] Neuroimmunomodulation
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / N-methyl D-aspartate receptor subtype 2A; 0 / NR2B NMDA receptor; 0 / Neurotoxins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, N-Methyl-D-Aspartate; 0 / bcl-2-Associated X Protein; 1HG84L3525 / Formaldehyde; 9006-59-1 / Ovalbumin; 9061-61-4 / Nerve Growth Factor; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3
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83. García JF, García JF, Maestre L, Lucas E, Sánchez-Verde L, Romero-Chala S, Piris MA, Roncador G: Genetic immunization: a new monoclonal antibody for the detection of BCL-6 protein in paraffin sections. J Histochem Cytochem; 2006 Jan;54(1):31-8
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  • [Title] Genetic immunization: a new monoclonal antibody for the detection of BCL-6 protein in paraffin sections.
  • A new anti-BCL-6 MAb (GI191E/A8) was produced by cloning full-length BCL-6 cDNA into a eukaryotic vector and delivering this into mouse epidermis using a helium gene gun.
  • A comparative study was made of the specificity and the effects of formalin fixation on immunohistochemistry quality of GI191E/A8 and two other anti-BCL-6 MAbs.
  • To evaluate its possible application to differential diagnosis of lymphomas, two tissue microarrays (89 diffuse large B-cell lymphomas and 24 B-cell chronic lymphocytic leukemia cases) were stained with GI191E/A8 and another anti-BCL-6 MAb produced by conventional means.
  • Using GI191E/A8, the detection of BCL-6 protein was significantly increased, and its specificity was independent of formalin-fixation time.
  • Using automatic quantified analysis, the correlation between the two anti-BCL-6 MAbs tested was identical in cases with overexpression or absence of BCL-6.
  • In cases with intermediate BCL-6 protein expression, detection with GI191E/A8 was more sensitive.
  • A significant association of higher BCL-6 expression and longer median overall survival times in diffuse large B-cell lymphomas was found.
  • [MeSH-minor] Animals. Cell Line, Tumor. Diagnosis, Differential. Fixatives. Formaldehyde. Humans. Immunohistochemistry. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / metabolism. Mice. Mice, Inbred BALB C. Palatine Tonsil / metabolism. Paraffin Embedding. Survival Analysis. Tissue Array Analysis

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  • (PMID = 16046671.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / BCL6 protein, human; 0 / DNA-Binding Proteins; 0 / Fixatives; 1HG84L3525 / Formaldehyde
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84. Weng Y, Gao ZF, Liu K, Zhang WJ, Ke XY, Li M: [Factors affecting the prognosis of diffuse large B-cell lymphoma in Chinese]. Zhonghua Nei Ke Za Zhi; 2005 Sep;44(9):681-3
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  • [Title] [Factors affecting the prognosis of diffuse large B-cell lymphoma in Chinese].
  • OBJECTIVE: To study the correlation between clinical prognosis and clinicopathologic features, origin and cell proliferous index of diffuse large B-cell lymphoma (DLBCL) in China.
  • Immunohistochemistry stain was used to check the expression of CD(45)RO, CD(3), CD(20), CD(79)a, CD(45)RA, Ki-67, p53 and bcl-6.
  • 23 patients 38.3% died during follow-up, the longest survival period lasting 108 months.16 died in the first year after establishment of diagnosis (16/23, 69.6%).
  • Ki-67, p53, bcl-6 were expressed in some cases (48/53, 90.6%; 26/46, 56.5%; 21/41, 51.2%).
  • The expression of bcl-6 protein was somewhat related with prognosis (P = 0.0049), but the expression of p53 was not (P = 0.5948).
  • Most of the cases died in the first year after establishment of diagnosis.
  • IPI can be used to predict the clinical outcome.
  • The expression of bcl-6 protein was somewhat related with clinical prognosis, but that of p53 was not.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Cell Proliferation. Child. China. DNA-Binding Proteins / metabolism. Female. Follow-Up Studies. Humans. Immunohistochemistry. Ki-67 Antigen / metabolism. Male. Middle Aged. Prognosis. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 16202261.001).
  • [ISSN] 0578-1426
  • [Journal-full-title] Zhonghua nei ke za zhi
  • [ISO-abbreviation] Zhonghua Nei Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / DNA-Binding Proteins; 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53
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85. Willenbrock K, Bräuninger A, Hansmann ML: Frequent occurrence of B-cell lymphomas in angioimmunoblastic T-cell lymphoma and proliferation of Epstein-Barr virus-infected cells in early cases. Br J Haematol; 2007 Sep;138(6):733-9
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  • [Title] Frequent occurrence of B-cell lymphomas in angioimmunoblastic T-cell lymphoma and proliferation of Epstein-Barr virus-infected cells in early cases.
  • Secondary lymphomas occurring in the setting of angioimmunoblastic T-cell lymphoma (AILT) are considered to be rare.
  • A previous study detected a dysregulated hypermutation process in B-cells of AILT.
  • The present study aimed at estimating the frequency of B-cell lymphomas in AILT.
  • By studying the expression of EBV and activation-induced cytidine deaminase (AID) as an indicator of hypermutating cells, we assessed whether B-cell lymphoproliferations in AILT were strictly associated with EBV and whether hypermutation might contribute to lymphomagenesis.
  • Among 161 cases of AILT, diagnosed between 1996 and 2005 at the lymph node registry, Frankfurt, Germany, 19 cases were detected that also had B-cell non-Hodgkin lymphoma (NHL) and two cases had classical Hodgkin lymphoma (HL).
  • EBV was detected in tumour cells of 7/18 NHL and both HL, suggesting that factors other than EBV contribute to lymphomagenesis.
  • AID was expressed in AILT in large cells disseminated in the tissue, implying that the process of somatic hypermutation is ongoing in AILT, although the GC architecture is disrupted.
  • This might be relevant in the development of secondary lymphomas.
  • [MeSH-major] Epstein-Barr Virus Infections / pathology. Herpesvirus 4, Human. Lymphoma, B-Cell / virology. Lymphoma, T-Cell, Peripheral / pathology
  • [MeSH-minor] B-Lymphocytes / pathology. Biomarkers, Tumor / analysis. Cell Proliferation. Clone Cells. Cytidine Deaminase / analysis. DNA-Binding Proteins / analysis. Gene Rearrangement, B-Lymphocyte. Humans. Immunohistochemistry. In Situ Hybridization. Neprilysin / analysis. Polymerase Chain Reaction / methods. RNA, Viral / analysis. Somatic Hypermutation, Immunoglobulin. T-Lymphocytes / pathology

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  • (PMID = 17672882.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / RNA, Viral; EC 3.4.24.11 / Neprilysin; EC 3.5.4.5 / Cytidine Deaminase
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86. Yun SJ, Lee KH, Yang DW, Lee JB, Kim SJ, Lee SC, Won YH: Primary cutaneous spindle cell B-cell lymphoma with multiple figurate erythema-like manifestation. J Cutan Pathol; 2009 Jan;36(1):49-52
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  • [Title] Primary cutaneous spindle cell B-cell lymphoma with multiple figurate erythema-like manifestation.
  • Spindle-shaped cells with elongated, twisted nuclei containing dispersed chromatin were also seen.
  • Immunohistochemical analysis showed that all of the cells were strongly positive for CD20, CD21, CD79a and CD45, while they were negative for CD3, CD5, CD10, CD23, CD35, CD43, CD45RO and CD68.
  • The spindle cells were also negative for smooth-muscle actin, desmin, S-100 and CD34.
  • They consistently expressed nuclear bcl-6, but did not express bcl-2, multiple myeloma-1 and p16.
  • We diagnosed him with primary cutaneous spindle cell B-cell lymphoma (PCSBCL) and treated him with six cycles of cyclophosphamide, adriamycin, vincristine, prednisone and rituximab (R-CHOP) chemotherapy; his skin lesions disappeared completely.
  • Immunohistochemical profiles suggest that PCSBCL is a variant of primary cutaneous follicle center lymphoma.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology. Skin Neoplasms / pathology

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  • (PMID = 19125734.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone
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87. Rohde G, Kermer P, Reed JC, Bähr M, Weishaupt JH: Neuron-specific overexpression of the co-chaperone Bcl-2-associated athanogene-1 in superoxide dismutase 1(G93A)-transgenic mice. Neuroscience; 2008 Dec 10;157(4):844-9
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  • [Title] Neuron-specific overexpression of the co-chaperone Bcl-2-associated athanogene-1 in superoxide dismutase 1(G93A)-transgenic mice.
  • Bcl-2-associated athanogene-1 (BAG1) binds heat-shock protein 70 (Hsp70)/Hsc70, increases intracellular chaperone activity in neurons and proved to be protective in several models for neurodegeneration.
  • Moreover, expression of mtSOD1 decreases BAG1 levels in a motoneuronal cell line.
  • [MeSH-minor] Age Factors. Amyotrophic Lateral Sclerosis / genetics. Amyotrophic Lateral Sclerosis / metabolism. Amyotrophic Lateral Sclerosis / mortality. Amyotrophic Lateral Sclerosis / pathology. Animals. Disease Models, Animal. Humans. Mice. Mice, Transgenic. Motor Activity / genetics. Phosphopyruvate Hydratase / metabolism. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. Spinal Cord / pathology. Survival Analysis

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  • (PMID = 18955116.001).
  • [ISSN] 0306-4522
  • [Journal-full-title] Neuroscience
  • [ISO-abbreviation] Neuroscience
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL2-associated athanogene 1 protein; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Transcription Factors; EC 1.15.1.- / SOD1 G93A protein; EC 1.15.1.1 / Superoxide Dismutase; EC 4.2.1.11 / Phosphopyruvate Hydratase
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88. Jin Y, Hu J, Wang Q, Li Z, Chen Y: Effects of Oxymatrine on the apoptosis of human esophageal carcinoma Eca109 cell line and its mechanism. J Huazhong Univ Sci Technolog Med Sci; 2008 Jun;28(3):314-6
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  • [Title] Effects of Oxymatrine on the apoptosis of human esophageal carcinoma Eca109 cell line and its mechanism.
  • The effects of Oxymatrine (Oxy) on the proliferation and apoptosis of human esophageal carcinoma Eca109 cell line and the mechanism were investigated.
  • The human esophageal carcinoma Eca109 cells were cultured in vitro.
  • The Oxy-induced apoptosis of Eca 109 cells was assayed by using flow cytometry.
  • The expressions of p-ERK(1/2), Cyclin D1, p21(waf/cip1), Bax and Bcl-2 were detected by Western blot.
  • Flow cytometry revealed that Oxy could induce the apoptosis of Eca109 cells.
  • Western blot showed that Oxy of different concentrations suppressed the expressions of p-ERK(1/2), Cyclin D1 and Bcl-2, but up-regulated the expression of p21(waf/cip1) and Bax, and the ratio of Bax/Bcl-2 was increased.
  • It was suggested the Oxy could induce the apoptosis of Eca109 cells, which might be related to the upregulation of p21(waf/cip1) and the downregulation of p-ERK(1/2), Cyclin D1 and p21(waf/cip1).
  • The possible pathway may be related to Bcl-2/Bax.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Antiviral Agents / pharmacology. Cell Line, Tumor. Cyclin-Dependent Kinase Inhibitor p21 / biosynthesis. Dose-Response Relationship, Drug. Flow Cytometry. Humans. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. bcl-2-Associated X Protein / biosynthesis

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  • [Cites] Oncogene. 2004 Apr 12;23(16):2838-49 [15077147.001]
  • [Cites] In Vivo. 2006 Sep-Oct;20(5):599-604 [17091766.001]
  • [Cites] Nat Cell Biol. 2007 Feb;9(2):160-70 [17330329.001]
  • [Cites] Curr Med Chem. 2007;14(5):601-23 [17346150.001]
  • (PMID = 18563331.001).
  • [ISSN] 1672-0733
  • [Journal-full-title] Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban
  • [ISO-abbreviation] J. Huazhong Univ. Sci. Technol. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Alkaloids; 0 / Antineoplastic Agents; 0 / Antiviral Agents; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Quinolizines; 0 / bcl-2-Associated X Protein; 85U4C366QS / oxymatrine; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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89. Timmerman JM, Vose JM, Czerwinski DK, Weng WK, Ingolia D, Mayo M, Denney DW, Levy R: Tumor-specific recombinant idiotype immunisation after chemotherapy as initial treatment for follicular non-Hodgkin lymphoma. Leuk Lymphoma; 2009 Jan;50(1):37-46
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  • [Title] Tumor-specific recombinant idiotype immunisation after chemotherapy as initial treatment for follicular non-Hodgkin lymphoma.
  • Tumor-specific variable regions of the clonal immunoglobulin (idiotype, Id) expressed by B cell non-Hodgkin lymphoma (NHL) can be targeted by active immunotherapy.
  • We conducted a phase I/II trial to determine the safety and immunogenicity of a patient-specific, recombinant, mammalian cell-derived Id protein conjugated to keyhole limpet hemocyanin (Id-KLH; MyVax personalised immunotherapy) in 22 patients with follicular NHL in first remission after chemotherapy.
  • Evoked anti-Id antibodies recognised both recombinant Id and native Id, and could specifically stain autologous tumor cells.
  • Immunisation of follicular lymphoma patients with MyVax Id-KLH is safe and patients often mount tumor-specific immune responses.

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  • [Cites] Cell Immunol. 1992 Oct 15;144(2):443-54 [1394453.001]
  • [Cites] J Immunol. 2008 Sep 15;181(6):4131-40 [18768870.001]
  • [Cites] J Natl Cancer Inst. 2006 Sep 20;98(18):1292-301 [16985248.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1504-8 [16690968.001]
  • [Cites] J Clin Oncol. 2006 Jul 1;24(19):3107-12 [16754937.001]
  • [Cites] J Clin Oncol. 1999 Apr;17(4):1244 [10561185.001]
  • [Cites] Blood. 2000 Feb 15;95(4):1342-9 [10666209.001]
  • [Cites] Nat Med. 2000 Jun;6(6):667-72 [10835683.001]
  • [Cites] Clin Immunol. 2001 Feb;98(2):175-9 [11161973.001]
  • [Cites] Clin Cancer Res. 2001 Mar;7(3 Suppl):902s-908s [11300490.001]
  • [Cites] Blood. 2002 Mar 1;99(5):1517-26 [11861263.001]
  • [Cites] Blood. 2002 Apr 1;99(7):2562-8 [11895794.001]
  • [Cites] Blood. 2002 Sep 15;100(6):2257-9 [12200395.001]
  • [Cites] Blood. 2004 Sep 1;104(5):1258-65 [15126323.001]
  • [Cites] Nat Med. 2004 Sep;10(9):909-15 [15340416.001]
  • [Cites] Adv Pharmacol. 2004;51:271-93 [15464914.001]
  • [Cites] N Engl J Med. 1982 Mar 4;306(9):517-22 [6173751.001]
  • [Cites] J Immunol Methods. 1986 May 1;89(1):61-72 [3084658.001]
  • [Cites] J Immunol. 1987 Jan 15;138(2):628-34 [3491853.001]
  • [Cites] J Immunol. 1987 Oct 15;139(8):2825-33 [3498771.001]
  • [Cites] N Engl J Med. 1989 Sep 28;321(13):851-7 [2475779.001]
  • [Cites] Mol Immunol. 1992 Feb;29(2):193-203 [1542297.001]
  • [Cites] N Engl J Med. 1992 Oct 22;327(17):1209-15 [1406793.001]
  • [Cites] J Exp Med. 1994 Jan 1;179(1):195-202 [7505798.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jun 7;91(12):5700-4 [7911244.001]
  • [Cites] Nat Med. 1996 Jan;2(1):52-8 [8564842.001]
  • [Cites] Gene Ther. 1996 Nov;3(11):988-93 [8940639.001]
  • [Cites] Blood. 1997 May 1;89(9):3129-35 [9129015.001]
  • [Cites] J Immunol. 1997 Dec 1;159(11):5516-27 [9548492.001]
  • [Cites] Blood. 1998 Aug 15;92(4):1184-90 [9694706.001]
  • [Cites] J Clin Oncol. 1998 Aug;16(8):2825-33 [9704735.001]
  • [Cites] Nat Med. 1999 Oct;5(10):1171-7 [10502821.001]
  • [Cites] J Clin Oncol. 2004 Dec 1;22(23):4717-24 [15483014.001]
  • [Cites] Clin Cancer Res. 2004 Dec 15;10(24):8309-17 [15623607.001]
  • [Cites] Curr Opin Oncol. 2005 Sep;17(5):432-40 [16093791.001]
  • [Cites] J Clin Oncol. 2005 Aug 20;23(24):5696-704 [16110029.001]
  • [Cites] Nat Med. 2005 Sep;11(9):986-91 [16116429.001]
  • [Cites] Leuk Res. 2006 Mar;30(3):277-82 [16112730.001]
  • [Cites] Cancer Res. 2006 Apr 15;66(8):4496-502 [16618777.001]
  • [CommentIn] Leuk Lymphoma. 2009 Jan;50(1):1-2 [19172492.001]
  • (PMID = 19125383.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / RR-00070-CAP; United States / NCI NIH HHS / CA / K08 CA111827-02; United States / NCI NIH HHS / CA / CA111827-03; United States / NCI NIH HHS / CA / CA111827-02; United States / NCI NIH HHS / CA / K08 CA111827-03; United States / NCRR NIH HHS / RR / M01 RR000070
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cancer Vaccines; 0 / Immunoglobulin Idiotypes; 0 / Recombinant Proteins
  • [Other-IDs] NLM/ NIHMS217707; NLM/ PMC2914563
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90. Senff NJ, Noordijk EM, Kim YH, Bagot M, Berti E, Cerroni L, Dummer R, Duvic M, Hoppe RT, Pimpinelli N, Rosen ST, Vermeer MH, Whittaker S, Willemze R, European Organization for Research and Treatment of Cancer, International Society for Cutaneous Lymphoma: European Organization for Research and Treatment of Cancer and International Society for Cutaneous Lymphoma consensus recommendations for the management of cutaneous B-cell lymphomas. Blood; 2008 Sep 1;112(5):1600-9
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  • [Title] European Organization for Research and Treatment of Cancer and International Society for Cutaneous Lymphoma consensus recommendations for the management of cutaneous B-cell lymphomas.
  • Primary cutaneous B-cell lymphomas (CBCL) represent approximately 20% to 25% of all primary cutaneous lymphomas.
  • With the advent of the World Health Organization-European Organization for Research and Treatment of Cancer (EORTC) Consensus Classification for Cutaneous Lymphomas in 2005, uniform terminology and classification for this rare group of neoplasms were introduced.
  • However, staging procedures and treatment strategies still vary between different cutaneous lymphoma centers, which may be because consensus recommendations for the management of CBCL have never been published.
  • Based on an extensive literature search and discussions within the EORTC Cutaneous Lymphoma Group and the International Society for Cutaneous Lymphomas, the present report aims to provide uniform recommendations for the management of the 3 main groups of CBCL.
  • Despite these limitations, there was consensus among the members of the multidisciplinary expert panel that these recommendations reflect the state-of-the-art management as currently practiced in major cutaneous lymphoma centers.
  • They may therefore contribute to uniform staging and treatment and form the basis for future clinical trials in patients with a CBCL.
  • [MeSH-major] Lymphoma, B-Cell / therapy. Skin Neoplasms / therapy
  • [MeSH-minor] Anti-Bacterial Agents / therapeutic use. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Agents / therapeutic use. Humans. Interferon Type I / administration & dosage. Lyme Disease / complications. Lyme Disease / drug therapy. Lymphoma, B-Cell, Marginal Zone / diagnosis. Lymphoma, B-Cell, Marginal Zone / pathology. Lymphoma, B-Cell, Marginal Zone / therapy. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Large B-Cell, Diffuse / therapy. Neoplasm Staging / methods. Radiotherapy Dosage. Recombinant Proteins. Rituximab

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  • (PMID = 18567836.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Practice Guideline; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Interferon Type I; 0 / Recombinant Proteins; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 123
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91. Singla R, Kumar P, Bahl A, Kumar S, Saran RK, Kar P: A case of primary rectal non-Hodgkin's lymphoma treated with chemotherapy. Trop Gastroenterol; 2008 Oct-Dec;29(4):227-8
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  • [Title] A case of primary rectal non-Hodgkin's lymphoma treated with chemotherapy.
  • Primary rectal non-Hodgkin's lymphoma is a rare disease.
  • Surgery has been proposed as the primary treatment modality for colorectal lymphomas.
  • We report a case of rectal non-Hodgkin's lymphoma (B cell large cell type, Ann Arbor Stage 1E) who responded completely to systemic chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Non-Hodgkin / drug therapy. Rectal Neoplasms / drug therapy

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  • (PMID = 19323094.001).
  • [ISSN] 0250-636X
  • [Journal-full-title] Tropical gastroenterology : official journal of the Digestive Diseases Foundation
  • [ISO-abbreviation] Trop Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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92. Watanuki J, Hatakeyama K, Sonoki T, Tatetsu H, Yoshida K, Fujii S, Mizutani M, Abo T, Kurimoto M, Matsuoka H, Matsuno F, Nakakuma H: Bone marrow large B cell lymphoma bearing cyclin D3 expression: clinical, morphologic, immunophenotypic, and genotypic analyses of seven patients. Int J Hematol; 2009 Sep;90(2):217-25
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  • [Title] Bone marrow large B cell lymphoma bearing cyclin D3 expression: clinical, morphologic, immunophenotypic, and genotypic analyses of seven patients.
  • We report seven large B cell lymphoma patients showing the involvement of tumor cells with cyclin D3 (CCND3) expression in bone marrow (BM) at the initial diagnosis.
  • The tumor cells were divided into those with a lymphoplasmacytoid or blastoid appearance.
  • Six cases were confirmed to express CD5 antigen on tumor cells.
  • Further studies are required to determine whether CCND3 expression is associated with a unique subset of diffuse large B cell lymphoma.
  • [MeSH-major] B-Lymphocytes / physiology. Bone Marrow Cells / physiology. Cyclins / genetics. Genotype. Lymphoma, Large B-Cell, Diffuse / genetics

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  • [Cites] J Clin Pathol. 1995 Mar;48(3):189-93 [7730473.001]
  • [Cites] Br J Haematol. 2000 Dec;111(3):826-34 [11122144.001]
  • [Cites] Blood. 2002 Feb 1;99(3):815-21 [11806981.001]
  • [Cites] Blood. 2001 Jul 1;98(1):217-23 [11418483.001]
  • [Cites] Blood. 2008 Sep 1;112(5):1570-80 [18725575.001]
  • [Cites] Int J Hematol. 2008 Oct;88(3):299-303 [18758895.001]
  • [Cites] Int J Hematol. 2008 Dec;88(5):536-42 [18972186.001]
  • [Cites] Blood. 2003 Oct 15;102(8):3003-9 [12842981.001]
  • [Cites] N Engl J Med. 2005 Feb 24;352(8):804-15 [15728813.001]
  • [Cites] J Clin Pathol. 1992 Sep;45(9):770-5 [1401205.001]
  • [Cites] Blood. 2001 Nov 1;98(9):2837-44 [11675358.001]
  • [Cites] Br J Haematol. 2007 Feb;136(3):351 [17233843.001]
  • [Cites] Br J Haematol. 1991 Mar;77(3):301-10 [2012754.001]
  • [Cites] Am J Clin Pathol. 2007 May;127(5):762-9 [17439835.001]
  • [Cites] Mt Sinai J Med. 2003 Mar;70(2):133-8 [12634906.001]
  • [Cites] Int J Cancer. 2007 Nov 15;121(10):2205-11 [17657714.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):13931-6 [8943038.001]
  • [Cites] Blood. 2008 Jun 15;111(12 ):5683-90 [18391076.001]
  • [Cites] Rinsho Ketsueki. 2002 Oct;43(10):943-8 [12462031.001]
  • [Cites] Blood. 2007 Apr 15;109(8):3451-61 [17170124.001]
  • [Cites] N Engl J Med. 1999 Nov 11;341(20):1520-9 [10559454.001]
  • [Cites] Nucleic Acids Res. 2006 Jan 1;34(Database issue):D781-4 [16381979.001]
  • [Cites] Cell. 2000 Sep 1;102(5):553-63 [11007474.001]
  • [Cites] Br J Haematol. 1999 Aug;106(2):477-85 [10460609.001]
  • [Cites] Br J Haematol. 1989 Oct;73(2):199-204 [2479409.001]
  • [Cites] Int J Hematol. 1996 Jan;63(1):71-6 [8713579.001]
  • [Cites] Clin Cancer Res. 2005 Dec 1;11(23):8265-72 [16322284.001]
  • [Cites] Nucleic Acids Res. 1997 Sep 1;25(17):3389-402 [9254694.001]
  • [Cites] J Exp Med. 2007 Mar 19;204(3):633-43 [17353367.001]
  • [Cites] Leukemia. 2002 May;16(5):937-9 [11986957.001]
  • (PMID = 19639271.001).
  • [ISSN] 1865-3774
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / CCND3 protein, human; 0 / Cyclin D3; 0 / Cyclins
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93. Tari A, Asaoku H, Kashiwado K, Yoshino T, Kitadai Y, Tanaka S, Fujihara M: Predictive value of endoscopy and endoscopic ultrasonography for regression of gastric diffuse large B-cell lymphomas after Helicobacter pylori eradication. Dig Endosc; 2009 Oct;21(4):219-27
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  • [Title] Predictive value of endoscopy and endoscopic ultrasonography for regression of gastric diffuse large B-cell lymphomas after Helicobacter pylori eradication.
  • BACKGROUND: Some gastric diffuse large B-cell lymphomas have been reported to regress completely after the successful eradication of Helicobacter pylori.
  • The aim of this study was to investigate the clinical characteristics of gastric diffuse large B-cell lymphomas without any detectable mucosa-associated lymphoid tissue (MALT) lymphoma that went into complete remission after successful H. pylori eradication.
  • PATIENTS AND METHODS: We examined the effect of H. pylori eradication in 15 H. pylori-positive gastric diffuse large B-cell lymphoma patients without any evidence of an associated MALT lymphoma (clinical stage I by the Lugano classification) by endoscopic examination including biopsies, endoscopic ultrasonography, computed tomography, and bone marrow aspiration.
  • RESULTS: H. pylori eradication was successful in all the patients and complete remission was achieved in four patients whose clinical stage was I.
  • CONCLUSION: In gastric diffuse large B-cell lymphomas without a concomitant MALT lymphoma but associated with H. pylori infection, only superficial cases and lesions limited to the shallow portion of the submucosa regressed completely after successful H. pylori eradication.
  • The endoscopic appearance and the rating of the depth of invasion by endosonography are both valuable for predicting the efficacy of H. pylori eradication in treating gastric diffuse large B-cell lymphomas.
  • [MeSH-major] Endoscopy. Endosonography. Helicobacter Infections / drug therapy. Helicobacter pylori. Lymphoma, Large B-Cell, Diffuse / diagnosis. Stomach Neoplasms / diagnosis


94. Roychoudhury P, Ghosh U, Bhattacharyya NP, Chaudhuri K: Activation of mitochondrial promoter P(H)-binding protein in a radio-resistant Chinese hamster cell strain associated with Bcl-2. Biochem Biophys Res Commun; 2006 Nov 17;350(2):272-6
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  • [Title] Activation of mitochondrial promoter P(H)-binding protein in a radio-resistant Chinese hamster cell strain associated with Bcl-2.
  • Previously, we have shown that up regulation of mitochondrial genes ND1, ND4, and COX1 transcribed from the heavy strand promoter (P(H)) has been increased in a radio-resistant cell strain designated as M5 in comparison with the parental Chinese hamster V79 cells.
  • These genes are also up regulated in Chinese hamster V79 cells VB13 that express exogenous human Bcl2.
  • In the present study, the expression of the gene ND6 that is expressed from the light strand promoter (P(L)) was found to be similar in both the cell lines, as determined by RT-PCR.
  • To test the possibility that this differential expression of mitochondrial genes under these two promoters was mediated by differences in proteins' affinity to interact with these promoters, we have carried out electrophoretic mobility shift assay (EMSA) using mitochondrial cell extracts from these two cell lines.
  • Our result of these experiments revealed that two different proteins formed complex with the synthetic promoters and higher amount of protein from M5 cell extracts interacted with the P(H) promoter in comparison to that observed with cell extracts from Chinese hamster V79 cells.
  • These results showed that differential mitochondrial gene expression observed earlier in the radio-resistant M5 cells was due to enhanced interaction proteins with the promoters P(H) and mediated by the expression of Bcl2.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Genes, Mitochondrial. Mitochondrial Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Radiation Tolerance
  • [MeSH-minor] Animals. Cell Line. Cricetinae. Cricetulus. Electrophoretic Mobility Shift Assay. Gamma Rays. Gene Expression Regulation, Enzymologic. Humans. Male. Mitochondria / enzymology. Mitochondria / radiation effects. NADH Dehydrogenase / biosynthesis. NADH Dehydrogenase / genetics. Promoter Regions, Genetic. Protein Subunits / biosynthesis. Protein Subunits / genetics

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  • (PMID = 17007815.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Mitochondrial Proteins; 0 / Protein Subunits; 0 / Proto-Oncogene Proteins c-bcl-2; EC 1.6.99.3 / NADH Dehydrogenase
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95. Schulze-Bergkamen H, Ehrenberg R, Hickmann L, Vick B, Urbanik T, Schimanski CC, Berger MR, Schad A, Weber A, Heeger S, Galle PR, Moehler M: Bcl-x(L) and Myeloid cell leukaemia-1 contribute to apoptosis resistance of colorectal cancer cells. World J Gastroenterol; 2008 Jun 28;14(24):3829-40
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  • [Title] Bcl-x(L) and Myeloid cell leukaemia-1 contribute to apoptosis resistance of colorectal cancer cells.
  • AIM: To explore the role of Bcl-x(L) and Myeloid cell leukaemia (Mcl)-1 for the apoptosis resistance of colorectal carcinoma (CRC) cells towards current treatment modalities.
  • METHODS: Bcl-x(L) and Mcl-1 mRNA and protein expression were analyzed in CRC cell lines as well as human CRC tissue by Western blot, quantitative PCR and immunohistochemistry.
  • Bcl-x(L) and Mcl-1 protein expression was knocked down or increased in CRC cell lines by applying specific siRNAs or expression plasmids, respectively.
  • After modulation of protein expression, CRC cells were treated with chemotherapeutic agents, an antagonistic epidermal growth factor receptor (EGFR1) antibody, an EGFR1 tyrosine kinase inhibitor, or with the death receptor ligand TRAIL.
  • Apoptosis induction and cell viability were analyzed.
  • RESULTS: Here we show that in human CRC tissue and various CRC cell lines both Bcl-x(L) and Mcl-1 are expressed.
  • Bcl-x(L) expression was higher in CRC tissue than in surrounding non-malignant tissue, both on protein and mRNA level.
  • Mcl-1 mRNA expression was significantly lower in malignant tissues.
  • Viability rates of CRC cells were significantly decreased after knock down of Bcl-x(L) expression, and, to a lower extent, after knock down of Mcl-1 expression.
  • Furthermore, cells with reduced Bcl-x(L) or Mcl-1 expression was more sensitive towards oxaliplatin- and irinotecan-induced apoptosis, and in the case of Bcl-x(L) also towards 5-FU-induced apoptosis.
  • On the other hand, upregulation of Bcl-x(L) by transfection of an expression plasmid decreased chemotherapeutic drug-induced apoptosis.
  • EGF treatment clearly induced Bcl-x(L) and Mcl-1 expression in CRC cells.
  • Apoptosis induction upon EGFR1 blockage by cetuximab or PD168393 was increased by inhibiting Mcl-1 and Bcl-x(L) expression.
  • More strikingly, CD95- and TRAIL-induced apoptosis was increased by Bcl-x(L) knock down.
  • CONCLUSION: Our data suggest that Bcl-x(L) and, to a lower extent, Mcl-1, are important anti-apoptotic factors in CRC.
  • Specific downregulation of Bcl-x(L) is a promising approach to sensitize CRC cells towards chemotherapy and targeted therapy.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Colorectal Neoplasms / metabolism. Colorectal Neoplasms / pathology. Proto-Oncogene Proteins c-bcl-2 / metabolism. bcl-X Protein / metabolism
  • [MeSH-minor] Antigens, CD95 / metabolism. Camptothecin / analogs & derivatives. Camptothecin / pharmacology. Cell Line, Tumor. Cell Survival / drug effects. Fluorouracil / pharmacology. Humans. Myeloid Cell Leukemia Sequence 1 Protein. Organoplatinum Compounds / pharmacology. RNA, Messenger / metabolism. Receptor, Epidermal Growth Factor / antagonists & inhibitors. TNF-Related Apoptosis-Inducing Ligand / metabolism

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  • [Cites] Nat Med. 1999 Feb;5(2):157-63 [9930862.001]
  • [Cites] Dig Dis Sci. 1998 Dec;43(12):2641-8 [9881495.001]
  • [Cites] Oncogene. 1999 Aug 19;18(33):4654-62 [10467412.001]
  • [Cites] Mol Cancer Ther. 2005 Mar;4(3):451-6 [15767554.001]
  • [Cites] Jpn J Clin Oncol. 2005 Aug;35(8):453-63 [16024531.001]
  • [Cites] Cancer Biol Ther. 2005 Mar;4(3):267-76 [15753661.001]
  • [Cites] Int J Oncol. 2006 Jan;28(1):25-32 [16327976.001]
  • [Cites] J Hepatol. 2006 Jan;44(1):151-7 [16289418.001]
  • [Cites] J Biol Chem. 2006 Apr 14;281(15):10153-63 [16478725.001]
  • [Cites] Clin Cancer Res. 2006 Apr 15;12(8):2640-6 [16638878.001]
  • [Cites] Semin Oncol. 2006 Aug;33(4):369-85 [16890793.001]
  • [Cites] Oncogene. 2006 Aug 24;25(37):5145-54 [16636678.001]
  • [Cites] BMC Cancer. 2006;6:232 [17014711.001]
  • [Cites] FEBS Lett. 2006 Dec 11;580(28-29):6565-9 [17113582.001]
  • [Cites] Oncogene. 2007 Feb 26;26(9):1324-37 [17322918.001]
  • [Cites] Clin Cancer Res. 2007 Apr 1;13(7):2226-35 [17404107.001]
  • [Cites] Curr Top Med Chem. 2007;7(10):961-5 [17508927.001]
  • [Cites] Pathology. 2007 Jun;39(3):334-8 [17558861.001]
  • [Cites] Cancer Cell. 2007 Jul;12(1):66-80 [17613437.001]
  • [Cites] Int J Biochem Cell Biol. 2007;39(7-8):1462-75 [17403612.001]
  • [Cites] Anticancer Agents Med Chem. 2007 Sep;7(5):492-503 [17896910.001]
  • [Cites] Expert Opin Ther Targets. 2007 Oct;11(10):1299-314 [17907960.001]
  • [Cites] Genes Dev. 2000 Jan 1;14(1):23-7 [10640272.001]
  • [Cites] Mol Cell Biol. 2000 Apr;20(8):2687-95 [10733571.001]
  • [Cites] Nat Med. 2000 May;6(5):513-9 [10802706.001]
  • [Cites] Clin Cancer Res. 2000 Jun;6(6):2547-55 [10873111.001]
  • [Cites] Science. 2000 Nov 3;290(5493):989-92 [11062132.001]
  • [Cites] J Clin Pathol. 2002 Mar;55(3):206-11 [11896073.001]
  • [Cites] Leukemia. 2002 Apr;16(4):444-54 [11960321.001]
  • [Cites] Nature. 2002 Jul 11;418(6894):244-51 [12110901.001]
  • [Cites] Genes Dev. 2003 Jun 15;17(12):1475-86 [12783855.001]
  • [Cites] Cancer Res. 2003 Aug 15;63(16):5118-25 [12941843.001]
  • [Cites] Lancet. 2003 Oct 25;362(9393):1401-3 [14585643.001]
  • [Cites] Cancer Cell. 2004 Jan;5(1):37-49 [14749125.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):1110-3 [14871845.001]
  • [Cites] Semin Oncol. 2004 Feb;31(1):90-119 [14970941.001]
  • [Cites] Cancer Res. 2004 May 15;64(10):3517-24 [15150106.001]
  • [Cites] Carcinogenesis. 2004 Oct;25(10):1867-77 [15205359.001]
  • [Cites] Nature. 1987 May 28-Jun 3;327(6120):293-7 [3587348.001]
  • [Cites] J Immunol Methods. 1991 Jun 3;139(2):271-9 [1710634.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3516-20 [7682708.001]
  • [Cites] Cell. 1994 Aug 26;78(4):539-42 [8069905.001]
  • [Cites] Cancer Res. 1995 Jan 15;55(2):237-41 [7812951.001]
  • [Cites] Cancer Res. 1996 May 15;56(10):2422-7 [8625322.001]
  • [Cites] Exp Cell Res. 1998 Apr 10;240(1):107-21 [9570926.001]
  • [Cites] Br J Cancer. 1998 Oct;78(8):1035-42 [9792147.001]
  • [Cites] Clin Cancer Res. 1996 Jul;2(7):1215-9 [9816290.001]
  • [Cites] J Clin Invest. 1999 Jul;104(2):155-62 [10411544.001]
  • (PMID = 18609706.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Antineoplastic Agents; 0 / BCL2L1 protein, human; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Organoplatinum Compounds; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / bcl-X Protein; 04ZR38536J / oxaliplatin; 7673326042 / irinotecan; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ PMC2721439
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96. Marín García D, Cárdenas Lafuente F, Utrilla Ayala Mdel C, Galán Jurado MV, Jiménez Martín JJ, García Ordóñez MA: [Primary diffuse large B-cell lymphoma of the rectum simulating a rectal adenocarcinoma]. Gastroenterol Hepatol; 2010 Feb;33(2):92-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Primary diffuse large B-cell lymphoma of the rectum simulating a rectal adenocarcinoma].
  • [Transliterated title] Linfoma de tipo B difuso de células grandes primario rectal que simula un adenocarcinoma de recto.
  • Colorectal lymphoma is an extremely infrequent entity, representing less than 0.5% of all primary colorectal neoplasms.
  • Colorectal localization accounts for 15-20% of all gastrointestinal lymphomas, after the stomach and small intestine.
  • Because the symptoms are non-specific, this disease is usually diagnosed in the advanced stages.
  • Dawson's criteria are highly useful in the differential diagnosis between primary colorectal involvement and gastrointestinal tract involvement secondary to systemic lymphoma, which is important due to the distinct prognosis and treatment of these entities.
  • We report the case of a B-cell non-Hodgkin's lymphoma that was difficult to diagnose and was treated with R-CHOP polychemotherapy.
  • [MeSH-major] Adenocarcinoma / diagnosis. Lymphoma, Large B-Cell, Diffuse / diagnosis. Rectal Neoplasms / diagnosis
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colonoscopy. Cyclophosphamide / therapeutic use. Diagnosis, Differential. Doxorubicin / therapeutic use. Humans. Immunohistochemistry. Male. Meta-Analysis as Topic. Middle Aged. Neoplasm Staging. Prednisone / therapeutic use. Prognosis. Radiography, Abdominal. Rectum / pathology. Tomography, X-Ray Computed. Vincristine / therapeutic use

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  • [Copyright] Copyright 2009 Elsevier España, S.L. All rights reserved.
  • (PMID = 19875198.001).
  • [ISSN] 0210-5705
  • [Journal-full-title] Gastroenterología y hepatología
  • [ISO-abbreviation] Gastroenterol Hepatol
  • [Language] spa
  • [Publication-type] Case Reports; Comparative Study; English Abstract; Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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97. Kahl BS: Special problems in B-cell lymphoma: an historical perspective. Hematology Am Soc Hematol Educ Program; 2008;:340
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  • [Title] Special problems in B-cell lymphoma: an historical perspective.

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  • (PMID = 19074107.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Historical Article; Introductory Journal Article
  • [Publication-country] United States
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98. Spender LC, Inman GJ: Targeting the BCL-2 family in malignancies of germinal centre origin. Expert Opin Ther Targets; 2009 Dec;13(12):1459-72
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  • [Title] Targeting the BCL-2 family in malignancies of germinal centre origin.
  • The germinal centre is a dynamic microenvironment where B-cell responses are honed.
  • Antigen-specific cells undergo clonal expansion followed by antibody affinity maturation and class switching through somatic hypermutation and recombination of immunoglobulin genes respectively.
  • The huge proliferative capacity of the B-cells and the potential for generating non-functional or autoreactive immunoglobulins, necessitate strict control measures.
  • Pro-apoptotic signalling pathways via B-cell receptors, FAS and the TGF-beta receptor, ALK5, ensure that apoptosis of germinal centre B-cells is the norm and cells only survive to differentiate fully if they receive sufficient pro-survival signals to overcome their 'primed for death' status.
  • Several of the B-cell signalling pathways converge on the intrinsic apoptotic machinery to control expression of the BCL-2 family of apoptosis regulators including BIM, the pro-survival factor BCL-X(L) and the BH3-only protein, BIK (recently identified as a mediator of a TGF-beta-induced default apoptosis pathway in human B-cells).
  • It is a foreseeable hazard that cells undergoing genetic mutation and recombination events might unintentionally target some of these factors, resulting in defective programmed cell death.
  • Here we discuss the function of BCL-2 family proteins in germinal centre reactions, their deregulation in malignancies of germinal centre origin, and the potential for targeting BCL-2-related proteins therapeutically in lymphomas.
  • [MeSH-major] Genes, bcl-2 / drug effects. Genes, bcl-2 / genetics. Germinal Center / physiology. Neoplasms / genetics

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  • (PMID = 19922301.001).
  • [ISSN] 1744-7631
  • [Journal-full-title] Expert opinion on therapeutic targets
  • [ISO-abbreviation] Expert Opin. Ther. Targets
  • [Language] eng
  • [Grant] United Kingdom / Worldwide Cancer Research / / 03-0900
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 112
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99. Zhou Z, Peng X, Insolera R, Fink DJ, Mata M: IL-10 promotes neuronal survival following spinal cord injury. Exp Neurol; 2009 Nov;220(1):183-90
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  • We have previously reported that the anti-inflammatory cytokine IL-10 induces a number of signaling cascades through the IL-10 receptor in spinal cord neurons in vitro to activate NF-kappaB transcription Bcl-2 and Bcl-x(L) and that, after exposure to glutamate IL-10, blocks cytochrome c release and caspase cleavage.
  • Injection of the vector 30 minutes after lateral hemisection injury resulted in increased neuronal survival in the anterior quadrant of the spinal cord and improved motor function up to 6 weeks after injury, that correlated with translocation of p50 and p65 NF-kappaB to the nucleus and increased expression of Bcl-2 and Bcl-x(L) in anterior quadrant neurons.
  • [MeSH-minor] Animals. Anti-Inflammatory Agents / metabolism. Apoptosis Regulatory Proteins / metabolism. Cell Survival / genetics. Cells, Cultured. Disease Models, Animal. Female. Rats. Rats, Sprague-Dawley. Receptors, Interleukin-10 / genetics. Receptors, Interleukin-10 / metabolism. Signal Transduction / genetics. Signal Transduction / immunology. Simplexvirus / genetics. Spinal Cord / immunology. Spinal Cord / metabolism. Transfection / methods. Treatment Outcome

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  • [Cites] J Neurotrauma. 1999 Oct;16(10):851-63 [10547095.001]
  • [Cites] J Neurochem. 2009 Sep;110(5):1617-27 [19575707.001]
  • [Cites] Exp Neurol. 2000 Dec;166(2):213-26 [11085887.001]
  • [Cites] Exp Neurol. 2001 Mar;168(1):144-54 [11170729.001]
  • [Cites] Annu Rev Immunol. 2001;19:683-765 [11244051.001]
  • [Cites] J Neurosci. 2001 May 1;21(9):3104-12 [11312295.001]
  • [Cites] J Neurotrauma. 2002 May;19(5):653-66 [12042099.001]
  • [Cites] J Neurosci. 2003 Sep 24;23(25):8682-91 [14507967.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Dec;44(12):5206-11 [14638718.001]
  • [Cites] Neuroscience. 2004;124(4):945-52 [15026134.001]
  • [Cites] J Clin Immunol. 1992 Jul;12(4):239-47 [1512298.001]
  • [Cites] J Neurotrauma. 1995 Feb;12(1):1-21 [7783230.001]
  • [Cites] Exp Neurol. 1999 Aug;158(2):444-50 [10415151.001]
  • [Cites] Nat Med. 1999 Aug;5(8):943-6 [10426320.001]
  • [Cites] Exp Neurol. 1999 Oct;159(2):484-93 [10506519.001]
  • [Cites] Virology. 2005 Jun 5;336(2):173-83 [15892959.001]
  • [Cites] J Neurosci. 2006 Apr 26;26(17):4672-80 [16641248.001]
  • [Cites] Arch Phys Med Rehabil. 2007 Nov;88(11):1384-93 [17964877.001]
  • [Cites] Gene Ther. 2008 Feb;15(3):183-90 [18033311.001]
  • [Cites] Brain Behav Immun. 2009 Jan;23(1):92-100 [18835435.001]
  • [Cites] Neurology. 2009 Jan 6;72(1):14-9 [18987350.001]
  • [Cites] Eur J Neurosci. 2000 Jul;12(7):2265-72 [10947805.001]
  • (PMID = 19716366.001).
  • [ISSN] 1090-2430
  • [Journal-full-title] Experimental neurology
  • [ISO-abbreviation] Exp. Neurol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS043247; United States / NINDS NIH HHS / NS / R01 NS043247-05
  • [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 / Anti-Inflammatory Agents; 0 / Apoptosis Regulatory Proteins; 0 / Receptors, Interleukin-10; 130068-27-8 / Interleukin-10
  • [Other-IDs] NLM/ NIHMS146458; NLM/ PMC2788918
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100. Ozören N, Inohara N, Núñez G: A putative role for human BFK in DNA damage-induced apoptosis. Biotechnol J; 2009 Jul;4(7):1046-54
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  • Human BFK (BCL-2 family kin) is a novel pro-apoptotic BCL-2 family member specifically expressed in the gastrointestinal tract.
  • BFK has the characteristic BH3 domain, which was shown to be essential for the apoptosis-inducing activity of pro-apoptotic BCL-2 family members.
  • When overexpressed, BFK interacts with BCL-XL and BCL-W but not BCL-2 or BAD in co-immunoprecipitations studies.
  • A recombinant version of the protein containing all residues downstream of the putative caspase cleavage site induces apoptosis in human colon cancer cells, HCT116, and in wild-type mouse embryonic fibroblasts (MEFs), which can be reversed by co-expression of BCL-XL or BCL-W.
  • [MeSH-major] Apoptosis / physiology. DNA Damage. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] Animals. Apoptosis Regulatory Proteins / metabolism. Cell Line. Cell Line, Tumor. Colon / metabolism. Colonic Neoplasms / metabolism. HCT116 Cells. Humans. Immunohistochemistry. Mice. Rabbits. bcl-2 Homologous Antagonist-Killer Protein / metabolism. bcl-2-Associated X Protein / metabolism. bcl-Associated Death Protein / metabolism. bcl-X Protein / metabolism

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  • (PMID = 19557800.001).
  • [ISSN] 1860-7314
  • [Journal-full-title] Biotechnology journal
  • [ISO-abbreviation] Biotechnol J
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BAD protein, human; 0 / BAK1 protein, human; 0 / BAX protein, human; 0 / BCL2L1 protein, human; 0 / BCL2L15 protein, human; 0 / BCL2L2 protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2 Homologous Antagonist-Killer Protein; 0 / bcl-2-Associated X Protein; 0 / bcl-Associated Death Protein; 0 / bcl-X Protein
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