[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 103
1. Hailfinger S, Lenz G, Ngo V, Posvitz-Fejfar A, Rebeaud F, Guzzardi M, Penas EM, Dierlamm J, Chan WC, Staudt LM, Thome M: Essential role of MALT1 protease activity in activated B cell-like diffuse large B-cell lymphoma. Proc Natl Acad Sci U S A; 2009 Nov 24;106(47):19946-51
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Essential role of MALT1 protease activity in activated B cell-like diffuse large B-cell lymphoma.
  • Mucosa-associated lymphoid tissue transformation protein 1 (MALT1) is a proto-oncogene that contributes to tumorigenesis in diffuse large B-cell lymphoma (DLBCL) of the activated B-cell (ABC) subtype, the least curable subtype of DLBCL.
  • Here we report that MALT1 is constitutively active in DLBCL lines of the ABC but not the GCB subtype.
  • Inhibition of the MALT1 proteolytic activity led to reduced expression of growth factors and apoptosis inhibitors, and specifically affected the growth and survival of ABC DLBCL lines.
  • These results demonstrate a key role for the proteolytic activity of MALT1 in DLBCL of the ABC subtype, and provide a rationale for the development of pharmacological inhibitors of MALT1 in DLBCL therapy.

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • SciCrunch. ArrayExpress: Data: Microarray .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Virol. 1999 Oct;73(10):7981-7 [10482545.001]
  • [Cites] Mol Cell Biol. 1999 Sep;19(9):5923-9 [10454539.001]
  • [Cites] J Biol Chem. 2005 Jul 22;280(29):27345-55 [15886205.001]
  • [Cites] Adv Immunol. 2005;87:163-208 [16102574.001]
  • [Cites] Immunol Rev. 2006 Apr;210:67-85 [16623765.001]
  • [Cites] Nature. 2006 May 4;441(7089):106-10 [16572121.001]
  • [Cites] Nature. 2006 Aug 10;442(7103):651-6 [16862125.001]
  • [Cites] Nat Rev Immunol. 2006 Nov;6(11):799-812 [17063183.001]
  • [Cites] Immunity. 2006 Nov;25(5):701-15 [17098202.001]
  • [Cites] Leukemia. 2007 Jan;21(1):30-6 [17096016.001]
  • [Cites] J Cardiovasc Pharmacol. 2007 Sep;50(3):247-56 [17878751.001]
  • [Cites] Nat Immunol. 2008 Mar;9(3):263-71 [18223652.001]
  • [Cites] Nat Immunol. 2008 Mar;9(3):272-81 [18264101.001]
  • [Cites] Science. 2008 Mar 21;319(5870):1676-9 [18323416.001]
  • [Cites] Blood. 2008 Apr 1;111(7):3701-13 [18160665.001]
  • [Cites] Nat Rev Immunol. 2008 Jul;8(7):495-500 [18575460.001]
  • [Cites] Neurotherapeutics. 2008 Jul;5(3):399-408 [18625451.001]
  • [Cites] Curr Opin Support Palliat Care. 2008 Sep;2(3):218-22 [18685424.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2421-8 [18192506.001]
  • [Cites] N Engl J Med. 2008 Nov 27;359(22):2313-23 [19038878.001]
  • [Cites] Handb Exp Pharmacol. 2009;(189):85-110 [19048198.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6069-76 [19380866.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):28-40 [15671525.001]
  • [Cites] Mol Cell Biol. 2001 Jun;21(12):3964-73 [11359904.001]
  • [Cites] Mol Cell Biol. 2001 Aug;21(16):5299-305 [11463813.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Nat Rev Cancer. 2002 Apr;2(4):301-10 [12001991.001]
  • [Cites] Nat Rev Immunol. 2002 Dec;2(12):920-32 [12461565.001]
  • [Cites] Immunity. 2003 Nov;19(5):749-58 [14614861.001]
  • [Cites] Leukemia. 2004 Mar;18(3):597-606 [14712288.001]
  • [Cites] Nat Rev Immunol. 2004 May;4(5):348-59 [15122200.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Mar 1;89(5):1890-3 [1371884.001]
  • [Cites] Cancer Res. 1996 Dec 1;56(23):5499-505 [8968107.001]
  • [Cites] Science. 1998 Sep 11;281(5383):1680-3 [9733516.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Aug 3;96(16):9136-41 [10430908.001]
  • [ErratumIn] Proc Natl Acad Sci U S A. 2013 Feb 12;110(7):2677
  • (PMID = 19897720.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE41034
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antineoplastic Agents; 0 / BCL10 protein, human; 0 / CARD Signaling Adaptor Proteins; 0 / Caspase Inhibitors; 0 / NF-kappa B; 0 / Neoplasm Proteins; EC 3.4.22.- / Caspases; EC 3.4.22.- / MALT1 protein, human; EC 4.6.1.2 / CARD11 protein, human; EC 4.6.1.2 / Guanylate Cyclase
  • [Other-IDs] NLM/ PMC2785272
  •  go-up   go-down


2. Lenz G, Nagel I, Siebert R, Roschke AV, Sanger W, Wright GW, Dave SS, Tan B, Zhao H, Rosenwald A, Muller-Hermelink HK, Gascoyne RD, Campo E, Jaffe ES, Smeland EB, Fisher RI, Kuehl WM, Chan WC, Staudt LM: Aberrant immunoglobulin class switch recombination and switch translocations in activated B cell-like diffuse large B cell lymphoma. J Exp Med; 2007 Mar 19;204(3):633-43
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant immunoglobulin class switch recombination and switch translocations in activated B cell-like diffuse large B cell lymphoma.
  • To elucidate the mechanisms underlying chromosomal translocations in diffuse large B cell lymphoma (DLBCL), we investigated the nature and extent of immunoglobulin class switch recombination (CSR) in these tumors.
  • We used Southern blotting to detect legitimate and illegitimate CSR events in tumor samples of the activated B cell-like (ABC), germinal center B cell-like (GCB), and primary mediastinal B cell lymphoma (PMBL) subgroups of DLBCL.
  • The frequency of legitimate CSR was lower in ABC DLBCL than in GCB DLBCL and PMBL.
  • In contrast, ABC DLBCL had a higher frequency of internal deletions within the switch mu (Smu) region compared with GCB DLBCL and PMBL.
  • ABC DLBCLs also had frequent deletions within Sgamma and other illegitimate switch recombinations.
  • Sequence analysis revealed ongoing Smu deletions within ABC DLBCL tumor clones, which were accompanied by ongoing duplications and activation-induced cytidine deaminase-dependent somatic mutations.
  • These findings suggest that ABC DLBCLs have abnormalities in the regulation of CSR that could predispose to chromosomal translocations.
  • Accordingly, aberrant switch recombination was responsible for translocations in ABC DLBCLs involving BCL6, MYC, and a novel translocation partner, SPIB.

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Eur J Immunol. 2007 Jan;37(1):235-9 [17183606.001]
  • [Cites] Immunity. 2006 Aug;25(2):225-36 [16919487.001]
  • [Cites] Blood. 2000 Feb 1;95(3):1032-8 [10648419.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Immunity. 2000 Aug;13(2):199-212 [10981963.001]
  • [Cites] Cell. 2000 Sep 1;102(5):553-63 [11007474.001]
  • [Cites] Cell. 2000 Sep 1;102(5):565-75 [11007475.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1999;64:71-8 [11232339.001]
  • [Cites] Curr Opin Oncol. 2001 Sep;13(5):325-34 [11555708.001]
  • [Cites] Nature. 2001 Dec 6;414(6864):660-5 [11740565.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Trends Immunol. 2002 Jan;23(1):31-9 [11801452.001]
  • [Cites] Science. 2002 Feb 15;295(5558):1301-6 [11847344.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):9984-9 [12114543.001]
  • [Cites] Immunity. 2002 Jul;17(1):51-62 [12150891.001]
  • [Cites] Am J Pathol. 2002 Aug;161(2):413-20 [12163366.001]
  • [Cites] Mod Pathol. 2002 Nov;15(11):1172-80 [12429796.001]
  • [Cites] Blood. 2003 Feb 1;101(3):1015-23 [12393575.001]
  • [Cites] J Exp Med. 2003 Jun 16;197(12):1767-78 [12810694.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] J Exp Med. 2003 Sep 15;198(6):851-62 [12975453.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3871-9 [12933571.001]
  • [Cites] Nat Immunol. 2004 May;5(5):481-7 [15077110.001]
  • [Cites] Nat Rev Immunol. 2004 Jul;4(7):541-52 [15229473.001]
  • [Cites] Cell. 2004 Aug 20;118(4):431-8 [15315756.001]
  • [Cites] Immunity. 2004 Jul;21(1):81-93 [15345222.001]
  • [Cites] Blood. 1996 Jul 15;88(2):674-81 [8695815.001]
  • [Cites] J Exp Med. 1996 Jul 1;184(1):203-14 [8691135.001]
  • [Cites] Blood. 1996 Aug 1;88(3):985-94 [8704258.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):13931-6 [8943038.001]
  • [Cites] Blood. 1997 Jun 1;89(11):3909-18 [9166827.001]
  • [Cites] EMBO J. 1997 Dec 1;16(23):7118-29 [9384589.001]
  • [Cites] J Biol Chem. 1999 Jun 25;274(26):18470-6 [10373455.001]
  • [Cites] J Exp Med. 2004 Nov 1;200(9):1111-21 [15504820.001]
  • [Cites] J Exp Med. 2004 Nov 1;200(9):1103-10 [15520243.001]
  • [Cites] Blood. 2004 Nov 15;104(10):3318-25 [15304391.001]
  • [Cites] Leukemia. 2004 Dec;18(12):2026-31 [15496980.001]
  • [Cites] Nature. 2004 Dec 2;432(7017):635-9 [15577913.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):28-40 [15671525.001]
  • [Cites] Nat Immunol. 2005 Jul;6(7):655-61 [15970938.001]
  • [Cites] Adv Immunol. 2005;87:163-208 [16102574.001]
  • [Cites] J Exp Med. 2005 Aug 15;202(4):561-8 [16103411.001]
  • [Cites] Mol Cell. 2006 Jan 20;21(2):201-14 [16427010.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):311-7 [16492805.001]
  • [Cites] Nature. 2006 Mar 2;440(7080):105-9 [16400328.001]
  • [Cites] Curr Opin Immunol. 2006 Apr;18(2):164-74 [16464563.001]
  • [Cites] Blood. 2006 May 15;107(10):4090-100 [16424392.001]
  • [Cites] N Engl J Med. 2006 Jun 8;354(23):2431-42 [16760443.001]
  • [Cites] Nat Immunol. 2006 Jul;7(7):773-82 [16767092.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jan 4;97(1):228-33 [10618400.001]
  • (PMID = 17353367.001).
  • [ISSN] 0022-1007
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA114778-01; United States / NCI NIH HHS / CA / U01 CA084967; United States / NCI NIH HHS / CA / U01 CA114778-01; United States / NCI NIH HHS / CA / U01-CA84967
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2137913
  •  go-up   go-down


3. Mandelbaum J, Bhagat G, Tang H, Mo T, Brahmachary M, Shen Q, Chadburn A, Rajewsky K, Tarakhovsky A, Pasqualucci L, Dalla-Favera R: BLIMP1 is a tumor suppressor gene frequently disrupted in activated B cell-like diffuse large B cell lymphoma. Cancer Cell; 2010 Dec 14;18(6):568-79
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BLIMP1 is a tumor suppressor gene frequently disrupted in activated B cell-like diffuse large B cell lymphoma.
  • Diffuse large B cell lymphoma (DLBCL) is a heterogeneous disease composed of at least two distinct subtypes: germinal center B cell-like (GCB) and activated B cell-like (ABC) DLBCL.
  • In this report we show that the BLIMP1/PRDM1 gene is inactivated by multiple mechanisms, including homozygous deletions, truncating or missense mutations, and transcriptional repression by constitutively active BCL6, in ∼53% of ABC-DLBCL.
  • In vivo, conditional deletion of Blimp1 in mouse B cells promotes the development of lymphoproliferative disorders recapitulating critical features of the human ABC-DLBCL.
  • These results demonstrate that BLIMP1 is a bona fide tumor-suppressor gene whose loss contributes to lymphomagenesis by blocking plasma cell differentiation.

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • [Cites] Am J Pathol. 2008 Jul;173(1):242-52 [18583325.001]
  • [Cites] Blood Cells Mol Dis. 2008 Jul-Aug;41(1):95-9 [18346918.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Sep 9;105(36):13520-5 [18765795.001]
  • [Cites] Blood. 2009 Apr 16;113(16):3754-64 [19047678.001]
  • [Cites] Blood. 2009 May 7;113(19):4586-94 [19202128.001]
  • [Cites] Nature. 2009 Jun 4;459(7247):717-21 [19412164.001]
  • [Cites] Nature. 2009 Aug 13;460(7257):909-13 [19578360.001]
  • [Cites] Blood. 2009 Dec 17;114(26):5315-21 [19855081.001]
  • [Cites] Nature. 2010 Jan 7;463(7277):88-92 [20054396.001]
  • [Cites] Int J Cancer. 2010 Mar 15;126(6):1316-26 [19530237.001]
  • [Cites] Nat Genet. 2010 Feb;42(2):181-5 [20081860.001]
  • [Cites] Blood. 2010 Feb 4;115(5):975-84 [19965633.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Blood. 2000 Mar 15;95(6):2084-92 [10706878.001]
  • [Cites] Immunity. 2000 Aug;13(2):199-212 [10981963.001]
  • [Cites] J Immunol. 2000 Nov 15;165(10):5462-71 [11067898.001]
  • [Cites] Hum Mol Genet. 2001 Mar 15;10(6):591-7 [11230178.001]
  • [Cites] Nat Immunol. 2000 Dec;1(6):526-32 [11101876.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Blood. 2002 Apr 1;99(7):2285-90 [11895757.001]
  • [Cites] Immunity. 2002 Jul;17(1):51-62 [12150891.001]
  • [Cites] Nat Rev Immunol. 2002 Dec;2(12):920-32 [12461565.001]
  • [Cites] Blood. 2003 Apr 15;101(8):2914-23 [12515714.001]
  • [Cites] J Exp Med. 2003 Sep 15;198(6):851-62 [12975453.001]
  • [Cites] Immunity. 2003 Oct;19(4):607-20 [14563324.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3871-9 [12933571.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Blood. 2008 Sep 1;112(5):1804-12 [18552212.001]
  • [Cites] Am J Pathol. 2004 Jul;165(1):159-66 [15215171.001]
  • [Cites] J Immunol. 2004 Jul 15;173(2):1158-65 [15240705.001]
  • [Cites] Blood. 1992 Oct 1;80(7):1781-7 [1356511.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Apr 1;90(7):2935-9 [8385351.001]
  • [Cites] Science. 1993 Oct 29;262(5134):747-50 [8235596.001]
  • [Cites] EMBO J. 1995 Dec 15;14(24):6209-17 [8557040.001]
  • [Cites] Nucleic Acids Res. 1997 Mar 15;25(6):1317-8 [9092650.001]
  • [Cites] Science. 1997 Apr 25;276(5312):596-9 [9110979.001]
  • [Cites] Nature. 2004 Dec 2;432(7017):635-9 [15577913.001]
  • [Cites] Blood. 2005 Mar 1;105(5):1851-61 [15550490.001]
  • [Cites] Cancer Cell. 2005 May;7(5):445-55 [15894265.001]
  • [Cites] Nature. 2005 Jul 14;436(7048):207-13 [15937476.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1164-74 [15855278.001]
  • [Cites] Nat Immunol. 2005 Oct;6(10):1054-60 [16142238.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):311-7 [16492805.001]
  • [Cites] Blood. 2006 May 15;107(10):4090-100 [16424392.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 9;103(19):7396-401 [16651521.001]
  • [Cites] Nat Immunol. 2006 Jul;7(7):773-82 [16767092.001]
  • [Cites] Nat Immunol. 2007 Jul;8(7):705-14 [17558410.001]
  • [Cites] Cancer Cell. 2007 Sep;12(3):280-92 [17785208.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3150-7 [17682124.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2332-43 [17625604.001]
  • [Cites] Nat Rev Immunol. 2008 Jan;8(1):22-33 [18097447.001]
  • [Cites] Science. 2008 Mar 21;319(5870):1676-9 [18323416.001]
  • [CommentIn] Cancer Cell. 2010 Dec 14;18(6):537-9 [21156275.001]
  • (PMID = 21156281.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE12195
  • [Grant] United States / NCI NIH HHS / CA / R37 CA037295-28; United States / NCI NIH HHS / CA / R01 CA037295; United States / NCI NIH HHS / CA / R37 CA037295; United States / NCI NIH HHS / CA / P01 CA092625; United States / NCI NIH HHS / CA / CA-37295; United States / NCI NIH HHS / CA / CA-092625; United States / NCI NIH HHS / CA / P01 CA092625-10; United States / NCI NIH HHS / CA / CA092625-10
  • [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 / Bcl6 protein, mouse; 0 / DNA-Binding Proteins; 0 / Prdm1 protein, mouse; 0 / Transcription Factors
  • [Other-IDs] NLM/ NIHMS250122; NLM/ PMC3030476
  •  go-up   go-down


Advertisement
4. Davis RE, Zhang YQ, Southall N, Staudt LM, Austin CP, Inglese J, Auld DS: A cell-based assay for IkappaBalpha stabilization using a two-color dual luciferase-based sensor. Assay Drug Dev Technol; 2007 Feb;5(1):85-103
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A cell-based assay for IkappaBalpha stabilization using a two-color dual luciferase-based sensor.
  • A cell-sensor assay for stabilization of IkappaBalpha was developed in the activated B cell-like diffuse large B-cell lymphoma cell line OCI-Ly3.
  • This cell line expresses known nuclear factor kappaB (NFkappaB) target genes due to high constitutive activity of IkappaB kinase (IKK), which phosphorylates the protein IkappaBalpha leading to proteasomal degradation of IkappaBalpha and activation of NFkappaB.
  • The cell-sensor assay uses green and red light-emitting beetle luciferases, with the green luciferase fused to IkappaBalpha (IkappaBalpha-CBG68) and the red luciferase (CBR) present in its native state.
  • The IkappaBalpha-CBG68 reporter functions as a sensor of IKK and proteasome activity, while CBR serves to normalize for cell number and nonspecific effects.
  • [MeSH-major] Biological Assay / methods. I-kappa B Proteins / analysis. I-kappa B Proteins / metabolism. Luciferases. Lymphoma, B-Cell / metabolism. Microscopy, Fluorescence, Multiphoton / methods. Neoplasm Proteins / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cell Line, Tumor. Humans

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17355202.001).
  • [ISSN] 1540-658X
  • [Journal-full-title] Assay and drug development technologies
  • [ISO-abbreviation] Assay Drug Dev Technol
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / I-kappa B Proteins; 0 / Neoplasm Proteins; 139874-52-5 / NF-kappaB inhibitor alpha; EC 1.13.12.- / Luciferases
  •  go-up   go-down


5. Thomas RK, Sos ML, Zander T, Mani O, Popov A, Berenbrinker D, Smola-Hess S, Schultze JL, Wolf J: Inhibition of nuclear translocation of nuclear factor-kappaB despite lack of functional IkappaBalpha protein overcomes multiple defects in apoptosis signaling in human B-cell malignancies. Clin Cancer Res; 2005 Nov 15;11(22):8186-94
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of nuclear translocation of nuclear factor-kappaB despite lack of functional IkappaBalpha protein overcomes multiple defects in apoptosis signaling in human B-cell malignancies.
  • PURPOSE: Defective apoptosis signaling is a typical feature of classic Hodgkin's lymphoma, multiple myeloma, and activated B-cell-like diffuse large B-cell lymphoma.
  • EXPERIMENTAL DESIGN: We investigated the effect of different inhibitors of NF-kappaB on classic Hodgkin's lymphoma, multiple myeloma, and activated B-cell-like diffuse large B-cell lymphoma cell lines harboring different molecular defects in apoptosis signaling both quantitatively and qualitatively.
  • Surprisingly, 15-deoxy-Delta12,14-prostaglandin J(2) and the IkappaB kinase inhibitor curcumin both reduced nuclear levels of p65 in cell lines lacking IkappaBalpha, suggesting that inhibition of nuclear translocation of NF-kappaB can occur in the absence of IkappaBalpha.
  • CONCLUSIONS: These results show that molecular defects in apoptotic signaling, such as IkappaBalpha mutations, can be circumvented by targeting NF-kappaB through inhibition of the IkappaB kinase complex followed by induction of apoptosis in classic Hodgkin's lymphoma, multiple myeloma, and activated B-cell-like diffuse large B-cell lymphoma.
  • [MeSH-major] Apoptosis / physiology. B-Lymphocytes / metabolism. Cell Nucleus / metabolism. NF-kappa B / metabolism
  • [MeSH-minor] Active Transport, Cell Nucleus / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Chromans / pharmacology. Dose-Response Relationship, Drug. HSP27 Heat-Shock Proteins. Heat-Shock Proteins / metabolism. Humans. I-kappa B Kinase / metabolism. I-kappa B Proteins / genetics. I-kappa B Proteins / metabolism. Mutation. Neoplasm Proteins / metabolism. Prostaglandin D2 / analogs & derivatives. Prostaglandin D2 / pharmacology. Signal Transduction / drug effects. Thiazolidinediones / pharmacology. X-Linked Inhibitor of Apoptosis Protein / metabolism

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16299251.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 15-deoxy-delta(12,14)-prostaglandin J2; 0 / Chromans; 0 / HSP27 Heat-Shock Proteins; 0 / HSPB1 protein, human; 0 / Heat-Shock Proteins; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Thiazolidinediones; 0 / X-Linked Inhibitor of Apoptosis Protein; 139874-52-5 / NF-kappaB inhibitor alpha; EC 2.7.11.10 / I-kappa B Kinase; I66ZZ0ZN0E / troglitazone; RXY07S6CZ2 / Prostaglandin D2
  •  go-up   go-down


6. Culpin RE, Proctor SJ, Angus B, Crosier S, Anderson JJ, Mainou-Fowler T: A 9 series microRNA signature differentiates between germinal centre and activated B-cell-like diffuse large B-cell lymphoma cell lines. Int J Oncol; 2010 Aug;37(2):367-76
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A 9 series microRNA signature differentiates between germinal centre and activated B-cell-like diffuse large B-cell lymphoma cell lines.
  • The microRNAs are endogenous, non-coding RNAs that play key roles in a range of pathophysiological processes by up- or down-regulating gene expression.
  • Diffuse large B-cell lymphoma (DLBCL) is an aggressive non-Hodgkin's lymphoma with a heterogeneous biology, which has impeded the clinical assessment of patients.
  • Recent immunohistochemical approaches have identified two different prognostic groups: the more indolent germinal centre (GC)- and the higher risk activated B-cell (ABC)-like phenotypes.
  • The present study uses microRNA profiling and a number of well-characterised B-cell lymphoma cell lines to identify microRNA signatures that are correctly assigned to the DLBCL prognostic subgroups and distinguish DLBCL from other more indolent lymphoma, including follicular lymphoma (FL).
  • We identified a 9 microRNA signature that discriminated between ABC- and GC-like DLBCL.
  • This included 3 newly identified microRNAs, not previously associated with DLBCL and predicted to target genes that are de-regulated in lymphoma.
  • DLBCL was distinguished from FL by 4 microRNAs and a total of 18 microRNAs were identified that differentiated between all lymphoma and control populations.
  • In conclusion, the present study identified a microRNA signature that correctly classified GC and ABC phenotypes in DLBCL cell lines.
  • [MeSH-major] Gene Expression Profiling. Germinal Center / metabolism. Lymphoma, Large B-Cell, Diffuse / genetics. MicroRNAs / genetics
  • [MeSH-minor] Antigens, CD19 / metabolism. B-Lymphocytes / metabolism. B-Lymphocytes / pathology. Cell Line, Tumor. Cluster Analysis. Diagnosis, Differential. Humans. Lymphocyte Activation / genetics. Oligonucleotide Array Sequence Analysis

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20596664.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, CD19; 0 / MicroRNAs
  •  go-up   go-down


7. Ferch U, Kloo B, Gewies A, Pfänder V, Düwel M, Peschel C, Krappmann D, Ruland J: Inhibition of MALT1 protease activity is selectively toxic for activated B cell-like diffuse large B cell lymphoma cells. J Exp Med; 2009 Oct 26;206(11):2313-20
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of MALT1 protease activity is selectively toxic for activated B cell-like diffuse large B cell lymphoma cells.
  • Diffuse large B cell lymphoma (DLBCL) is the most common type of lymphoma in humans.
  • The aggressive activated B cell-like (ABC) subtype of DLBCL is characterized by constitutive NF-kappaB activity and requires signals from CARD11, BCL10, and the paracaspase MALT1 for survival.
  • Yet, the relevance of MALT1 proteolytic activity for malignant cell growth is unknown.
  • Here, we demonstrate preassembled CBM complexes and constitutive proteolysis of the two known MALT1 substrates in ABC-DLBCL, but not in germinal center B cell-like (GCB) DLBCL.
  • ABC-DLBCL cell treatment with a MALT1 protease inhibitor blocks A20 and BCL10 cleavage, reduces NF-kappaB activity, and decreases the expression of NF-kappaB targets genes.
  • Finally, MALT1 paracaspase inhibition results in death and growth retardation selectively in ABC-DLBCL cells.
  • Thus, our results indicate a growth-promoting role for MALT1 paracaspase activity in ABC-DLBCL and suggest that a pharmacological MALT1 protease inhibition could be a promising approach for lymphoma treatment.
  • [MeSH-major] Caspase Inhibitors. Cytotoxicity, Immunologic / drug effects. Lymphocyte Activation / drug effects. Lymphoma, Large B-Cell, Diffuse / enzymology. Lymphoma, Large B-Cell, Diffuse / pathology. Neoplasm Proteins / antagonists & inhibitors. Protease Inhibitors / pharmacology
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / metabolism. CARD Signaling Adaptor Proteins / metabolism. Caspases / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. DNA, Neoplasm / metabolism. Guanylate Cyclase / metabolism. Humans. NF-kappa B / metabolism. Protein Binding / drug effects

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • SciCrunch. OMIM: Data: Gene Annotation .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2009 Jun 4;459(7247):717-21 [19412164.001]
  • [Cites] Nat Rev Drug Discov. 2009 Jan;8(1):33-40 [19116625.001]
  • [Cites] J Exp Med. 2009 May 11;206(5):977-80 [19380636.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Mol Cell Biol. 2000 Apr;20(8):2687-95 [10733571.001]
  • [Cites] Biochem Pharmacol. 2000 Oct 15;60(8):1143-51 [11007952.001]
  • [Cites] Mol Cell. 2000 Oct;6(4):961-7 [11090634.001]
  • [Cites] Curr Opin Oncol. 2001 Sep;13(5):325-34 [11555708.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Immunol Rev. 2003 Jun;193:93-100 [12752674.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] J Exp Med. 2003 Sep 15;198(6):851-62 [12975453.001]
  • [Cites] Immunity. 2003 Nov;19(5):749-58 [14614861.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3871-9 [12933571.001]
  • [Cites] Science. 2003 Nov 28;302(5650):1581-4 [14576442.001]
  • [Cites] Nat Rev Immunol. 2004 May;4(5):348-59 [15122200.001]
  • [Cites] Ann Oncol. 1998 Jul;9(7):717-20 [9739436.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):28-40 [15671525.001]
  • [Cites] Cell Death Differ. 2006 May;13(5):687-92 [16485032.001]
  • [Cites] Nature. 2006 May 4;441(7089):106-10 [16572121.001]
  • [Cites] Nat Rev Drug Discov. 2006 Sep;5(9):785-99 [16955069.001]
  • [Cites] Nat Rev Immunol. 2006 Nov;6(11):799-812 [17063183.001]
  • [Cites] Nat Immunol. 2007 Sep;8(9):984-91 [17660823.001]
  • [Cites] J Exp Med. 2009 May 11;206(5):981-9 [19380639.001]
  • [Cites] Nature. 2009 Jun 4;459(7247):712-6 [19412163.001]
  • [Cites] Cell. 2008 Feb 8;132(3):344-62 [18267068.001]
  • [Cites] Nat Immunol. 2008 Mar;9(3):263-71 [18223652.001]
  • [Cites] Nat Immunol. 2008 Mar;9(3):272-81 [18264101.001]
  • [Cites] Science. 2008 Mar 21;319(5870):1676-9 [18323416.001]
  • [Cites] Blood. 2008 Apr 1;111(7):3701-13 [18160665.001]
  • [CommentIn] J Exp Med. 2009 Oct 26;206(11):2309-12 [19841088.001]
  • [ErratumIn] J Exp Med. 2009 Nov 23;206(12):2851
  • (PMID = 19841089.001).
  • [ISSN] 1540-9538
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / BCL10 protein, human; 0 / CARD Signaling Adaptor Proteins; 0 / Caspase Inhibitors; 0 / DNA, Neoplasm; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Protease Inhibitors; EC 3.4.22.- / Caspases; EC 3.4.22.- / MALT1 protein, human; EC 4.6.1.2 / CARD11 protein, human; EC 4.6.1.2 / Guanylate Cyclase
  • [Other-IDs] NLM/ PMC2768866
  •  go-up   go-down


8. Li D, Xie P, Mi C: Primary testicular diffuse large B-cell lymphoma shows an activated B-cell-like phenotype. Pathol Res Pract; 2010 Sep 15;206(9):611-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary testicular diffuse large B-cell lymphoma shows an activated B-cell-like phenotype.
  • The most common type of primary testicular lymphoma is diffuse large B-cell type, which has a poor prognosis relative to other extra-nodal diffuse large B-cell lymphomas (DLBCL).
  • These constitute a heterogeneous group of lymphomas with germinal center B-cell-like and activated B-cell-like subtypes.
  • Such a distinction theoretically utilizes the immunohistochemical expression of CD10, Bcl-6, and MUM1.
  • The purpose of this study was that we could stratify primary testicular lymphoma of diffuse large B-cell type according to this scheme, and further elucidate the reason why primary testicular diffuse large B-cell lymphoma possesses a poor clinical outcome.
  • Seventeen Chinese patients with primary testicular DLBCL were examined by means of a 3-antibody panel (CD10, Bcl-6, MUM1).
  • Among these 17 cases, 16 were assigned to the activated B-cell-like subtypes.
  • One case was classified as germinal center B-cell-like type.
  • The majority of primary testicular DLBCLs have activated B-cell-like subtype characteristics and high proliferative activity.
  • [MeSH-major] B-Lymphocytes / pathology. Biomarkers, Tumor / analysis. Lymphoma, Large B-Cell, Diffuse / pathology. Testicular Neoplasms / pathology

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • MedlinePlus Health Information. consumer health - Testicular Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Crown Copyright 2010. Published by Elsevier GmbH. All rights reserved.
  • (PMID = 20627604.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor
  •  go-up   go-down


9. Iqbal J, Neppalli VT, Wright G, Dave BJ, Horsman DE, Rosenwald A, Lynch J, Hans CP, Weisenburger DD, Greiner TC, Gascoyne RD, Campo E, Ott G, Müller-Hermelink HK, Delabie J, Jaffe ES, Grogan TM, Connors JM, Vose JM, Armitage JO, Staudt LM, Chan WC: BCL2 expression is a prognostic marker for the activated B-cell-like type of diffuse large B-cell lymphoma. J Clin Oncol; 2006 Feb 20;24(6):961-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BCL2 expression is a prognostic marker for the activated B-cell-like type of diffuse large B-cell lymphoma.
  • BACKGROUND: The role of BCL2 as a predictor of survival in diffuse large B-cell lymphoma (DLBCL) is controversial.
  • DLBCL is heterogeneous, and the expression of BCL2 is variable within the two major subgroups of DLBCL, germinal center B-cell-like (GCB) and activated B-cell-like (ABC) DLBCL, as well as primary mediastinal DLBCL.
  • PATIENTS AND METHODS: In this study, we investigated the correlation of BCL2 expression with survival in the two major subgroups of DLBCL, as well as the mechanisms of BCL2 expression.
  • RESULTS: There was no significant correlation between BCL2 protein expression and overall survival within the GCB subgroup, but BCL2 expression had a significant adverse effect on overall survival within the ABC subgroup (P = .008).
  • The t(14;18) was frequently observed in the GCB subgroup and was highly associated with BCL2 expression.
  • Patients with ABC DLBCL did not exhibit t(14;18) but had a markedly higher frequency of chromosome 18q21 amplification, on which BCL2 resides.
  • Thus, alternative mechanisms such as 18q21 amplification or activation of the nuclear factor-kappa B pathway, as reported previously, seem to be mainly responsible for the upregulation of BCL2 expression in the ABC subgroup.
  • CONCLUSION: Treating all DLBCL as a single entity ignores the mechanistic differences in BCL2 upregulation and obscures the prognostic significance of BCL2 expression.
  • Hence, the significance of BCL2 and other biomarkers should be assessed in the context of DLBCL subgroups in future studies.
  • [MeSH-major] Biomarkers, Tumor / analysis. Lymphoma, B-Cell / chemistry. Lymphoma, Large B-Cell, Diffuse / chemistry. Proto-Oncogene Proteins c-bcl-2 / analysis
  • [MeSH-minor] Aged. Chromosomes, Human, Pair 18. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Predictive Value of Tests. Prognosis. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Survival Analysis. Translocation, Genetic. Up-Regulation


10. Fu K, Weisenburger DD, Choi WW, Perry KD, Smith LM, Shi X, Hans CP, Greiner TC, Bierman PJ, Bociek RG, Armitage JO, Chan WC, Vose JM: Addition of rituximab to standard chemotherapy improves the survival of both the germinal center B-cell-like and non-germinal center B-cell-like subtypes of diffuse large B-cell lymphoma. J Clin Oncol; 2008 Oct 1;26(28):4587-94
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Addition of rituximab to standard chemotherapy improves the survival of both the germinal center B-cell-like and non-germinal center B-cell-like subtypes of diffuse large B-cell lymphoma.
  • PURPOSE: Diffuse large B-cell lymphoma (DLBCL) includes at least two prognostically important subtypes (ie, germinal center B-cell-like [GCB] and activated B-cell-like [ABC] DLBCL), which initially were characterized by gene expression profiling and subsequently were confirmed by immunostaining.
  • However, with the addition of rituximab to standard chemotherapy, the prognostic significance of this subclassification of DLBCL is unclear.
  • PATIENTS AND METHODS: We studied 243 patient cases of de novo DLBCL, which included 131 patient cases treated with rituximab plus standard chemotherapy (rituximab group) and 112 patient cases treated with only standard chemotherapy (control group).
  • The cases were assigned to GCB or non-GCB subgroups (the latter of which included both ABC DLBCL and unclassifiable DLBCL) on the basis of immunophenotype by using the Hans method.
  • Compared with the control group, addition of rituximab improved the 3-year overall survival (OS; 42% v 77%; P < .001) of patients with DLBCL.
  • CONCLUSION: In this retrospective study, we have shown that the subclassification of DLBCL on the basis of the cell of origin continues to have prognostic importance in the rituximab era.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Large B-Cell, Diffuse / drug therapy

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18662967.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; BZ114NVM5P / Mitoxantrone; VB0R961HZT / Prednisone; CHOP protocol; MCOP protocol
  •  go-up   go-down


11. Tay K, Shapiro G, Disinski M, Chirieac LR, Pittaluga S, Jaffe ES, Janik JE, Wiestner A, Wilson WH, Dunleavy K: Phase I/II study of a hybrid schedule of flavopiridol in relapsed/refractory mantle cell lymphoma (MCL) and diffuse large B-cell lymphoma (DLBCL). J Clin Oncol; 2009 May 20;27(15_suppl):8563
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I/II study of a hybrid schedule of flavopiridol in relapsed/refractory mantle cell lymphoma (MCL) and diffuse large B-cell lymphoma (DLBCL).
  • Because flavopiridol decreases cyclin D1 and mcl-1 and induces apoptosis in MCL cells, is significantly toxic for cell lines derived from the activated B-cell-like type of DLBCL (OCI-Ly3) and down-regulates NF-kappa B, we investigated the hybrid schedule in MCL and DLBCL.
  • 10 had MCL and 10 had DLBCL.
  • Responses were PR in 2 (1 MCL; 1 DLBCL) pts (10%); SD in 5 (25%); and PD in 13 (65%).
  • CONCLUSIONS: The hybrid schedule of flavopiridol has modest activity in relapsed MCL and DLBCL.
  • Analysis of cell cycle and transcriptional cdk targets is ongoing.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27961020.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


12. Dasmahapatra G, Lembersky D, Kramer L, Fisher RI, Friedberg J, Dent P, Grant S: The pan-HDAC inhibitor vorinostat potentiates the activity of the proteasome inhibitor carfilzomib in human DLBCL cells in vitro and in vivo. Blood; 2010 Jun 3;115(22):4478-87
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pan-HDAC inhibitor vorinostat potentiates the activity of the proteasome inhibitor carfilzomib in human DLBCL cells in vitro and in vivo.
  • Interactions between histone deacetylase inhibitors (HDACIs) and the novel proteasome inhibitor carfilzomib (CFZ) were investigated in GC- and activated B-cell-like diffuse large B-cell lymphoma (ABC-DLBCL) cells.
  • Coadministration of subtoxic or minimally toxic concentrations of CFZ) with marginally lethal concentrations of HDACIs (vorinostat, SNDX-275, or SBHA) synergistically increased mitochondrial injury, caspase activation, and apoptosis in both GC- and ABC-DLBCL cells.
  • CFZ/vorinostat induced pronounced lethality in 3 primary DLBCL specimens but minimally affected normal CD34(+) hematopoietic cells.
  • Bortezomib-resistant GC (SUDHL16) and ABC (OCI-LY10) cells exhibited partial cross-resistance to CFZ.
  • However, CFZ/vorinostat dramatically induced resistant cell apoptosis, accompanied by increased JNK activation and gammaH2A.X expression.
  • These findings indicate that HDACIs increase CFZ activity in GC- and ABC-DLBCL cells sensitive or resistant to bortezomib through a JNK-dependent mechanism in association with DNA damage and inhibition of nuclear factor-kappaB activation.
  • Together, they support further investigation of strategies combining CFZ and HDACIs in DLBCL.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Vorinostat .
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • Hazardous Substances Data Bank. CHYMOTRYPSIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Blood. 2009 Oct 15;114(16):3439-47 [19671918.001]
  • [Cites] Nature. 2000 Nov 23;408(6811):433-9 [11100718.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10833-8 [11535817.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] N Engl J Med. 2002 Jan 24;346(4):235-42 [11807147.001]
  • [Cites] Science. 2002 May 3;296(5569):922-7 [11934988.001]
  • [Cites] J Biol Chem. 2002 May 10;277(19):16639-47 [11872748.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 15;100(8):4389-94 [12677000.001]
  • [Cites] J Biol Chem. 2003 Sep 5;278(36):33714-23 [12821677.001]
  • [Cites] Oncogene. 2004 Sep 2;23(40):6693-701 [15235588.001]
  • [Cites] Mol Cell Biol. 2004 Nov;24(22):9695-704 [15509775.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 17;95(6):3003-7 [9501205.001]
  • [Cites] Cell Death Differ. 1998 Dec;5(12):1062-75 [9894613.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):673-8 [15637150.001]
  • [Cites] N Engl J Med. 2005 Jun 16;352(24):2487-98 [15958804.001]
  • [Cites] Mol Cell Biol. 2005 Jul;25(13):5429-44 [15964800.001]
  • [Cites] J Biol Chem. 2005 Jul 22;280(29):26729-34 [15937340.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3183-90 [16046532.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11658-66 [16357177.001]
  • [Cites] Blood. 2006 Jan 1;107(1):232-40 [16166589.001]
  • [Cites] Clin Cancer Res. 2006 May 15;12(10):2955-60 [16707588.001]
  • [Cites] Nat Rev Drug Discov. 2006 Sep;5(9):769-84 [16955068.001]
  • [Cites] J Clin Oncol. 2006 Oct 20;24(30):4867-74 [17001068.001]
  • [Cites] Blood. 2006 Nov 15;108(10):3441-9 [16728695.001]
  • [Cites] Nat Rev Drug Discov. 2007 Jan;6(1):21-2 [17269160.001]
  • [Cites] J Biol Chem. 2007 Jun 15;282(24):17330-4 [17478428.001]
  • [Cites] Cancer Res. 2007 Jul 1;67(13):6383-91 [17616698.001]
  • [Cites] Cancer Res. 2007 Sep 15;67(18):8536-43 [17875693.001]
  • [Cites] FEBS Lett. 2007 Oct 30;581(26):5075-81 [17927986.001]
  • [Cites] Blood. 2007 Nov 1;110(9):3281-90 [17591945.001]
  • [Cites] Clin Cancer Res. 2008 Jan 15;14(2):549-58 [18223231.001]
  • [Cites] Ann Oncol. 2008 May;19(5):964-9 [18296419.001]
  • [Cites] Blood. 2008 Aug 15;112(4):981-9 [18495956.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2489-99 [18565852.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2439-49 [18614762.001]
  • [Cites] Mol Cancer Ther. 2008 Oct;7(10):3285-97 [18852132.001]
  • [Cites] Cancer Cell. 2009 Jan 6;15(1):57-66 [19111881.001]
  • [Cites] J Mol Biol. 2009 Feb 6;385(5):1409-21 [19109974.001]
  • [Cites] Blood. 2009 May 7;113(19):4667-76 [19050304.001]
  • [Cites] Clin Cancer Res. 2009 May 15;15(10):3354-65 [19417023.001]
  • [Cites] Cancer Biol Ther. 2009 May;8(9):808-19 [19270531.001]
  • [Cites] Nature. 2009 Jun 4;459(7247):717-21 [19412164.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6069-76 [19380866.001]
  • [Cites] Blood. 2009 Jul 30;114(5):1046-52 [19436050.001]
  • [Cites] Clin Cancer Res. 2009 Aug 15;15(16):5250-7 [19671864.001]
  • [Cites] Cell. 2009 Sep 4;138(5):1019-31 [19698979.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jan 4;97(1):377-82 [10618426.001]
  • [CommentIn] NIH Guide Grants Contracts. 2015 Dec 18;:NOT-OD-16-040 [26693581.001]
  • [CommentIn] Fed Regist. 2015 Dec 10;80(237):76703-76704 [27737268.001]
  • (PMID = 20233973.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 1P50 CA130805; United States / NCI NIH HHS / CA / CA63753; United States / NCI NIH HHS / CA / R01 CA100866; United States / NCI NIH HHS / CA / R01 CA063753; United States / NCI NIH HHS / CA / R01 CA093738; United States / NCI NIH HHS / CA / CA100866; United States / NCI NIH HHS / CA / P50 CA130805; United States / NCI NIH HHS / CA / R01 CA141703; United States / NCI NIH HHS / CA / CA93738; United States / NIDDK NIH HHS / DK / R01 DK052825; United States / NCI NIH HHS / CA / R01 CA150214
  • [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 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / NF-kappa B; 0 / Oligopeptides; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 58IFB293JI / vorinostat; 69G8BD63PP / Bortezomib; 72X6E3J5AR / carfilzomib; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.4.21.1 / Chymotrypsin
  • [Other-IDs] NLM/ PMC2881506
  •  go-up   go-down


13. Hoefnagel JJ, Dijkman R, Basso K, Jansen PM, Hallermann C, Willemze R, Tensen CP, Vermeer MH: Distinct types of primary cutaneous large B-cell lymphoma identified by gene expression profiling. Blood; 2005 May 1;105(9):3671-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct types of primary cutaneous large B-cell lymphoma identified by gene expression profiling.
  • In the European Organization for Research and Treatment of Cancer (EORTC) classification 2 types of primary cutaneous large B-cell lymphoma (PCLBCL) are distinguished: primary cutaneous follicle center cell lymphomas (PCFCCL) and PCLBCL of the leg (PCLBCL-leg).
  • To establish a molecular basis for this subdivision in the EORTC classification, we investigated the gene expression profiles of 21 PCLBCLs by oligonucleotide microarray analysis.
  • Hierarchical clustering based on a B-cell signature (7450 genes) classified PCLBCL into 2 distinct subgroups consisting of, respectively, 8 PCFCCLs and 13 PCLBCLsleg.
  • PCLBCLs-leg showed increased expression of genes associated with cell proliferation; the proto-oncogenes Pim-1, Pim-2, and c-Myc; and the transcription factors Mum1/IRF4 and Oct-2.
  • In the group of PCFCCL high expression of SPINK2 was observed.
  • Further analysis suggested that PCFCCLs and PCLBCLs-leg have expression profiles similar to that of germinal center B-cell-like and activated B-cell-like diffuse large B-cell lymphoma, respectively.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, B-Cell / classification. Lymphoma, B-Cell / genetics. Skin Neoplasms / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biopsy. Cell Proliferation. Female. Gene Expression Profiling. Humans. Leg / pathology. Lymphoma, Follicular / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Skin / pathology

  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15308563.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


14. Ding H, Gabali AM, Jenson SD, Lim MS, Elenitoba-Johnson KS: P38 mitogen activated protein kinase expression and regulation by interleukin-4 in human B cell non-Hodgkin lymphomas. J Hematop; 2009;2(4):195-204
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] P38 mitogen activated protein kinase expression and regulation by interleukin-4 in human B cell non-Hodgkin lymphomas.
  • The prevalence and regulation of p38 mitogen activated protein kinase (MAPK) expression in human lymphomas have not been extensively studied.
  • In order to elucidate the role of p38 MAPK in lymphomagenesis, we examined the expression of native and phosphorylated p38 (p-p38) MAPK in cell lines derived from human hematopoietic neoplasms including B cell lymphoma-derived cell lines using Western blot analysis.
  • The p-p38 MAPK protein was also analyzed in 30 B cell non-Hodgkin lymphoma (NHL) tissue biopsies by immunohistochemistry.
  • Our results show that the expression of p38 MAPK was up-regulated in most of the cell lines as compared with peripheral blood lymphocytes, while the expression of p-p38 MAPK was more variable.
  • A subset of B cell NHL biopsies showed increased expression of p-p38 MAPK relative to reactive germinal center cells.
  • Interleukin-4 (IL-4) induced a dose-dependent increase in the expression of p-p38 MAPK (1.6- to 2.8-fold) in cell lines derived from activated B cell-like diffuse large B cell lymphoma (DLBCL) but not those from germinal center-like DLBCL.
  • The in vitro kinase activity of p38 MAPK, however, was induced (1.6- to 3.2-fold) in all five cell lines by IL-4.
  • Quantitative fluorescent RT-PCR demonstrated that all four isoforms of p38 MAPK gene were expressed in the lymphoma cell lines, with p38gamma and p38beta isoforms being predominant.
  • IL-4 stimulation increased the expression of beta, gamma, and delta isoforms but not alpha isoform in two cell lines.
  • In conclusion, there is constitutive expression and activation of p38 MAPK in a large number of B-lymphoma-derived cell lines and primary lymphoma tissues, supportive of its role in lymphomagenesis.
  • The differential IL-4 regulation of p38 MAPK expression in cell lines derived from DLBCL may relate to the cellular origin of these neoplasms.

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Endocrinology. 2000 Sep;141(9):3225-34 [10965893.001]
  • [Cites] Oncogene. 2000 Mar 16;19(12):1596-604 [10734320.001]
  • [Cites] Leuk Lymphoma. 2001 Aug;42(4):689-98 [11697499.001]
  • [Cites] J Leukoc Biol. 2002 Mar;71(3):503-10 [11867688.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 10;100(12):7259-64 [12756297.001]
  • [Cites] Int J Hematol. 2003 May;77(4):364-70 [12774925.001]
  • [Cites] Leuk Lymphoma. 2003 Jun;44(6):897-903 [12854886.001]
  • [Cites] Mol Cell Proteomics. 2004 Aug;3(8):820-33 [15169874.001]
  • [Cites] Trends Cell Biol. 1997 Sep;7(9):353-61 [17708980.001]
  • [Cites] Am J Pathol. 2008 Aug;173(2):463-9 [18599603.001]
  • [Cites] Biochem Biophys Res Commun. 1996 Nov 12;228(2):334-40 [8920915.001]
  • [Cites] Science. 1997 Jan 3;275(5296):90-4 [8974401.001]
  • [Cites] J Biol Chem. 1997 Feb 7;272(6):3296-301 [9013568.001]
  • [Cites] Nature. 1997 Mar 20;386(6622):296-9 [9069290.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Jun 27;235(3):533-8 [9207191.001]
  • [Cites] J Biol Chem. 1997 Aug 1;272(31):19509-17 [9235954.001]
  • [Cites] J Biol Chem. 1997 Aug 15;272(33):20490-4 [9252360.001]
  • [Cites] J Biol Chem. 1997 Sep 19;272(38):23668-74 [9295308.001]
  • [Cites] J Biol Chem. 1997 Nov 28;272(48):30122-8 [9374491.001]
  • [Cites] J Neurosci. 1998 Jan 1;18(1):112-8 [9412491.001]
  • [Cites] J Biol Chem. 1998 Jan 16;273(3):1741-8 [9430721.001]
  • [Cites] Biotechniques. 1998 Jun;24(6):954-8, 960, 962 [9631186.001]
  • [Cites] J Biol Chem. 1998 Jun 26;273(26):16415-20 [9632706.001]
  • [Cites] J Biol Chem. 1998 Sep 18;273(38):24832-8 [9733787.001]
  • [Cites] J Immunol. 1998 Oct 1;161(7):3225-36 [9759836.001]
  • [Cites] J Immunol. 1999 Apr 1;162(7):4246-52 [10201954.001]
  • [Cites] J Biol Chem. 1999 Aug 13;274(33):23570-6 [10438538.001]
  • [Cites] Pharmacol Ther. 1999 May-Jun;82(2-3):389-97 [10454214.001]
  • [Cites] Science. 1995 Nov 24;270(5240):1326-31 [7481820.001]
  • [Cites] J Biol Chem. 1995 Nov 17;270(46):27395-8 [7499191.001]
  • [Cites] Science. 1994 Aug 5;265(5173):808-11 [7914033.001]
  • [Cites] Cell. 1994 Sep 23;78(6):1027-37 [7923353.001]
  • [Cites] Nature. 1994 Dec 22-29;372(6508):739-46 [7997261.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Dec 19;92(26):12230-4 [8618875.001]
  • [Cites] Mol Cell Biol. 1996 Mar;16(3):1247-55 [8622669.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 30;93(9):4355-9 [8633070.001]
  • [Cites] J Biol Chem. 1996 Jul 26;271(30):17920-6 [8663524.001]
  • [Cites] J Biol Chem. 1999 Oct 15;274(42):30127-31 [10514501.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] EMBO J. 2000 Mar 15;19(6):1301-11 [10716930.001]
  • [Cites] Br J Haematol. 2001 Mar;112(3):760-7 [11260081.001]
  • (PMID = 20309428.001).
  • [ISSN] 1865-5785
  • [Journal-full-title] Journal of hematopathology
  • [ISO-abbreviation] J Hematop
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2798936
  • [Keywords] NOTNLM ; IL-4 / In vitro kinase assay / Isoforms / RT-PCR / p-p38 / p38 MAPK
  •  go-up   go-down


15. Ding BB, Yu JJ, Yu RY, Mendez LM, Shaknovich R, Zhang Y, Cattoretti G, Ye BH: Constitutively activated STAT3 promotes cell proliferation and survival in the activated B-cell subtype of diffuse large B-cell lymphomas. Blood; 2008 Feb 1;111(3):1515-23
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Constitutively activated STAT3 promotes cell proliferation and survival in the activated B-cell subtype of diffuse large B-cell lymphomas.
  • Diffuse large B-cell lymphoma (DLBCL) consists of at least 2 phenotypic subtypes; that is, the germinal center B-cell-like (GCB-DLBCL) and the activated B-cell-like (ABC-DLBCL) groups.
  • It has been shown that GCB-DLBCL responds favorably to chemotherapy and expresses high levels of BCL6, a transcription repressor known to play a causative role in lymphomagenesis.
  • In comparison, ABC-DLBCL has lower levels of BCL6, constitutively activated nuclear factor-kappaB, and tends to be refractory to chemotherapy.
  • As a result, high-level STAT3 expression and activation are preferentially detected in ABC-DLBCL and BCL6-negative normal germinal center B cells.
  • Most importantly, inactivating STAT3 by either AG490 or small interference RNA in ABC-DLBCL cells inhibits cell proliferation and triggers apoptosis.
  • These phenotypes are accompanied by decreased expression of several known STAT3 target genes, including c-Myc, JunB, and Mcl-1, and increased expression of the cell- cycle inhibitor p27.
  • In addition to identifying STAT3 as a novel BCL6 target gene, our results define a second oncogenic pathway, STAT3 activation, which operates in ABC-DLBCL, suggesting that STAT3 may be a new therapeutic target in these aggressive lymphomas.

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Immunol. 2002 Jan 1;168(1):466-74 [11751994.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1085-91 [16223771.001]
  • [Cites] J Clin Invest. 2002 May;109(9):1143-8 [11994402.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] J Immunol. 2002 Aug 15;169(4):1922-9 [12165517.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):15018-23 [12407182.001]
  • [Cites] Blood. 2003 Apr 15;101(8):2914-23 [12515714.001]
  • [Cites] J Exp Med. 2003 Jul 21;198(2):211-21 [12860928.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] J Exp Med. 2003 Sep 15;198(6):851-62 [12975453.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Oncogene. 2004 Jan 22;23(3):839-44 [14737119.001]
  • [Cites] Leuk Lymphoma. 2003;44 Suppl 3:S5-12 [15202519.001]
  • [Cites] Blood. 2004 Jul 15;104(2):543-9 [15044251.001]
  • [Cites] J Immunol. 2004 Jul 15;173(2):1158-65 [15240705.001]
  • [Cites] Cell. 2004 Oct 1;119(1):75-86 [15454082.001]
  • [Cites] J Immunol Methods. 1983 Dec 16;65(1-2):55-63 [6606682.001]
  • [Cites] Biochem Biophys Res Commun. 1994 Jul 29;202(2):1181-7 [7519422.001]
  • [Cites] Nucleic Acids Res. 1995 Dec 11;23(23):4878-84 [8532532.001]
  • [Cites] Nature. 1996 Feb 15;379(6566):645-8 [8628398.001]
  • [Cites] EMBO J. 1998 Nov 16;17(22):6670-7 [9822610.001]
  • [Cites] J Exp Med. 1999 Jan 4;189(1):63-73 [9874564.001]
  • [Cites] Cancer Cell. 2004 Nov;6(5):439-44 [15542427.001]
  • [Cites] Nature. 2004 Dec 2;432(7017):635-9 [15577913.001]
  • [Cites] J Immunol. 2005 Jan 1;174(1):205-14 [15611242.001]
  • [Cites] Nature. 2005 Jan 20;433(7023):278-85 [15662416.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1777-84 [15507530.001]
  • [Cites] Blood. 2005 Mar 1;105(5):1851-61 [15550490.001]
  • [Cites] Nat Rev Immunol. 2005 Mar;5(3):230-42 [15738953.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2924-32 [15591113.001]
  • [Cites] J Biol Chem. 2005 Apr 1;280(13):13114-21 [15659391.001]
  • [Cites] J Pathol. 2005 May;206(1):76-86 [15772984.001]
  • [Cites] J Cell Sci. 2005 May 1;118(Pt 9):1873-83 [15860730.001]
  • [Cites] Cancer Cell. 2005 May;7(5):445-55 [15894265.001]
  • [Cites] Nat Med. 2005 Jun;11(6):623-9 [15895073.001]
  • [Cites] Nat Med. 2005 Jun;11(6):595-6 [15937466.001]
  • [Cites] Cancer Res. 2005 Aug 1;65(15):6516-20 [16061629.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1392-9 [15870177.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):311-7 [16492805.001]
  • [Cites] Blood. 2006 May 15;107(10):4090-100 [16424392.001]
  • [Cites] Nature. 2006 May 4;441(7089):106-10 [16572121.001]
  • [Cites] J Exp Med. 2007 Mar 19;204(3):633-43 [17353367.001]
  • [Cites] Mol Cell Biol. 2005 Sep;25(17):7432-40 [16107692.001]
  • [Cites] Nat Med. 2005 Dec;11(12):1314-21 [16288283.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Cancer Invest. 2000;18(4):356-65 [10808372.001]
  • [Cites] Oncogene. 2000 May 15;19(21):2474-88 [10851046.001]
  • [Cites] Immunity. 2000 Aug;13(2):199-212 [10981963.001]
  • [Cites] J Exp Med. 2000 Dec 18;192(12):1841-8 [11120780.001]
  • [Cites] J Clin Invest. 2001 Feb;107(3):351-62 [11160159.001]
  • [Cites] Blood. 2001 Aug 1;98(3):762-70 [11468177.001]
  • [Cites] Mol Cell Biol. 2001 Oct;21(19):6615-25 [11533249.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Genes Dev. 2002 Mar 15;16(6):681-6 [11914273.001]
  • (PMID = 17951530.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA085573; United States / NCI NIH HHS / CA / R01 CA85573
  • [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 / BCL6 protein, human; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / STAT3 Transcription Factor; 0 / Tyrphostins; 0 / alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide
  • [Other-IDs] NLM/ PMC2214773
  •  go-up   go-down


16. Compagno M, Lim WK, Grunn A, Nandula SV, Brahmachary M, Shen Q, Bertoni F, Ponzoni M, Scandurra M, Califano A, Bhagat G, Chadburn A, Dalla-Favera R, Pasqualucci L: Mutations of multiple genes cause deregulation of NF-kappaB in diffuse large B-cell lymphoma. Nature; 2009 Jun 4;459(7247):717-21
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutations of multiple genes cause deregulation of NF-kappaB in diffuse large B-cell lymphoma.
  • Diffuse large B-cell lymphoma (DLBCL), the most common form of lymphoma in adulthood, comprises multiple biologically and clinically distinct subtypes including germinal centre B-cell-like (GCB) and activated B-cell-like (ABC) DLBCL.
  • Gene expression profile studies have shown that its most aggressive subtype, ABC-DLBCL, is associated with constitutive activation of the NF-kappaB transcription complex.
  • However, except for a small fraction of cases, it remains unclear whether NF-kappaB activation in these tumours represents an intrinsic program of the tumour cell of origin or a pathogenetic event.
  • Here we show that >50% of ABC-DLBCL and a smaller fraction of GCB-DLBCL carry somatic mutations in multiple genes, including negative (TNFAIP3, also called A20) and positive (CARD11, TRAF2, TRAF5, MAP3K7 (TAK1) and TNFRSF11A (RANK)) regulators of NF-kappaB.
  • When reintroduced in cell lines carrying biallelic inactivation of the gene, A20 induced apoptosis and cell growth arrest, indicating a tumour suppressor role.
  • Thus, our results demonstrate that NF-kappaB activation in DLBCL is caused by genetic lesions affecting multiple genes, the loss or activation of which may promote lymphomagenesis by leading to abnormally prolonged NF-kappaB responses.

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • COS Scholar Universe. author profiles.
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Blood. 2009 May 14;113(20):4918-21 [19258598.001]
  • [Cites] Science. 2000 Sep 29;289(5488):2350-4 [11009421.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):341-6 [11460166.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):346-51 [11460167.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Science. 2002 Feb 1;295(5556):868-72 [11786607.001]
  • [Cites] Nat Rev Immunol. 2002 Oct;2(10):725-34 [12360211.001]
  • [Cites] EMBO J. 2002 Oct 15;21(20):5375-85 [12374738.001]
  • [Cites] Mol Cell. 2002 Oct;10(4):693-5 [12419209.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3871-9 [12933571.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Nature. 2004 Aug 5;430(7000):694-9 [15258597.001]
  • [Cites] Nat Immunol. 2004 Oct;5(10):1052-60 [15334086.001]
  • [Cites] Blood. 1992 Oct 1;80(7):1781-7 [1356511.001]
  • [Cites] Cell. 1994 Aug 26;78(4):681-92 [8069916.001]
  • [Cites] Science. 1995 Sep 8;269(5229):1424-7 [7544915.001]
  • [Cites] Science. 1995 Dec 22;270(5244):2008-11 [8533096.001]
  • [Cites] Science. 1996 Apr 12;272(5259):263-7 [8602510.001]
  • [Cites] Nature. 1997 Nov 13;390(6656):175-9 [9367155.001]
  • [Cites] Immunity. 1997 Nov;7(5):715-25 [9390694.001]
  • [Cites] Nature. 2004 Dec 2;432(7017):635-9 [15577913.001]
  • [Cites] Blood. 2004 Dec 15;104(13):4088-96 [15331443.001]
  • [Cites] Blood. 2005 Mar 1;105(5):1851-61 [15550490.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):311-7 [16492805.001]
  • [Cites] Immunol Rev. 2006 Apr;210:171-86 [16623771.001]
  • [Cites] Nature. 2006 May 4;441(7089):106-10 [16572121.001]
  • [Cites] Nature. 2006 May 25;441(7092):431-6 [16724054.001]
  • [Cites] Nat Rev Immunol. 2006 Nov;6(11):799-812 [17063183.001]
  • [Cites] Cancer Cell. 2007 Sep;12(3):280-92 [17785208.001]
  • [Cites] Genes Chromosomes Cancer. 2008 Jan;47(1):1-7 [17886247.001]
  • [Cites] Science. 2008 Mar 21;319(5870):1676-9 [18323416.001]
  • [Cites] Blood. 2000 Mar 15;95(6):2084-92 [10706878.001]
  • (PMID = 19412164.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE12195/ GSE15127
  • [Grant] United States / NCI NIH HHS / CA / P01 CA092625-020003; United States / NIAID NIH HHS / AI / R01 AI066116-05; United States / NCI NIH HHS / CA / U54CA121852; United States / NCI NIH HHS / CA / P01 CA092625; United States / NCI NIH HHS / CA / P01 CA92625-07; United States / NCI NIH HHS / CA / U54 CA121852; United States / NIAID NIH HHS / AI / R01AI066116; United States / NIAID NIH HHS / AI / R01 AI066116; United States / NIAID NIH HHS / AI / AI066116-05; United States / NCI NIH HHS / CA / U54 CA121852-05; United States / NCI NIH HHS / CA / CA092625-020003
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / NF-kappa B; 0 / Nuclear Proteins; EC 6.3.2.19 / TNFAIP3 protein, human
  • [Other-IDs] NLM/ NIHMS151757; NLM/ PMC2973325
  •  go-up   go-down


17. Bea S, Zettl A, Wright G, Salaverria I, Jehn P, Moreno V, Burek C, Ott G, Puig X, Yang L, Lopez-Guillermo A, Chan WC, Greiner TC, Weisenburger DD, Armitage JO, Gascoyne RD, Connors JM, Grogan TM, Braziel R, Fisher RI, Smeland EB, Kvaloy S, Holte H, Delabie J, Simon R, Powell J, Wilson WH, Jaffe ES, Montserrat E, Muller-Hermelink HK, Staudt LM, Campo E, Rosenwald A, Lymphoma/Leukemia Molecular Profiling Project: Diffuse large B-cell lymphoma subgroups have distinct genetic profiles that influence tumor biology and improve gene-expression-based survival prediction. Blood; 2005 Nov 1;106(9):3183-90
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diffuse large B-cell lymphoma subgroups have distinct genetic profiles that influence tumor biology and improve gene-expression-based survival prediction.
  • Gene-expression profiling has identified 3 major subgroups of diffuse large B-cell lymphoma (DLBCL): germinal center B-cell-like (GCB), activated B-cell-like (ABC), and primary mediastinal DLBCL (PMBCL).
  • Using comparative genomic hybridization (CGH), we investigated the genetic alterations of 224 cases of untreated DLBCL (87 GCB-DLBCL, 77 ABC-DLBCL, 19 PMBCL, and 41 unclassified DLBCL) previously characterized by gene-expression profiling.
  • The DLBCL subgroups differed significantly in the frequency of particular chromosomal aberrations.
  • ABC-DLBCL had frequent trisomy 3, gains of 3q and 18q21-q22, and losses of 6q21-q22, whereas GCB-DLBCL had frequent gains of 12q12, and PMBCL had gains of 9p21-pter and 2p14-p16.
  • Parallel analysis of CGH alterations, locus-specific gene-expression profiles, and global gene-expression signatures revealed that DNA amplifications and gains had a substantial impact on the expression of genes in the involved chromosomal regions, and some genes were overexpressed in a DLBCL subgroup-specific fashion.
  • Unexpectedly, specific chromosomal alterations were associated with significant changes in gene-expression signatures that reflect various aspects of lymphoma cell biology as well as the host response to the lymphoma.
  • In addition, gains involving the chromosomal region 3p11-p12 provided prognostic information that was statistically independent of the previously defined gene-expression-based survival model, thereby improving its predictive power.

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 1989 Apr 20;320(16):1047-54 [2648153.001]
  • [Cites] Cancer Res. 2004 Sep 15;64(18):6453-60 [15374954.001]
  • [Cites] Blood. 1996 Jun 15;87(12):5269-78 [8652842.001]
  • [Cites] Blood. 1997 Jun 1;89(11):3909-18 [9166827.001]
  • [Cites] Blood. 1998 Jul 1;92(1):234-40 [9639522.001]
  • [Cites] Genes Chromosomes Cancer. 1999 Jun;25(2):123-33 [10337996.001]
  • [Cites] Blood. 1999 Jun 15;93(12):4365-74 [10361135.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):28-40 [15671525.001]
  • [Cites] Blood. 1999 Nov 1;94(9):3114-20 [10556197.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10209-13 [10954754.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jan 30;98(3):1124-9 [11158605.001]
  • [Cites] Genes Chromosomes Cancer. 2001 Apr;30(4):393-401 [11241792.001]
  • [Cites] Immunity. 2001 Sep;15(3):375-85 [11567628.001]
  • [Cites] Cancer Res. 2001 Nov 15;61(22):8143-9 [11719443.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Feb;33(2):114-22 [11793437.001]
  • [Cites] Cancer Genet Cytogenet. 2002 Jan 15;132(2):125-32 [11850073.001]
  • [Cites] Blood. 2002 Apr 1;99(7):2285-90 [11895757.001]
  • [Cites] Blood. 2002 Apr 1;99(7):2554-61 [11895793.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Mod Pathol. 2002 Aug;15(8):807-16 [12181265.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):12963-8 [12297621.001]
  • [Cites] Cancer Res. 2002 Nov 1;62(21):6240-5 [12414653.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] J Exp Med. 2003 Sep 15;198(6):851-62 [12975453.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3871-9 [12933571.001]
  • [Cites] Blood. 2004 Jun 1;103(11):4251-8 [14976040.001]
  • [Cites] Am J Pathol. 2004 Jul;165(1):159-66 [15215171.001]
  • [Cites] J Clin Oncol. 2004 Sep 1;22(17):3498-506 [15337798.001]
  • [Cites] Blood. 1996 Feb 15;87(4):1571-8 [8608249.001]
  • (PMID = 16046532.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / UO1-CA84 967
  • [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
  • [Other-IDs] NLM/ PMC1895326
  •  go-up   go-down


18. Pasqualucci L, Compagno M, Houldsworth J, Monti S, Grunn A, Nandula SV, Aster JC, Murty VV, Shipp MA, Dalla-Favera R: Inactivation of the PRDM1/BLIMP1 gene in diffuse large B cell lymphoma. J Exp Med; 2006 Feb 20;203(2):311-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inactivation of the PRDM1/BLIMP1 gene in diffuse large B cell lymphoma.
  • PR domain containing 1 with zinc finger domain (PRDM1)/B lymphocyte-induced maturation protein 1 (BLIMP1) is a transcriptional repressor expressed in a subset of germinal center (GC) B cells and in all plasma cells, and required for terminal B cell differentiation.
  • The BLIMP1 locus lies on chromosome 6q21-q22.1, a region frequently deleted in B cell lymphomas, suggesting that it may harbor a tumor suppressor gene.
  • We report here that the BLIMP1 gene is inactivated by structural alterations in 24% (8 out of 34) activated B cell-like diffuse large cell lymphoma (ABC-DLBCL), but not in GC B cell-like (n = 0/37) or unclassified (n = 0/21) DLBCL.
  • Furthermore, most non-GC type DLBCL cases (n = 20/26, 77%) lack BLIMP1 protein expression, despite the presence of BLIMP1 mRNA.
  • These results indicate that a sizable fraction of ABC-DLBCL carry an inactive BLIMP1 gene, and suggest that the same gene is inactivated by epigenetic mechanisms in an additional large number of cases.

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Exp Med. 1998 Aug 3;188(3):515-25 [9687529.001]
  • [Cites] Blood. 1998 Jul 1;92(1):234-40 [9639522.001]
  • [Cites] J Pathol. 2005 May;206(1):76-86 [15772984.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1164-74 [15855278.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3183-90 [16046532.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Mol Cell Biol. 2000 Apr;20(7):2592-603 [10713181.001]
  • [Cites] Immunity. 2000 Aug;13(2):199-212 [10981963.001]
  • [Cites] J Immunol. 2000 Nov 15;165(10):5462-71 [11067898.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):341-6 [11460166.001]
  • [Cites] Immunity. 2002 Jul;17(1):51-62 [12150891.001]
  • [Cites] Nat Rev Immunol. 2002 Dec;2(12):920-32 [12461565.001]
  • [Cites] J Immunol. 2003 Mar 15;170(6):3125-33 [12626569.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] J Exp Med. 2003 Sep 15;198(6):851-62 [12975453.001]
  • [Cites] Immunity. 2003 Oct;19(4):607-20 [14563324.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3871-9 [12933571.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Genes Chromosomes Cancer. 1991 May;3(3):189-201 [1868033.001]
  • [Cites] Mol Cell Biol. 1992 May;12(5):1940-9 [1569931.001]
  • [Cites] Blood. 1992 Oct 1;80(7):1781-7 [1356511.001]
  • [Cites] Blood. 1993 Oct 1;82(7):2157-62 [8104536.001]
  • [Cites] Cell. 1994 Apr 22;77(2):297-306 [8168136.001]
  • [Cites] Science. 1997 Apr 25;276(5312):596-9 [9110979.001]
  • [Cites] Blood. 2005 Mar 1;105(5):1851-61 [15550490.001]
  • (PMID = 16492805.001).
  • [ISSN] 0022-1007
  • [Journal-full-title] The Journal of experimental medicine
  • [ISO-abbreviation] J. Exp. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA092625; United States / NCI NIH HHS / CA / CA-092625
  • [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 / Codon, Nonsense; 0 / RNA Splice Sites; 0 / Repressor Proteins; 0 / Transcription Factors; 138415-26-6 / PRDM1 protein, human
  • [Other-IDs] NLM/ PMC2118216
  •  go-up   go-down


19. Calado DP, Zhang B, Srinivasan L, Sasaki Y, Seagal J, Unitt C, Rodig S, Kutok J, Tarakhovsky A, Schmidt-Supprian M, Rajewsky K: Constitutive canonical NF-κB activation cooperates with disruption of BLIMP1 in the pathogenesis of activated B cell-like diffuse large cell lymphoma. Cancer Cell; 2010 Dec 14;18(6):580-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Constitutive canonical NF-κB activation cooperates with disruption of BLIMP1 in the pathogenesis of activated B cell-like diffuse large cell lymphoma.
  • Diffuse large B cell lymphoma (DLBCL) comprises disease entities with distinct genetic profiles, including germinal center B cell (GCB)-like and activated B cell (ABC)-like DLBCLs.
  • Major differences between these two subtypes include genetic aberrations leading to constitutive NF-κB activation and interference with terminal B cell differentiation through BLIMP1 inactivation, observed in ABC- but not GCB-DLBCL.
  • Using conditional gain-of-function and/or loss-of-function mutagenesis in the mouse, we show that constitutive activation of the canonical NF-κB pathway cooperates with disruption of BLIMP1 in the development of a lymphoma that resembles human ABC-DLBCL.
  • Our work suggests that both NF-κB signaling, as an oncogenic event, and BLIMP1, as a tumor suppressor, play causal roles in the pathogenesis of ABC-DLBCL.

  • COS Scholar Universe. author profiles.
  • Jackson Laboratory JAX®Mice Database. culture/stock collections - B6(Cg)-Gt(ROSA)26Sor<tm4(Ikbkb)Rsky>/J (subscription/membership/fee required).
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • [Cites] Clin Cancer Res. 2009 Sep 1;15(17):5494-502 [19706817.001]
  • [Cites] Nature. 2009 Jun 4;459(7247):717-21 [19412164.001]
  • [Cites] N Engl J Med. 2010 Apr 15;362(15):1417-29 [20393178.001]
  • [Cites] Cold Spring Harb Perspect Biol. 2010 Jun;2(6):a000109 [20516126.001]
  • [Cites] Cancer Cell. 2007 Aug;12(2):131-44 [17692805.001]
  • [Cites] J Immunol. 2010 Jul 1;185(1):220-30 [20505142.001]
  • [Cites] J Immunol. 2010 Jul 1;185(1):211-9 [20505144.001]
  • [Cites] Cancer Cell. 2010 Dec 14;18(6):568-79 [21156281.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] J Exp Med. 2000 Apr 17;191(8):1281-92 [10770796.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10209-13 [10954754.001]
  • [Cites] J Immunol. 2000 Nov 15;165(10):5462-71 [11067898.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Bioinformatics. 2003 Jan 22;19(2):295-6 [12538257.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] BMC Dev Biol. 2001;1:4 [11299042.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Curr Biol. 1994 Jul 1;4(7):573-83 [7953531.001]
  • [Cites] J Exp Med. 1996 May 1;183(5):2303-12 [8642339.001]
  • [Cites] Science. 1997 Apr 25;276(5312):596-9 [9110979.001]
  • [Cites] Science. 1998 Jul 3;281(5373):96-9 [9651253.001]
  • [Cites] Clin Cancer Res. 2005 Feb 1;11(3):1065-72 [15709173.001]
  • [Cites] Blood. 2005 Mar 1;105(5):1851-61 [15550490.001]
  • [Cites] Nature. 2005 Jul 14;436(7048):207-13 [15937476.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):311-7 [16492805.001]
  • [Cites] Blood. 2006 May 15;107(10):4090-100 [16424392.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 May 9;103(19):7396-401 [16651521.001]
  • [Cites] Immunity. 2006 Jun;24(6):729-39 [16782029.001]
  • [Cites] Cancer Cell. 2007 Aug;12(2):115-30 [17692804.001]
  • [Cites] Nature. 2010 Jan 7;463(7277):88-92 [20054396.001]
  • [Cites] Cancer Cell. 2007 Sep;12(3):280-92 [17785208.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2332-43 [17625604.001]
  • [Cites] Science. 2008 Mar 21;319(5870):1676-9 [18323416.001]
  • [Cites] Annu Rev Immunol. 2008;26:133-69 [18370921.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Sep 9;105(36):13520-5 [18765795.001]
  • [Cites] Nature. 2009 Jun 4;459(7247):712-6 [19412163.001]
  • [CommentIn] Cancer Cell. 2010 Dec 14;18(6):537-9 [21156275.001]
  • (PMID = 21156282.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA092625-08; United States / NCI NIH HHS / CA / P01 CA092625; United States / NCI NIH HHS / CA / P01 CA092625-07; None / None / / P01 CA092625-07; United States / NCI NIH HHS / CA / P01CA092625; United States / NCI NIH HHS / CA / CA092625-08
  • [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 / NF-kappa B; 0 / Prdm1 protein, mouse; 0 / Transcription Factors; EC 2.7.11.10 / I-kappa B Kinase; EC 2.7.11.10 / Ikbkb protein, mouse
  • [Other-IDs] NLM/ NIHMS253996; NLM/ PMC3018685
  •  go-up   go-down


20. Tagawa H, Suguro M, Tsuzuki S, Matsuo K, Karnan S, Ohshima K, Okamoto M, Morishima Y, Nakamura S, Seto M: Comparison of genome profiles for identification of distinct subgroups of diffuse large B-cell lymphoma. Blood; 2005 Sep 1;106(5):1770-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of genome profiles for identification of distinct subgroups of diffuse large B-cell lymphoma.
  • Diffuse large B-cell lymphoma (DLBCL) comprises molecularly distinct subgroups such as activated B-cell-like (ABC) and germinal center B-cell-like (GCB) DLBCLs.
  • We previously reported that CD5(+) and CD5(-)CD10(+) DLBCL constitute clinically relevant subgroups.
  • To determine whether these 2 subgroups are related to ABC and GCB DLBCLs, we analyzed the genomic imbalance of 99 cases (36 CD5(+), 19 CD5(-)CD10(+), and 44 CD5(-)CD10(-)) using array-based comparative genomic hybridization (CGH).
  • Forty-six of these cases (22 CD5(+), 7 CD5(-)CD10(+), and 17 CD5(-)CD10(-)) were subsequently subjected to gene-expression profiling, resulting in their division into 28 ABC (19 CD5(+) and 9 CD5(-)CD10(-)) and 18 GCB (3 CD5(+), 7 CD5(-)CD10(+), and 8 CD5(-)CD10(-)) types.
  • A comparison of genome profiles of distinct subgroups of DLBCL demonstrated that (1) ABC DLBCL is characterized by gain of 3q, 18q, and 19q and loss of 6q and 9p21, and GCB DLBCL is characterized by gain of 1q, 2p, 7q, and 12q;.
  • (2) the genomic imbalances characteristic of the CD5(+) and CD5(-)CD10(+) groups were similar to those of the ABC and GCB types, respectively.
  • These findings suggest that CD5(+) and CD5(-)CD10(+) subgroups are included, respectively, in the ABC and GCB types.
  • Finally, when searching for genomic imbalances that affect patients' prognosis, we found that 9p21 loss (p16(INK4a) locus) marks the most aggressive type of DLBCL.
  • [MeSH-major] Antigens, CD / genetics. Gene Expression Profiling. Lymphoma, B-Cell / classification. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / classification. Lymphoma, Large B-Cell, Diffuse / genetics

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Blood. 2006 Apr 15;107(8):3052
  • (PMID = 15886317.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor
  •  go-up   go-down


21. Lenz G, Wright GW, Emre NC, Kohlhammer H, Dave SS, Davis RE, Carty S, Lam LT, Shaffer AL, Xiao W, Powell J, Rosenwald A, Ott G, Muller-Hermelink HK, Gascoyne RD, Connors JM, Campo E, Jaffe ES, Delabie J, Smeland EB, Rimsza LM, Fisher RI, Weisenburger DD, Chan WC, Staudt LM: Molecular subtypes of diffuse large B-cell lymphoma arise by distinct genetic pathways. Proc Natl Acad Sci U S A; 2008 Sep 9;105(36):13520-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular subtypes of diffuse large B-cell lymphoma arise by distinct genetic pathways.
  • Gene-expression profiling has been used to define 3 molecular subtypes of diffuse large B-cell lymphoma (DLBCL), termed germinal center B-cell-like (GCB) DLBCL, activated B-cell-like (ABC) DLBCL, and primary mediastinal B-cell lymphoma (PMBL).
  • To investigate whether these DLBCL subtypes arise by distinct pathogenetic mechanisms, we analyzed 203 DLBCL biopsy samples by high-resolution, genome-wide copy number analysis coupled with gene-expression profiling.
  • Of 272 recurrent chromosomal aberrations that were associated with gene-expression alterations, 30 were used differentially by the DLBCL subtypes (P < 0.006).
  • An amplicon on chromosome 19 was detected in 26% of ABC DLBCLs but in only 3% of GCB DLBCLs and PMBLs.
  • Knockdown of SPIB by RNA interference was toxic to ABC DLBCL cell lines but not to GCB DLBCL, PMBL, or myeloma cell lines, strongly implicating SPIB as an oncogene involved in the pathogenesis of ABC DLBCL.
  • Deletion of the INK4a/ARF tumor suppressor locus and trisomy 3 also occurred almost exclusively in ABC DLBCLs and was associated with inferior outcome within this subtype.
  • FOXP1 emerged as a potential oncogene in ABC DLBCL that was up-regulated by trisomy 3 and by more focal high-level amplifications.
  • In GCB DLBCL, amplification of the oncogenic mir-17-92 microRNA cluster and deletion of the tumor suppressor PTEN were recurrent, but these events did not occur in ABC DLBCL.
  • Together, these data provide genetic evidence that the DLBCL subtypes are distinct diseases that use different oncogenic pathways.

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • SciCrunch. ArrayExpress: Data: Microarray .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jul 5;102(27):9625-30 [15983384.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3183-90 [16046532.001]
  • [Cites] Adv Immunol. 2005;87:163-208 [16102574.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1770-7 [15886317.001]
  • [Cites] Cancer Res. 2004 May 1;64(9):3087-95 [15126345.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 15;101(24):9067-72 [15199222.001]
  • [Cites] Blood. 1997 Jun 1;89(11):3909-18 [9166827.001]
  • [Cites] EMBO J. 1997 Dec 1;16(23):7118-29 [9384589.001]
  • [Cites] Blood. 1998 Dec 1;92(11):4487-9 [9882102.001]
  • [Cites] Cancer Res. 2000 Feb 1;60(3):549-52 [10676635.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Curr Opin Oncol. 2001 Sep;13(5):325-34 [11555708.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Nat Rev Immunol. 2002 Dec;2(12):920-32 [12461565.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] J Exp Med. 2003 Sep 15;198(6):851-62 [12975453.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3871-9 [12933571.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):28-40 [15671525.001]
  • [Cites] J Biol Chem. 2005 Mar 4;280(9):7444-51 [15618216.001]
  • [Cites] Leukemia. 2005 Apr;19(4):652-8 [15703784.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):839-43 [15944709.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2477-85 [16317097.001]
  • [Cites] Nature. 2006 May 4;441(7089):106-10 [16572121.001]
  • [Cites] N Engl J Med. 2006 Jun 8;354(23):2419-30 [16760442.001]
  • [Cites] Leukemia. 2006 Jul;20(7):1300-3 [16673020.001]
  • [Cites] Nature. 2006 Nov 23;444(7118):444-54 [17122850.001]
  • [Cites] Nat Genet. 2007 Mar;39(3):347-51 [17293865.001]
  • [Cites] J Exp Med. 2007 Mar 19;204(3):633-43 [17353367.001]
  • [Cites] Trends Biochem Sci. 2007 Nov;32(11):509-19 [17949986.001]
  • [Cites] Science. 2008 Mar 21;319(5870):1676-9 [18323416.001]
  • [Cites] Blood. 2008 Apr 1;111(7):3701-13 [18160665.001]
  • [Cites] Leukemia. 2005 Aug;19(8):1299-305 [15944719.001]
  • (PMID = 18765795.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA114778; United States / NCI NIH HHS / CA / UO1-CA 114778; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins; 0 / Tumor Suppressor Proteins
  • [Other-IDs] NLM/ PMC2533222
  •  go-up   go-down


22. Davis RE, Ngo VN, Lenz G, Tolar P, Young RM, Romesser PB, Kohlhammer H, Lamy L, Zhao H, Yang Y, Xu W, Shaffer AL, Wright G, Xiao W, Powell J, Jiang JK, Thomas CJ, Rosenwald A, Ott G, Muller-Hermelink HK, Gascoyne RD, Connors JM, Johnson NA, Rimsza LM, Campo E, Jaffe ES, Wilson WH, Delabie J, Smeland EB, Fisher RI, Braziel RM, Tubbs RR, Cook JR, Weisenburger DD, Chan WC, Pierce SK, Staudt LM: Chronic active B-cell-receptor signalling in diffuse large B-cell lymphoma. Nature; 2010 Jan 7;463(7277):88-92
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chronic active B-cell-receptor signalling in diffuse large B-cell lymphoma.
  • A role for B-cell-receptor (BCR) signalling in lymphomagenesis has been inferred by studying immunoglobulin genes in human lymphomas and by engineering mouse models, but genetic and functional evidence for its oncogenic role in human lymphomas is needed.
  • Here we describe a form of 'chronic active' BCR signalling that is required for cell survival in the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL).
  • The signalling adaptor CARD11 is required for constitutive NF-kappaB pathway activity and survival in ABC DLBCL.
  • Roughly 10% of ABC DLBCLs have mutant CARD11 isoforms that activate NF-kappaB, but the mechanism that engages wild-type CARD11 in other ABC DLBCLs was unknown.
  • An RNA interference genetic screen revealed that a BCR signalling component, Bruton's tyrosine kinase, is essential for the survival of ABC DLBCLs with wild-type CARD11.
  • In addition, knockdown of proximal BCR subunits (IgM, Ig-kappa, CD79A and CD79B) killed ABC DLBCLs with wild-type CARD11 but not other lymphomas.
  • The BCRs in these ABC DLBCLs formed prominent clusters in the plasma membrane with low diffusion, similarly to BCRs in antigen-stimulated normal B cells.
  • Somatic mutations affecting the immunoreceptor tyrosine-based activation motif (ITAM) signalling modules of CD79B and CD79A were detected frequently in ABC DLBCL biopsy samples but rarely in other DLBCLs and never in Burkitt's lymphoma or mucosa-associated lymphoid tissue lymphoma.
  • In 18% of ABC DLBCLs, one functionally critical residue of CD79B, the first ITAM tyrosine, was mutated.
  • These mutations increased surface BCR expression and attenuated Lyn kinase, a feedback inhibitor of BCR signalling.
  • These findings establish chronic active BCR signalling as a new pathogenetic mechanism in ABC DLBCL, suggesting several therapeutic strategies.

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • SciCrunch. OMIM: Data: Gene Annotation .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Immunity. 1999 Nov;11(5):537-45 [10591179.001]
  • [Cites] Immunity. 2009 Jan 16;30(1):44-55 [19135393.001]
  • [Cites] J Immunol. 2001 Feb 1;166(3):1507-16 [11160190.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):4126-31 [12651942.001]
  • [Cites] Nat Rev Immunol. 2004 May;4(5):348-59 [15122200.001]
  • [Cites] Cell. 2004 Jun 11;117(6):787-800 [15186779.001]
  • [Cites] Mol Immunol. 2004 Jul;41(6-7):599-613 [15219998.001]
  • [Cites] Oncogene. 2004 Oct 18;23(48):8001-6 [15489917.001]
  • [Cites] J Immunol. 2004 Nov 1;173(9):5601-9 [15494510.001]
  • [Cites] Cancer Res. 1986 Jul;46(7):3211-24 [3011242.001]
  • [Cites] Nature. 1989 Mar 30;338(6214):383-4 [2927501.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Aug 1;89(15):6770-4 [1495966.001]
  • [Cites] Hybridoma. 1995 Jun;14(3):243-6 [7590786.001]
  • [Cites] Immunity. 1997 Jul;7(1):69-81 [9252121.001]
  • [Cites] Cell. 1997 Sep 19;90(6):1073-83 [9323135.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):28-40 [15671525.001]
  • [Cites] Adv Immunol. 2005;87:163-208 [16102574.001]
  • [Cites] Immunity. 1999 Nov;11(5):527-36 [10591178.001]
  • [Cites] Nat Immunol. 2005 Nov;6(11):1168-76 [16200067.001]
  • [Cites] Nature. 2006 May 4;441(7089):106-10 [16572121.001]
  • [Cites] J Exp Med. 2006 Jul 10;203(7):1785-94 [16818674.001]
  • [Cites] ChemMedChem. 2007 Jan;2(1):58-61 [17154430.001]
  • [Cites] J Cell Sci. 2007 Feb 1;120(Pt 3):379-83 [17251378.001]
  • [Cites] Assay Drug Dev Technol. 2007 Feb;5(1):49-64 [17355199.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Aug 14;104(33):13283-8 [17684099.001]
  • [Cites] Blood. 2008 Feb 15;111(4):2230-7 [18006696.001]
  • [Cites] Curr Protoc Mol Biol. 2004 May;Chapter 18:Unit 18.11 [18265343.001]
  • [Cites] Science. 2008 Mar 21;319(5870):1676-9 [18323416.001]
  • [Cites] PLoS Biol. 2008 Jun 24;6(6):e152 [18578569.001]
  • [Cites] N Engl J Med. 2008 Nov 27;359(22):2313-23 [19038878.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • (PMID = 20054396.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] ENG
  • [Databank-accession-numbers] GEO/ GSE18817
  • [Grant] United States / Intramural NIH HHS / / NIH0011349228; United States / PHS HHS / / NIH0011349228; United States / Howard Hughes Medical Institute / / ; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD79; 0 / CARD Signaling Adaptor Proteins; 0 / Receptors, Antigen, B-Cell; EC 2.7.10.1 / Agammaglobulinaemia tyrosine kinase; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / lyn protein-tyrosine kinase; EC 2.7.10.2 / src-Family Kinases; EC 4.6.1.2 / CARD11 protein, human; EC 4.6.1.2 / Guanylate Cyclase
  • [Other-IDs] NLM/ NIHMS178837; NLM/ PMC2845535
  •  go-up   go-down


23. Dunleavy K, Pittaluga S, Czuczman MS, Dave SS, Wright G, Grant N, Shovlin M, Jaffe ES, Janik JE, Staudt LM, Wilson WH: Differential efficacy of bortezomib plus chemotherapy within molecular subtypes of diffuse large B-cell lymphoma. Blood; 2009 Jun 11;113(24):6069-76
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential efficacy of bortezomib plus chemotherapy within molecular subtypes of diffuse large B-cell lymphoma.
  • Gene expression profiling of diffuse large B-cell lymphoma (DLBCL) has revealed distinct molecular subtypes that include germinal center B cell-like (GCB) and activated B cell-like (ABC) DLBCL.
  • ABC DLBCL has a worse survival after upfront chemotherapy and is characterized by constitutive activation of the antiapoptotic nuclear factor-kappa B (NF-kappaB) pathway, which can inhibit chemotherapy.
  • We hypothesized that inhibition of NF-kappaB might sensitize ABC but not GCB DLBCL to chemotherapy and improve outcome.
  • As the proteasome inhibitor bortezomib can inhibit NF-kappaB through blocking IkappaBalpha degradation, we investigated bortezomib alone followed by bortezomib and doxorubicin-based chemotherapy in recurrent DLBCL.
  • Tumor tissue was analyzed by gene expression profiling and/or immunohistochemistry to identify molecular DLBCL subtypes.
  • As a control, we showed that relapsed/refractory ABC and GCB DLBCL have equally poor survivals after upfront chemotherapy.
  • Bortezomib alone had no activity in DLBCL, but when combined with chemotherapy, it demonstrated a significantly higher response (83% vs 13%; P < .001) and median overall survival (10.8 vs 3.4 months; P = .003) in ABC compared with GCB DLBCL, respectively.
  • These results suggest bortezomib enhances the activity of chemotherapy in ABC but not GCB DLBCL, and provide a rational therapeutic approach based on genetically distinct DLBCL subtypes.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Large B-Cell, Diffuse / drug therapy. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Adolescent. Adult. Aged. B-Lymphocytes / drug effects. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Boronic Acids / administration & dosage. Bortezomib. Doxorubicin / administration & dosage. Female. Gene Expression Profiling. Germinal Center / drug effects. Humans. Immunoenzyme Techniques. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prognosis. Pyrazines / administration & dosage. Survival Rate. Treatment Outcome. Young Adult


24. Pike BL, Greiner TC, Wang X, Weisenburger DD, Hsu YH, Renaud G, Wolfsberg TG, Kim M, Weisenberger DJ, Siegmund KD, Ye W, Groshen S, Mehrian-Shai R, Delabie J, Chan WC, Laird PW, Hacia JG: DNA methylation profiles in diffuse large B-cell lymphoma and their relationship to gene expression status. Leukemia; 2008 May;22(5):1035-43
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA methylation profiles in diffuse large B-cell lymphoma and their relationship to gene expression status.
  • In an initial epigenetic characterization of diffuse large B-cell lymphoma (DLBCL), we evaluated the DNA methylation levels of over 500 CpG islands.
  • Interestingly, the methylation levels of a CpG island proximal to FLJ21062 differed between the activated B-cell-like (ABC-DLBCL) and germinal center B-cell-like (GCB-DLBCL) subtypes.
  • In addition, we compared the methylation and expression status of 67 genes proximal (within 500 bp) to the methylation assays.
  • However, many of these same genes were also poorly expressed in DLBCL tumors where their cognate CpG islands were hypomethylated.
  • Nevertheless, the proportional reductions in BNIP3, MGMT, RBP1, GATA4, IGSF4, CRABP1 and FLJ21062 expression with increasing methylation suggest that epigenetic processes strongly influence these genes.
  • Lastly, the moderate expression of several genes proximal to hypermethylated CpG tracts suggests that DNA methylation assays are not always accurate predictors of gene silencing.

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Cancer Res. 2007 Mar 15;67(6):2617-25 [17363581.001]
  • [Cites] J Natl Cancer Inst. 2002 Jan 2;94(1):26-32 [11773279.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] J Nutr. 2002 Aug;132(8 Suppl):2430S-2434S [12163706.001]
  • [Cites] Am J Pathol. 2002 Sep;161(3):1007-13 [12213729.001]
  • [Cites] Mol Cell Biol. 2002 Oct;22(19):6689-96 [12215526.001]
  • [Cites] Cancer Res. 2002 Oct 15;62(20):5902-5 [12384555.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] Clin Cancer Res. 2003 Sep 15;9(11):4034-42 [14519624.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Haematologica. 2004 Feb;89(2):154-64 [15003890.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 20;101(16):6062-7 [15075390.001]
  • [Cites] Clin Chem. 2004 Aug;50(8):1480-1 [15277367.001]
  • [Cites] J Clin Oncol. 2004 Sep 1;22(17):3498-506 [15337798.001]
  • [Cites] N Engl J Med. 2004 Nov 18;351(21):2159-69 [15548776.001]
  • [Cites] J Pharmacol Exp Ther. 2004 Dec;311(3):968-81 [15302897.001]
  • [Cites] Mol Cancer Ther. 2005 Jan;4(1):61-9 [15657354.001]
  • [Cites] Clin Cancer Res. 2005 Feb 1;11(3):1021-7 [15709167.001]
  • [Cites] Saudi Med J. 2005 Jul;26(7):1099-103 [16047061.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1770-7 [15886317.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6351-7 [16155019.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3183-90 [16046532.001]
  • [Cites] Nucleic Acids Res. 2005;33(21):6823-36 [16326863.001]
  • [Cites] Nat Genet. 2006 Feb;38(2):149-53 [16444255.001]
  • [Cites] Oncogene. 2006 Feb 9;25(6):959-68 [16205641.001]
  • [Cites] J Clin Oncol. 2006 Feb 20;24(6):995-1007 [16418498.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2477-85 [16317097.001]
  • [Cites] Nat Genet. 2006 May;38(5):540-9 [16642018.001]
  • [Cites] Hum Mutat. 2006 Jun;27(6):589-96 [16652338.001]
  • [Cites] Leuk Res. 2006 Jul;30(7):859-67 [16406514.001]
  • [Cites] Int J Cancer. 2006 Nov 1;119(9):2078-83 [16823849.001]
  • [Cites] Int J Hematol. 2006 Oct;84(3):248-55 [17050200.001]
  • [Cites] Cancer Res. 2006 Nov 15;66(22):10664-70 [17090521.001]
  • [Cites] Nucleic Acids Res. 2006;34(20):e136 [17041235.001]
  • [Cites] Carcinogenesis. 2007 Jan;28(1):60-70 [16774933.001]
  • [Cites] Cell Oncol. 2006;28(5-6):259-72 [17167179.001]
  • [Cites] Nucleic Acids Res. 2000 Apr 15;28(8):E32 [10734209.001]
  • (PMID = 18288132.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NHGRI NIH HHS / HG / P50-HG002790; United States / NCI NIH HHS / CA / U01 CA084967; United States / NHGRI NIH HHS / HG / P50 HG002790-02; United States / NIGMS NIH HHS / GM / GM072477-03; United States / NCI NIH HHS / CA / C06 CA62528-01; United States / NIGMS NIH HHS / GM / R01 GM072477-04; United States / NCI NIH HHS / CA / CA014089-30; United States / NHGRI NIH HHS / HG / P50 HG002790-04; United States / NCI NIH HHS / CA / CA014089-26; United States / NCI NIH HHS / CA / U01 CA084967-05; United States / NCI NIH HHS / CA / CA84967; United States / Intramural NIH HHS / / Z01 HG000185-07; United States / NCI NIH HHS / CA / CA36727; United States / NCI NIH HHS / CA / C06 CA062528; United States / NIGMS NIH HHS / GM / R01 GM072477-05; United States / NHGRI NIH HHS / HG / P50 HG002790-03; United States / NIGMS NIH HHS / GM / R01 GM072477-02; United States / NIGMS NIH HHS / GM / GM072477-02; United States / NCI NIH HHS / CA / CA084967-05; United States / NIGMS NIH HHS / GM / GM072477-01A1; United States / NIGMS NIH HHS / GM / R01 GM072477-01A1; United States / NHGRI NIH HHS / HG / HG002790-04; United States / Intramural NIH HHS / / Z99 HG999999; United States / NHGRI NIH HHS / HG / HG002790-03; United States / NCI NIH HHS / CA / P30 CA014089; United States / NCRR NIH HHS / RR / C06 RR10600-01; United States / NCI NIH HHS / CA / P30-CA014089; United States / NCI NIH HHS / CA / P30 CA036727; None / None / / P30 CA036727-24; United States / NIGMS NIH HHS / GM / GM072477-05; United States / NHGRI NIH HHS / HG / P50 HG002790-01A1; United States / NCRR NIH HHS / RR / C06 RR14514-01; United States / NCRR NIH HHS / RR / C06 RR014514; United States / NHGRI NIH HHS / HG / HG002790-02; United States / NIGMS NIH HHS / GM / R01 GM072477-03; United States / NIGMS NIH HHS / GM / GM072477-04; United States / NCI NIH HHS / CA / P30 CA014089-30; United States / NCI NIH HHS / CA / P30 CA036727-24; United States / NIGMS NIH HHS / GM / R01 GM072477; United States / NHGRI NIH HHS / HG / P50 HG002790; United States / NCI NIH HHS / CA / P30 CA014089-26; United States / NHGRI NIH HHS / HG / HG002790-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ NIHMS97202; NLM/ PMC2654231
  •  go-up   go-down


25. Lam LT, Davis RE, Pierce J, Hepperle M, Xu Y, Hottelet M, Nong Y, Wen D, Adams J, Dang L, Staudt LM: Small molecule inhibitors of IkappaB kinase are selectively toxic for subgroups of diffuse large B-cell lymphoma defined by gene expression profiling. Clin Cancer Res; 2005 Jan 1;11(1):28-40
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small molecule inhibitors of IkappaB kinase are selectively toxic for subgroups of diffuse large B-cell lymphoma defined by gene expression profiling.
  • Constitutive activation of the NF-kappaB pathway is required for survival of the activated B cell-like (ABC) subgroup of diffuse large B-cell lymphoma (DLBCL).
  • Here we show that a small molecule IkappaB kinase (IKK) inhibitor, PS-1145, and related compounds are toxic for ABC DLBCL cell lines but not for cell lines derived from the other prevalent form of DLBCL, germinal center B cell-like DLBCL.
  • Treatment of ABC lines with these inhibitors rapidly induced a series of gene expression changes that were attributable to cessation of constitutive IKK activity, similar to changes induced by acute expression of genetic inhibitors of NF-kappaB, confirming the effectiveness and specificity of this compound.
  • Before cell death, inhibition of IKK also induced features of apoptosis and an arrest in the G1 phase of the cell cycle.
  • In the presence of tamoxifen, p65-ERD reversed the toxicity of IKK inhibition and restored expression of many NF-kappaB target genes.
  • Another subgroup of DLBCL, primary mediastinal B-cell lymphoma (PMBL), also expresses NF-kappaB target genes, and treatment of a PMBL cell line with an IKK inhibitor was toxic and induced gene expression changes of a distinct group of NF-kappaB target genes.
  • These studies validate the NF-kappaB pathway as a promising therapeutic target in ABC DLBCL, PMBL, and other lymphomas that depend on the activity of NF-kappaB for survival and proliferation.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, B-Cell / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. Protein-Serine-Threonine Kinases / antagonists & inhibitors
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Apoptosis. Carbolines / pharmacology. Cell Cycle. Cell Line. Cell Line, Tumor. Cell Proliferation. Cell Survival. Dose-Response Relationship, Drug. Down-Regulation. Enzyme Inhibitors / pharmacology. Genes, Dominant. Heterocyclic Compounds, 3-Ring / pharmacology. Humans. I-kappa B Kinase. Inhibitory Concentration 50. L-Lactate Dehydrogenase / metabolism. Leukocytes, Mononuclear / cytology. NF-kappa B / metabolism. Protein Structure, Tertiary. Pyridines / pharmacology. Receptors, Estrogen / metabolism. Tamoxifen / pharmacology. Time Factors. Up-Regulation

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TAMOXIFEN .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Clin Cancer Res. 2005 Jan 1;11(1):2-6 [15671521.001]
  • (PMID = 15671525.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carbolines; 0 / Enzyme Inhibitors; 0 / Heterocyclic Compounds, 3-Ring; 0 / MLX105; 0 / NF-kappa B; 0 / PS1145; 0 / Pyridines; 0 / Receptors, Estrogen; 094ZI81Y45 / Tamoxifen; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 2.7.1.- / IKBKE protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.10 / CHUK protein, human; EC 2.7.11.10 / I-kappa B Kinase; EC 2.7.11.10 / IKBKB protein, human
  •  go-up   go-down


26. Lam LT, Wright G, Davis RE, Lenz G, Farinha P, Dang L, Chan JW, Rosenwald A, Gascoyne RD, Staudt LM: Cooperative signaling through the signal transducer and activator of transcription 3 and nuclear factor-{kappa}B pathways in subtypes of diffuse large B-cell lymphoma. Blood; 2008 Apr 1;111(7):3701-13
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cooperative signaling through the signal transducer and activator of transcription 3 and nuclear factor-{kappa}B pathways in subtypes of diffuse large B-cell lymphoma.
  • The activated B cell-like (ABC) subgroup of diffuse large B-cell lymphoma (DLBCL) is characterized by constitutive activation of the nuclear factor-kappaB (NF-kappaB) pathway.
  • In this study, we showed that the NF-kappaB pathway induced the expression of the cytokines interleukin (IL)-6 and IL-10 in ABC DLBCL cell lines, which also have high levels of total and phosphorylated signal transducer and activator of transcription (STAT) 3 protein, suggesting autocrine signaling.
  • Using RNA interference for STAT3, we defined a gene expression signature of IL-6 and IL-10 signaling through STAT3.
  • Based on this signature, we constructed a molecular predictor of STAT3 signaling that defined a subset of ABC DLBCL tumors with high expression of STAT3, IL-6, and/or IL-10 and their downstream targets.
  • Although the STAT3-high and STAT3-low subsets had equivalent expression of genes that distinguish ABC DLBCL from germinal center B cell-like DLBCL, STAT3-high ABC DLBCLs had higher expression of signatures that reflected NF-kappaB activity, proliferation, and glycolysis.
  • A small-molecule inhibitor of Janus kinase signaling, which blocked STAT3 signature expression, was toxic only for ABC DLBCL lines and synergized with an inhibitor of NF-kappaB signaling.
  • These findings suggest that the biological interplay between the STAT3 and NF-kappaB pathways may be exploited for the treatments of a subset of ABC DLBCLs.

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Oncogene. 2000 May 15;19(21):2468-73 [10851045.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2332-43 [17625604.001]
  • [Cites] Immunity. 2000 Aug;13(2):199-212 [10981963.001]
  • [Cites] Nat Genet. 2001 Jan;27(1):48-54 [11137997.001]
  • [Cites] Annu Rev Immunol. 2001;19:683-765 [11244051.001]
  • [Cites] Mol Cell Biol. 2001 Oct;21(19):6615-25 [11533249.001]
  • [Cites] Immunity. 2001 Sep;15(3):375-85 [11567628.001]
  • [Cites] Genome Biol. 2001;2(10):RESEARCH0041 [11597333.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Blood. 2002 Jan 15;99(2):618-26 [11781246.001]
  • [Cites] Bioorg Med Chem Lett. 2002 Apr 22;12(8):1219-23 [11934592.001]
  • [Cites] Mol Biol Cell. 2002 Jun;13(6):1977-2000 [12058064.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] J Immunol. 2002 Sep 1;169(5):2253-63 [12193690.001]
  • [Cites] J Exp Med. 2002 Sep 16;196(6):743-52 [12235208.001]
  • [Cites] Blood. 2003 Feb 1;101(3):1164-71 [12393423.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] J Cell Physiol. 2003 Nov;197(2):157-68 [14502555.001]
  • [Cites] Nat Med. 2004 Jan;10(1):48-54 [14702634.001]
  • [Cites] J Immunol. 2004 Jul 15;173(2):1158-65 [15240705.001]
  • [Cites] Science. 2004 Sep 3;305(5689):1466-70 [15353804.001]
  • [Cites] Adv Enzyme Regul. 1984;22:27-55 [6382953.001]
  • [Cites] Nature. 1986 Nov 6-12;324(6092):73-6 [3491322.001]
  • [Cites] Nature. 1988 Mar 3;332(6159):83-5 [3258060.001]
  • [Cites] Blood. 1989 Aug 1;74(2):798-804 [2787680.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Mar 1;89(5):1890-3 [1371884.001]
  • [Cites] Blood. 1993 Dec 15;82(12):3712-20 [8260708.001]
  • [Cites] Cell. 1994 Apr 8;77(1):63-71 [7512451.001]
  • [Cites] Cancer Res. 1996 Dec 1;56(23):5499-505 [8968107.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] J Biol Chem. 2004 Jan 16;279(3):1768-76 [14593105.001]
  • [Cites] Leukemia. 2004 Mar;18(3):597-606 [14712288.001]
  • [Cites] Nature. 1997 Jun 26;387(6636):917-21 [9202125.001]
  • [Cites] J Leukoc Biol. 1998 Jun;63(6):665-8 [9620657.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):28-40 [15671525.001]
  • [Cites] Cancer Res. 2005 Feb 1;65(3):939-47 [15705894.001]
  • [Cites] Annu Rev Immunol. 2005;23:1-21 [15771564.001]
  • [Cites] Nature. 2005 Jun 2;435(7042):677-81 [15902208.001]
  • [Cites] Adv Immunol. 2005;87:163-208 [16102574.001]
  • [Cites] Eur J Cancer. 2005 Nov;41(16):2502-12 [16199153.001]
  • [Cites] Nat Clin Pract Oncol. 2005 Jun;2(6):315-24 [16264989.001]
  • [Cites] Nat Med. 2005 Dec;11(12):1314-21 [16288283.001]
  • [Cites] J Clin Oncol. 2006 Feb 20;24(6):961-8 [16418494.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):311-7 [16492805.001]
  • [Cites] Immunol Rev. 2006 Apr;210:67-85 [16623765.001]
  • [Cites] Blood. 2006 May 15;107(10):4090-100 [16424392.001]
  • [Cites] Nature. 2006 May 4;441(7089):106-10 [16572121.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4266-73 [16439676.001]
  • [Cites] Cancer Cell. 2006 Nov;10(5):375-88 [17097560.001]
  • [Cites] Cancer Cell. 2006 Nov;10(5):389-99 [17097561.001]
  • [Cites] Nat Rev Immunol. 2007 Jan;7(1):41-51 [17186030.001]
  • [Cites] J Biol Chem. 2007 Feb 9;282(6):3428-32 [17178722.001]
  • [Cites] J Immunol. 2007 Mar 1;178(5):2623-9 [17312100.001]
  • [Cites] Oncogene. 2007 Feb 26;26(9):1324-37 [17322918.001]
  • [Cites] Blood. 2007 Apr 1;109(7):2700-7 [17119127.001]
  • [Cites] Genes Dev. 2007 Jun 1;21(11):1396-408 [17510282.001]
  • [Cites] Cell. 2007 Jun 15;129(6):1065-79 [17574021.001]
  • [Cites] Nat Rev Cancer. 2007 Sep;7(9):673-83 [17721432.001]
  • [Cites] Oncogene. 2000 May 15;19(21):2474-88 [10851046.001]
  • (PMID = 18160665.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084967; United States / NCI NIH HHS / CA / U01-CA84967; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / IL10 protein, human; 0 / IL6 protein, human; 0 / Interleukin-6; 0 / NF-kappa B; 0 / Protein Kinase Inhibitors; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 130068-27-8 / Interleukin-10; EC 2.7.10.2 / Janus Kinases
  • [Other-IDs] NLM/ PMC2275028
  •  go-up   go-down


27. Milhollen MA, Traore T, Adams-Duffy J, Thomas MP, Berger AJ, Dang L, Dick LR, Garnsey JJ, Koenig E, Langston SP, Manfredi M, Narayanan U, Rolfe M, Staudt LM, Soucy TA, Yu J, Zhang J, Bolen JB, Smith PG: MLN4924, a NEDD8-activating enzyme inhibitor, is active in diffuse large B-cell lymphoma models: rationale for treatment of NF-{kappa}B-dependent lymphoma. Blood; 2010 Sep 2;116(9):1515-23
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MLN4924, a NEDD8-activating enzyme inhibitor, is active in diffuse large B-cell lymphoma models: rationale for treatment of NF-{kappa}B-dependent lymphoma.
  • In most cancer cells tested, inhibition of NAE leads to induction of DNA rereplication, resulting in DNA damage and cell death.
  • However, in preclinical models of activated B cell-like (ABC) diffuse large B-cell lymphoma (DLBCL), we show that MLN4924 induces an alternative mechanism of action.
  • Treatment of ABC DLBCL cells with MLN4924 resulted in rapid accumulation of pIkappaBalpha, decrease in nuclear p65 content, reduction of nuclear factor-kappaB (NF-kappaB) transcriptional activity, and G(1) arrest, ultimately resulting in apoptosis induction, events consistent with potent NF-kappaB pathway inhibition.
  • Treatment of germinal-center B cell-like (GCB) DLBCL cells resulted in an increase in cellular Cdt-1 and accumulation of cells in S-phase, consistent with cells undergoing DNA rereplication.
  • In vivo administration of MLN4924 to mice bearing human xenograft tumors of ABC- and GCB-DLBCL blocked NAE pathway biomarkers and resulted in complete tumor growth inhibition.
  • In primary human tumor models of ABC-DLBCL, MLN4924 treatment resulted in NF-kappaB pathway inhibition accompanied by tumor regressions.
  • This work describes a novel mechanism of targeted NF-kappaB pathway modulation in DLBCL and provides strong rationale for clinical development of MLN4924 against NF-kappaB-dependent lymphomas.
  • [MeSH-major] Cyclopentanes / pharmacology. Germinal Center / drug effects. Lymphoma, Large B-Cell, Diffuse / drug therapy. Lymphoma, Large B-Cell, Diffuse / pathology. NF-kappa B / metabolism. Pyrimidines / pharmacology. Ubiquitins / antagonists & inhibitors
  • [MeSH-minor] Animals. Apoptosis / drug effects. B-Lymphocytes / drug effects. B-Lymphocytes / metabolism. Blotting, Western. Cell Cycle / drug effects. Cell Proliferation / drug effects. DNA Replication / drug effects. Female. Flow Cytometry. Humans. Mice. Mice, Inbred NOD. Mice, SCID. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Xenograft Model Antitumor Assays

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20525923.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ((1S,2S,4R)-4-(4-((1S)-2,3-dihydro-1H-inden-1-ylamino)-7H-pyrrolo(2,3-d)pyrimidin-7-yl)-2-hydroxycyclopentyl)methyl sulphamate; 0 / Cyclopentanes; 0 / NEDD8 protein, human; 0 / NF-kappa B; 0 / Pyrimidines; 0 / RNA, Messenger; 0 / Ubiquitins
  •  go-up   go-down


28. Lawrie CH, Soneji S, Marafioti T, Cooper CD, Palazzo S, Paterson JC, Cattan H, Enver T, Mager R, Boultwood J, Wainscoat JS, Hatton CS: MicroRNA expression distinguishes between germinal center B cell-like and activated B cell-like subtypes of diffuse large B cell lymphoma. Int J Cancer; 2007 Sep 1;121(5):1156-61
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA expression distinguishes between germinal center B cell-like and activated B cell-like subtypes of diffuse large B cell lymphoma.
  • Diffuse large B cell lymphoma (DLBCL) is an aggressive malignancy that accounts for nearly 40% of all lymphoid tumors.
  • This heterogeneous disease can be divided into germinal center B cell-like (GCB) and activated B cell-like (ABC) subtypes by gene expression and immunohistochemical profiling.
  • Using microarray analysis on prototypic cell lines, we identified microRNAs (miR-155, miR-21 and miR-221) that were more highly expressed in ABC-type than GCB-type cell lines.
  • These microRNAs were over-expressed in de novo DLBCL (n = 35), transformed DLBCL (n = 14) and follicular center lymphoma cases (n = 27) compared to normal B cells.
  • Consistent with the cell line model, expression levels were higher in DLBCL cases with an ABC-type immunophenotype than those that were GCB-type (p < 0.05).
  • Moreover, using multivariate analysis we found that expression of miR-21 was an independent prognostic indicator in de novo DLBCL (p < 0.05).
  • Interestingly, expression levels of both miR-155 and miR-21 were also higher in nonmalignant ABC than in GCB cells.
  • As we also demonstrate that expression of microRNAs can be measured reliably from routine paraffin-embedded biopsies of more than 8-years-old (p < 0.001), we suggest that microRNAs could be clinically useful molecular markers for DLBCL as well as other cancers.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. MicroRNAs / genetics
  • [MeSH-minor] Cell Line, Tumor. Disease-Free Survival. Humans. Prognosis. Regression Analysis. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17487835.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U137973817
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs
  •  go-up   go-down


29. Nyman H, Jerkeman M, Karjalainen-Lindsberg ML, Banham AH, Leppä S: Prognostic impact of activated B-cell focused classification in diffuse large B-cell lymphoma patients treated with R-CHOP. Mod Pathol; 2009 Aug;22(8):1094-101
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic impact of activated B-cell focused classification in diffuse large B-cell lymphoma patients treated with R-CHOP.
  • Gene expression profiling studies initially enabled diffuse large B-cell lymphoma to be divided into germinal center and activated B-cell-like subtypes, which define high- and low-risk patient groups when treated with chemotherapy.
  • The aim of this study was to determine whether modified immunohistochemical classification of cell of origin focusing on activated B-cell-like markers could be used to predict the outcome of immunochemotherapy-treated diffuse large B-cell lymphoma patients.
  • The expression of CD10, Bcl-6, MUM1/IRF4, Bcl-2, and FOXP1 was determined immunohistochemically from 88 samples of diffuse large B-cell lymphoma patients treated uniformly with R-CHOP.
  • When the modified classification using MUM1/IRF4 and FOXP1 positivities as activated B-cell-like markers was applied to distinguish the patients between the activated B-cell-like and other diffuse large B-cell lymphoma subtypes, a significantly worse outcome was seen for the patients with the activated B-cell-like phenotype (3-year failure-free survival 63 vs 82%, P=0.048, overall survival 69 vs 85%, P=0.110).
  • In conclusion, the data suggest that both the modified activated B-cell-like and Muris classifications define the non-germinal center phenotype as an adverse risk factor in R-CHOP-treated diffuse large B-cell lymphoma patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. B-Lymphocytes / pathology. Lymphoma, Large B-Cell, Diffuse / classification. Lymphoma, Large B-Cell, Diffuse / immunology. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Algorithms. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Biomarkers, Tumor / analysis. Cyclophosphamide / therapeutic use. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / genetics. Doxorubicin / therapeutic use. Forkhead Transcription Factors / biosynthesis. Forkhead Transcription Factors / genetics. Gene Expression. Gene Expression Profiling. Humans. Immunohistochemistry. Interferon Regulatory Factors / biosynthesis. Interferon Regulatory Factors / genetics. Kaplan-Meier Estimate. Lymphocyte Activation / immunology. Neprilysin / biosynthesis. Neprilysin / genetics. Phenotype. Prednisolone / therapeutic use. Prognosis. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Proto-Oncogene Proteins c-bcl-2 / genetics. Repressor Proteins / biosynthesis. Repressor Proteins / genetics. Rituximab. Vincristine / therapeutic use

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19448593.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [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 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / FOXP1 protein, human; 0 / Forkhead Transcription Factors; 0 / Interferon Regulatory Factors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Repressor Proteins; 0 / interferon regulatory factor-4; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; EC 3.4.24.11 / Neprilysin; VAP-cyclo protocol
  •  go-up   go-down


30. Poulsen CB, Borup R, Nielsen FC, Borregaard N, Hansen M, Grønbaek K, Møller MB, Ralfkiaer E: Microarray-based classification of diffuse large B-cell lymphoma. Eur J Haematol; 2005 Jun;74(6):453-65
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Microarray-based classification of diffuse large B-cell lymphoma.
  • OBJECTIVE: Hierarchical clusterings of diffuse large B-cell lymphoma (DLBCL) based on gene expression signatures have previously been used to classify DLBCL into Germinal Center B-cell (GCB) and Activated B-cell (ABC) types.
  • To examine if it was feasible to perform a cross-platform validation on the Affymetrix HG-U133A oligonucleotide arrays and improve the classification, we determined the expression profiles of pretreatment, diagnostic samples from 52 primary nodal DLBCL.
  • In this way, three subtypes, including the GCB type (n = 20), the ABC type (n = 25) and an intermediate group, Type-3 (n = 5), were distinguished.
  • The CD10 and Bcl-6 expression as well as t(14;18) translocation were prevalent, but not exclusive to the GCB type.
  • By contrast, MUM1 was only expressed in the ABC and in Type-3 samples.
  • The 5-year survival was similar between the groups, but GCB patients showed a better initial response to CHOP or CHOP-like regimens than the remaining patients and tended to have less advanced disease and lower IPI scores.
  • As a next step, an improved set of classifier genes was generated by analysis of 34 patients that were consistently classified as GCB or ABC in the above analyses.
  • CONCLUSION: We conclude that gene expression profiling with Affymetrix Genechips is efficient to distinguish between GCB and ABC types of DLBCL and that these are likely to represent separate biological entities.
  • The Genechip platform is highly standardised and therefore useful for future prospective investigations to establish the value of gene expression profiling in the clinical management of DLBCL.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Lymphoma, Large B-Cell, Diffuse / classification. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. B-Lymphocytes / pathology. Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 18 / genetics. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / genetics. Female. Gene Expression Profiling. Germinal Center / pathology. Humans. Lymphocyte Activation. Male. Middle Aged. Neprilysin / biosynthesis. Neprilysin / genetics. Translocation, Genetic / genetics

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15876249.001).
  • [ISSN] 0902-4441
  • [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] Denmark
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / DNA-Binding Proteins; EC 3.4.24.11 / Neprilysin
  •  go-up   go-down


31. Booman M, Douwes J, Glas AM, de Jong D, Schuuring E, Kluin PM: Primary testicular diffuse large B-cell lymphomas have activated B-cell-like subtype characteristics. J Pathol; 2006 Oct;210(2):163-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary testicular diffuse large B-cell lymphomas have activated B-cell-like subtype characteristics.
  • Diffuse large B-cell lymphomas (DLBCLs) constitute a heterogeneous group of lymphomas in which germinal centre B-cell-like and activated B-cell-like subtypes can be discerned based on pathology, clinical presentation, and gene expression patterns.
  • In the present study, cDNA microarray analysis, immunohistochemistry for CD10, Bcl6 and MUM1, and somatic hypermutation analysis of the immunoglobulin heavy chain gene rearrangements were used to determine the subtype of primary testicular DLBCL.
  • Immunohistochemistry revealed 14/22 testicular DLBCLs with an activated B-cell-like immunophenotype and 8/22 with an ambiguous immunophenotype co-expressing CD10 and high levels of MUM1. cDNA microarray analysis of these 22 and four additional cases showed a uniform activated B-cell-like gene expression pattern for both immunophenotypes.
  • It is concluded that primary testicular DLBCLs have uniform activated B-cell-like subtype characteristics despite a number of cases showing an ambiguous immunophenotype.
  • [MeSH-major] B-Lymphocytes / immunology. Lymphocyte Activation. Lymphoma, B-Cell / immunology. Lymphoma, Large B-Cell, Diffuse / immunology. Testicular Neoplasms / immunology

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • MedlinePlus Health Information. consumer health - Testicular Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16823896.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / DNA, Neoplasm; 0 / Immunoglobulin Variable Region; 0 / Interferon Regulatory Factors; 0 / Neoplasm Proteins; 0 / interferon regulatory factor-4; EC 3.4.24.11 / Neprilysin
  •  go-up   go-down


32. Saad AA, Awed NM, Abdel-Hafeez ZM, Kamal GM, Elsallaly HM, Alloub AI: Prognostic value of immunohistochemical classification of diffuse large B-cell lymphoma into germinal center B-cell and non-germinal center B-cell subtypes. Saudi Med J; 2010 Feb;31(2):135-41
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic value of immunohistochemical classification of diffuse large B-cell lymphoma into germinal center B-cell and non-germinal center B-cell subtypes.
  • OBJECTIVE: To study the expression of germinal center B-cell (GCB)/activated B-cell like-related proteins to get optimal stratification of diffuse large B-cell lymphoma (DLBCL) patients, and correlate this with the established clinical and laboratory parameters.
  • METHODS: This study was conducted retrospectively on 30 archival paraffin tissue blocks of DLBCL.
  • Each case included in this study was investigated by immunohistochemical reaction for multiple myeloma-1/interferon regulatory factor-4, B-cell/lymphoma 6, and cluster of differentiation10 monoclonal antibodies.
  • CONCLUSION: The subclassification of DLBCL into GCB and non-GCB groups using immunohistochemistry may be useful for identifying those patients whose prognosis is so poor that more aggressive therapy can be given at the time of diagnosis.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / classification

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20174727.001).
  • [ISSN] 0379-5284
  • [Journal-full-title] Saudi medical journal
  • [ISO-abbreviation] Saudi Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Saudi Arabia
  •  go-up   go-down


33. Anderson JJ, Fordham S, Overman L, Dignum H, Wood K, Proctor SJ, Crosier S, Angus B, Culpin RE, Mainou-Fowler T: Immunophenotyping of diffuse large B-cell lymphoma (DLBCL) defines multiple sub-groups of germinal centre-like tumours displaying different survival characteristics. Int J Oncol; 2009 Nov;35(5):961-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunophenotyping of diffuse large B-cell lymphoma (DLBCL) defines multiple sub-groups of germinal centre-like tumours displaying different survival characteristics.
  • Diffuse large B-cell lymphoma (DLBCL) forms a heterogeneous collection of aggressive non-Hodgkin's Lymphoma in which three principle classes of neoplasia have been defined according to gene expression and immunophenotyping studies.
  • A series of 155 DLBCL treated uniformly with anthracycline therapy in clinical trials, were stratified upon the basis of common biomarker expression with combination immunophenotype being related to patient overall survival.
  • Stratification of tumours with respect to combined expression profiles of the three biological markers (CD10, Bcl-6 and MUM-1) revealed six groups showing significant differences in survival (p=0.014).
  • The greatest difference resided between distinct populations of germinal centre (GC) cell tumours; the first being CD10-, Bcl-6+, MUM-1- and the second CD10+ Bcl-6+ MUM-1+ (p=0.002).
  • Of the three groups presenting a non-GC or activated B cell (NGC/ABC) phenotype, only one (CD10-, Bcl-6+ and MUM-1+) presented short-term median survival (27 months) comparable with poor prognosis GC sub-populations.
  • Within the remaining ABC tumour groups (CD10- Bcl-6- MUM-1- and CD10- Bcl-6- MUM-1+) patients presented intermediate median survival times of 54 and 58 months, respectively.
  • The first of these comprised two patient sub-populations with GC-like tumours together with one sub-population of NGC/ABC, the second two sub-populations of ABC-like tumours, and the final a single group of GC-like tumours associated with optimal long-term survival.
  • [MeSH-major] Biomarkers, Tumor / analysis. Lymphoma, Large B-Cell, Diffuse / metabolism. Lymphoma, Large B-Cell, Diffuse / mortality

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19787248.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-4; EC 3.4.24.11 / Neprilysin
  •  go-up   go-down


34. Blenk S, Engelmann J, Weniger M, Schultz J, Dittrich M, Rosenwald A, Müller-Hermelink HK, Müller T, Dandekar T: Germinal center B cell-like (GCB) and activated B cell-like (ABC) type of diffuse large B cell lymphoma (DLBCL): analysis of molecular predictors, signatures, cell cycle state and patient survival. Cancer Inform; 2007 Dec 12;3:399-420
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Germinal center B cell-like (GCB) and activated B cell-like (ABC) type of diffuse large B cell lymphoma (DLBCL): analysis of molecular predictors, signatures, cell cycle state and patient survival.
  • Aiming to find key genes and events, we analyze a large data set on diffuse large B-cell lymphoma (DLBCL) gene-expression (248 patients, 12196 spots).
  • We identify specific, activated B cell-like (ABC) and germinal center B cell-like (GCB) distinguishing genes.
  • CDKN2C) cell cycle genes.
  • Independently from previous classification by marker genes we confirm a clear binary class distinction between the ABC and GCB subgroups.
  • A key regulatory network, distinguishing marked over-expression in ABC from that in GCB, is built by: ASB13, BCL2, BCL6, BCL7A, CCND2, COL3A1, CTGF, FN1, FOXP1, IGHM, IRF4, LMO2, LRMP, MAPK10, MME, MYBL1, NEIL1 and SH3BP5.
  • It predicts and supports the aggressive behaviour of the ABC subgroup.
  • These results help to understand target interactions, improve subgroup diagnosis, risk prognosis as well as therapy in the ABC and GCB DLBCL subgroups.

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6567-72 [12011421.001]
  • [Cites] Nucleic Acids Res. 2002 Feb 15;30(4):e15 [11842121.001]
  • [Cites] Genes Dev. 2002 Feb 1;16(3):295-300 [11825871.001]
  • [Cites] Nat Med. 2002 Jan;8(1):68-74 [11786909.001]
  • [Cites] Bioinformatics. 2001;17 Suppl 1:S107-14 [11472999.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Genes Dev. 2005 May 1;19(9):1067-80 [15833912.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D433-7 [15608232.001]
  • [Cites] Cell. 1999 Jan 8;96(1):35-45 [9989495.001]
  • [Cites] N Engl J Med. 1993 Sep 30;329(14):987-94 [8141877.001]
  • [Cites] Genome Biol. 2004;5(10):R80 [15461798.001]
  • [Cites] Br J Cancer. 2003 Nov 17;89(10):1958-60 [14612909.001]
  • [Cites] Methods. 2003 Dec;31(4):265-73 [14597310.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Genome Res. 2003 Oct;13(10):2363-71 [14525934.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] Leukemia. 2003 Apr;17(4):789-95 [12682639.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Blood. 2005 Mar 1;105(5):1851-61 [15550490.001]
  • [Cites] Science. 2005 Feb 4;307(5710):724-7 [15692050.001]
  • (PMID = 19455257.001).
  • [ISSN] 1176-9351
  • [Journal-full-title] Cancer informatics
  • [ISO-abbreviation] Cancer Inform
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2675856
  • [Keywords] NOTNLM ; cancer / gene expression / immunity / prognosis / regulation
  •  go-up   go-down


35. Cheng J, Tu P, Shi QL, Zhou HB, Zhou ZY, Zhao YC, Ma HH, Zhou XJ: [Primary diffuse large B-cell lymphoma of central nervous system belongs to activated B-cell-like subgroup: a study of 47 cases]. Zhonghua Bing Li Xue Za Zhi; 2008 Jun;37(6):384-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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 central nervous system belongs to activated B-cell-like subgroup: a study of 47 cases].
  • OBJECTIVE: To investigate the histogenetic origin of primary central nervous system diffuse large B-cell lymphoma (DLBCL) with respect to the stage of B-cell differentiation, and identification of the relevant prognostic markers.
  • RESULTS: CD10, bcl-6, MUM-1 and FOXP1 expression in the tumor cells were 6.4%, 53.2%, 91.5% and 93.6% respectively.
  • There was no expression of CD138 in all the cases.
  • Among the 47 patients, 43 cases (91.5%) showed an activated B-cell-like (ABC) phenotype: 21 (44.7%) were bcl-6+ and MUM-1+, suggesting an "activated germinal center (GC) B-cell-like" in origin; 22 (46.8%) were exclusively MUM-1+, suggesting an "activated non-GCB" in origin.
  • No significant correlation of the classification and FOXP1 expression found on the outcome (P=0.279 and P=0.154).
  • CONCLUSIONS: Most primary central nervous system DLBCL are shown belonging to the ABC subgroup, suggesting that primary central nervous system DLBCL is quite similar to a DLBCL subset, which is derived from late GC to early post-GC B cell.
  • The classification and FOXP1 expression do not show prognostic value in primary central nervous system DLBCL.
  • [MeSH-major] Central Nervous System Neoplasms / diagnosis. Lymphoma, B-Cell / diagnosis. Lymphoma, Large B-Cell, Diffuse / diagnosis

  • Genetic Alliance. consumer health - Central Nervous System Lymphoma, Primary.
  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19031717.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


36. Sarosiek KA, Nechushtan H, Lu X, Rosenblatt JD, Lossos IS: Interleukin-4 distinctively modifies responses of germinal centre-like and activated B-cell-like diffuse large B-cell lymphomas to immuno-chemotherapy. Br J Haematol; 2009 Nov;147(3):308-18
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin-4 distinctively modifies responses of germinal centre-like and activated B-cell-like diffuse large B-cell lymphomas to immuno-chemotherapy.
  • Diffuse large B-cell lymphomas (DLBCLs) can be classified into two subtypes: germinal-centre B-cell (GCB)-like and Activated B-cell (ABC)-like tumours, which are associated with longer or shorter patient overall survival, respectively.
  • In our previous studies, we have shown that, although DLBCL tumours of GCB-like and ABC-like subtypes express similar levels of IL4 mRNA, they exhibit distinct patterns of IL-4-induced intracellular signalling and different expression of IL-4 target genes.
  • We hypothesized that these differences may contribute to the different clinical behaviour and outcome of DLBCL subtypes.
  • Herein, we demonstrated that IL-4 increased the sensitivity of GCB-like DLBCL to doxorubicin-induced apoptosis and complement-dependent rituximab cell killing.
  • In contrast, IL-4 protected ABC-like DLBCL from the cytotoxic effects of doxorubicin and rituximab.
  • The distinct effects of IL-4 on doxorubicin sensitivity in GCB-like and ABC-like DLBCL cells may be partially attributed to the contrasting effects of the cytokine on Bcl-2 and Bad protein levels in the DLBCL subtypes.
  • These findings suggest that the different effects of IL-4 on chemotherapy and immunotherapy-induced cytotoxicity of GCB- and ABC-like DLBCL could contribute to the different clinical outcomes exhibited by patients with these two subtypes of DLBCL.

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • Hazardous Substances Data Bank. RITUXIMAB .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2006 Jul 1;24(19):3121-7 [16754935.001]
  • [Cites] Blood. 2008 Nov 15;112(10):4098-108 [18716132.001]
  • [Cites] Blood. 2006 Dec 15;108(13):4178-86 [16946303.001]
  • [Cites] Mol Cell Biol. 2007 Mar;27(6):2166-79 [17210636.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Blood. 2000 Jun 15;95(12):3900-8 [10845926.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10209-13 [10954754.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1352-7 [11520782.001]
  • [Cites] Cell Immunol. 2001 Aug 1;211(2):131-42 [11591117.001]
  • [Cites] J Immunol Methods. 2001 Dec 1;258(1-2):183-91 [11684135.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] N Engl J Med. 2002 Jan 24;346(4):235-42 [11807147.001]
  • [Cites] Br J Haematol. 2001 Dec;115(4):807-11 [11843813.001]
  • [Cites] Blood. 2002 Apr 1;99(7):2285-90 [11895757.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Leuk Lymphoma. 2002 Jun;43(6):1313-21 [12153001.001]
  • [Cites] Leukemia. 2003 Apr;17(4):789-95 [12682639.001]
  • [Cites] J Clin Oncol. 2003 Apr 15;21(8):1466-71 [12697868.001]
  • [Cites] J Immunol. 2003 Aug 15;171(4):1722-31 [12902471.001]
  • [Cites] N Engl J Med. 2004 Apr 29;350(18):1828-37 [15115829.001]
  • [Cites] Gynecol Oncol. 2004 Sep;94(3):785-95 [15350374.001]
  • [Cites] Blood. 1990 Mar 1;75(5):1114-8 [2306518.001]
  • [Cites] Cell. 1997 Sep 19;90(6):1073-83 [9323135.001]
  • [Cites] FEBS Lett. 1997 Nov 17;417(3):360-4 [9409752.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2924-32 [15591113.001]
  • [Cites] Blood. 2005 May 15;105(10):3979-86 [15677569.001]
  • [Cites] Blood. 2006 Apr 15;107(8):3205-11 [16373664.001]
  • [Cites] Leuk Lymphoma. 2007 Jul;48(7):1290-8 [17613756.001]
  • [Cites] Cell Res. 2007 Nov;17(11):942-55 [17968425.001]
  • [Cites] J Clin Oncol. 2008 Jan 20;26(3):447-54 [18086797.001]
  • [Cites] Clin Cancer Res. 2006 Jul 1;12(13):4027-35 [16818702.001]
  • (PMID = 19694722.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA109335-03; United States / NCI NIH HHS / CA / R01 CA109335; United States / NCI NIH HHS / CA / R01 CA122105; United States / NCI NIH HHS / CA / R01 CA109335-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Neoplasm Proteins; 0 / Recombinant Proteins; 207137-56-2 / Interleukin-4; 4F4X42SYQ6 / Rituximab; 80168379AG / Doxorubicin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
  • [Other-IDs] NLM/ NIHMS139972; NLM/ PMC2763052
  •  go-up   go-down


37. Bai M, Skyrlas A, Agnantis NJ, Kamina S, Papoudou-Bai A, Kitsoulis P, Kanavaros P: B-cell differentiation, apoptosis and proliferation in diffuse large B-cell lymphomas. Anticancer Res; 2005 Jan-Feb;25(1A):347-62
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] B-cell differentiation, apoptosis and proliferation in diffuse large B-cell lymphomas.
  • Diffuse large B-cell lymphomas (DLBCL) represent the most common type of adult non-Hodgkin's lymphomas in Western countries and are characterized by heterogeneous clinical, histological, immunophenotypic and genetic features.
  • Recent investigations using cDNA and oligonucleotide microarrays have identified molecularly distinct groups of DLBCL with respect to the B-cell differentiation gene expression profile: the germinal center (GC) B-cell-like DLBCL, the activated B-cell-like DLBCL and the type 3 DLBCL.
  • The GC B-cell-like DLBCL were characterized by the expression of genes of the normal GC B-cells, the activated B-cell-like DLBCL were characterized by the expression of genes that are normally induced luring in vitro activation of peripheral blood B-cells, while the type 3 DLBCL did not express either set of genes at a high level.
  • Patients with GC B-cell-like DLBCL had more favorable clinical outcome than those with activated B-cell-like or type 3 DLBCL.
  • Immunohistochemical studies have shown that the bc16/CD10/MUM1/CD138 B-cell differentiation immunophenotypes are prognostically relevant and may predict the cDNA classification in a sizable fraction of DLBCL.
  • In the last few years, there has been accumulating molecular and immunohistochemical evidence indicating links between B-cell differentiation gene expression profiles and expression of apoptosis and cell cycle-associated genes in DLBCL.
  • The present review summarizes data with respect to the relationships between B-cell differentiation, apoptosis and proliferation in DLBCL.
  • [MeSH-major] B-Lymphocytes / pathology. Lymphoma, B-Cell / genetics. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Animals. Apoptosis / genetics. Cell Differentiation / genetics. Humans. Oligonucleotide Array Sequence Analysis

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15816558.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Greece
  • [Number-of-references] 163
  •  go-up   go-down


38. Dierlamm J, Murga Penas EM, Bentink S, Wessendorf S, Berger H, Hummel M, Klapper W, Lenze D, Rosenwald A, Haralambieva E, Ott G, Cogliatti SB, Möller P, Schwaenen C, Stein H, Löffler M, Spang R, Trümper L, Siebert R, Deutsche Krebshilfe Network Project "Molecular Mechanisms in Malignant Lymphomas": Gain of chromosome region 18q21 including the MALT1 gene is associated with the activated B-cell-like gene expression subtype and increased BCL2 gene dosage and protein expression in diffuse large B-cell lymphoma. Haematologica; 2008 May;93(5):688-96
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gain of chromosome region 18q21 including the MALT1 gene is associated with the activated B-cell-like gene expression subtype and increased BCL2 gene dosage and protein expression in diffuse large B-cell lymphoma.
  • BACKGROUND: The aim of this study was to determine the impact of a gain of the MALT1 gene on gene expression and clinical parameters in diffuse large B-cell lymphoma.
  • DESIGN AND METHODS: We analyzed 116 cases of diffuse large B-cell lymphoma by fluorescence in situ hybridization, array-based comparative genomic hybridization, and transcriptional profiling.
  • Cases with 18q21/MALT1 gain more frequently showed an activated B-cell-like (ABC) gene expression signature (65%) than a germinal center B-cell-like (GCB) one (23%) (p<0.001).
  • Ninety-eight genes including MALT1, BCL2, and some selected nuclear factor-kappaB target genes were differentially expressed between the two genetic groups of diffuse large B-cell lymphoma.
  • By global testing of each chromosome, we identified 33 genes, all located on chromosome 18q, which were differentially expressed between the two genetic groups independently of the ABC/GCB status.
  • CONCLUSIONS: In diffuse large B-cell lymphoma, gain of 18q21 including MALT1 is significantly associated with differential expression of genes located on 18q, the ABC gene expression subtype, increased BCL2 gene and protein expression and might indicate an unfavorable prognosis.
  • [MeSH-major] B-Lymphocytes / cytology. Caspases / genetics. Chromosomes, Human, Pair 18. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / metabolism. Neoplasm Proteins / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] Aged. Female. Gene Expression Profiling. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Nucleic Acid Hybridization. Prognosis. Transcription, Genetic

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Haematologica. 2008 May;93(5):641-5 [18450732.001]
  • (PMID = 18367485.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; EC 3.4.22.- / Caspases; EC 3.4.22.- / MALT1 protein, human
  •  go-up   go-down


39. Chen Y, Han T, Iqbal J, Irons R, Chan WC, Zhu X, Fu K: Diffuse large B-cell lymphoma in Chinese patients: immunophenotypic and cytogenetic analyses of 124 cases. Am J Clin Pathol; 2010 Feb;133(2):305-13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diffuse large B-cell lymphoma in Chinese patients: immunophenotypic and cytogenetic analyses of 124 cases.
  • In diffuse large B-cell lymphoma (DLBCL), BCL2 expression usually correlates with the t(14;18) (q32;q21) in germinal center B-cell (GCB) subtype and with gain/amplification of chromosome 18q21 in the activated B cell-like subtype.
  • We studied 124 Chinese DLBCL cases using immunohistochemical, conventional cytogenetics, and interphase fluorescence in situ hybridization analyses.
  • A cohort of 114 well-characterized DLBCL cases from Western populations was also analyzed for comparison.
  • BCL2 expression was associated with gain of chromosome 18/18q in the Chinese and Western cohorts.
  • More interestingly, BCL2 expression was associated with gain of chromosome 3/3q in Chinese DLBCL cases, whereas this association was less significant in Western cases.
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 18. Chromosomes, Human, Pair 3. Gene Amplification. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / immunology. Translocation, Genetic

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20093241.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.24.11 / Neprilysin
  •  go-up   go-down


40. Lu X, Chen J, Sasmono RT, Hsi ED, Sarosiek KA, Tiganis T, Lossos IS: T-cell protein tyrosine phosphatase, distinctively expressed in activated-B-cell-like diffuse large B-cell lymphomas, is the nuclear phosphatase of STAT6. Mol Cell Biol; 2007 Mar;27(6):2166-79
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] T-cell protein tyrosine phosphatase, distinctively expressed in activated-B-cell-like diffuse large B-cell lymphomas, is the nuclear phosphatase of STAT6.
  • Diffuse large B-cell lymphomas (DLBCLs) consist of clinically distinct subtypes: germinal center B-cell (GCB)-like and activated-B-cell (ABC)-like tumors, characterized by long and short survival, respectively.
  • We reported distinct interleukin 4 (IL-4) responsiveness and STAT6 signaling in these DLBCL subtypes.
  • Increased nuclear dephosphorylation of phospho-STAT6 (pSTAT6) was observed in ABC-like tumors, which exhibited a different expression profile of protein tyrosine phosphatases (PTPs).
  • Among the differentially expressed PTPs, only T-cell PTP (TCPTP) localizes to the nucleus.
  • Herein, we report that the elevated expression of TCPTP in ABC- versus GCB-like DLBCL tumors is not due to the distinct ontogeny of these neoplasms but rather may be an acquired feature of the tumors.
  • Taken together, these results identify TCPTP as a physiological regulator of STAT6 phosphorylation and suggest that specific increases in TCPTP expression in ABC-like DLBCLs may contribute to the different biological characteristics of these tumors.

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] EMBO J. 1999 Nov 15;18(22):6307-18 [10562543.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Semin Immunol. 2000 Aug;12(4):379-86 [10995584.001]
  • [Cites] J Biol Chem. 2000 Dec 15;275(50):39718-26 [10993888.001]
  • [Cites] J Biol Chem. 2001 Oct 5;276(40):37700-7 [11479308.001]
  • [Cites] J Biol Chem. 2001 Dec 7;276(49):46313-8 [11514572.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Mol Endocrinol. 2002 Jan;16(1):58-69 [11773439.001]
  • [Cites] Curr Biol. 2002 Mar 19;12(6):446-53 [11909529.001]
  • [Cites] Bioorg Med Chem Lett. 2002 Apr 22;12(8):1219-23 [11934592.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Mol Cell Biol. 1996 Oct;16(10):5811-20 [8816495.001]
  • [Cites] J Biol Chem. 1997 May 16;272(20):12968-77 [9148903.001]
  • [Cites] J Immunol. 1997 Aug 1;159(3):1255-64 [9233621.001]
  • [Cites] J Biol Chem. 1997 Aug 22;272(34):21548-57 [9261175.001]
  • [Cites] J Exp Med. 1997 Aug 29;186(5):683-93 [9271584.001]
  • [Cites] J Immunol. 1997 Oct 15;159(8):3757-66 [9378962.001]
  • [Cites] J Biol Chem. 1997 Nov 14;272(46):29322-9 [9361013.001]
  • [Cites] Mol Cell Biol. 1998 Mar;18(3):1622-34 [9488479.001]
  • [Cites] J Immunol. 1998 Jul 1;161(1):302-10 [9647237.001]
  • [Cites] Adv Exp Med Biol. 1998;452:37-43 [9889957.001]
  • [Cites] Gene. 1999 Sep 17;237(2):351-60 [10521659.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):28-40 [15671525.001]
  • [Cites] Nat Immunol. 2005 Mar;6(3):253-60 [15696169.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2924-32 [15591113.001]
  • [Cites] Curr Opin Cell Biol. 2005 Apr;17(2):203-9 [15780598.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(16):5662-8 [12138178.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):36563-9 [12121972.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Oct 4;297(4):811-7 [12359225.001]
  • [Cites] J Biol Chem. 2003 Feb 7;278(6):3903-11 [12459556.001]
  • [Cites] Mol Cell Biol. 2003 Mar;23(6):2096-108 [12612081.001]
  • [Cites] Leukemia. 2003 Apr;17(4):789-95 [12682639.001]
  • [Cites] J Biol Chem. 2003 May 9;278(19):16520-7 [12615921.001]
  • [Cites] Nat Rev Immunol. 2003 Nov;3(11):900-11 [14668806.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3075-86 [14701875.001]
  • [Cites] FASEB J. 2004 Jan;18(1):8-30 [14718383.001]
  • [Cites] Cell. 2004 Jun 11;117(6):699-711 [15186772.001]
  • [Cites] Blood. 1991 May 1;77(9):1859-70 [2018830.001]
  • [Cites] Science. 1991 Nov 1;254(5032):713-6 [1948050.001]
  • [Cites] J Clin Invest. 1993 Jan;91(1):88-93 [8423237.001]
  • [Cites] Biochemistry. 1993 Mar 9;32(9):2194-201 [8443161.001]
  • [Cites] Cancer Res. 1995 May 15;55(10):2173-6 [7743520.001]
  • [Cites] Cancer Res. 1995 Sep 1;55(17):3692-6 [7641177.001]
  • (PMID = 17210636.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109335; United States / NCI NIH HHS / CA / CA109335
  • [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 / STAT6 Transcription Factor; 207137-56-2 / Interleukin-4; EC 3.1.3.48 / PTPN2 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 2; EC 3.1.3.48 / Protein Tyrosine Phosphatases
  • [Other-IDs] NLM/ PMC1820499
  •  go-up   go-down


41. Liu YH, Li L, Liu G, Zhuang HG, Luo DL, Luo XL, Xu J: [Gene expression profiling of diffuse large B-cell lymphoma in China]. Zhonghua Bing Li Xue Za Zhi; 2007 Feb;36(2):79-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Gene expression profiling of diffuse large B-cell lymphoma in China].
  • OBJECTIVE: Gene expression profiling of diffuse large B-cell lymphoma (DLBCL) of different immunophenotypes.
  • METHODS: The study included 156 cases of DLBCL, which were subclassified by immunohistochemistry including CD10, bcl-6 and MUM1.
  • Affymetrix U133 plus2.0 oligonucleotide microarrays were used to obtain differential gene expression profiling of 9 DLBCL (3 representative cases from each immunophenotypical group) and 3 tonsils.
  • RESULTS: The immunohistochemistry subclassified 156 cases of DLBCL into 3 groups: CD10(+) and/or bcl-6(+), MUM1(-) (group 1); CD10(+) and/or bcl-6(+), MUM1(+) (group 2); CD10(-) and bcl-6(-), MUM1(+) (group 3).
  • By gene expression array, 9 lymphomas and 3 tonsils were clustered in an unsupervised fashion into 4 groups (A, B, C and D), which were in accordance with the immunophenotypical groups (group 1, 2, 3 and normal).
  • A total of 81 genes were markedly decreased and 86 genes were over-expressed in all DLBCL groups.
  • Although Group B lymphomas showed mixed immunophenotypical features of both germinal center B-cell-like DLBCL (Group A) and activated B-cell-like lymphomas (Group C), gene profile clustering showed that Group B was dissimilar to Group A or Group C, with 45 over-expressed and 27 uniquely expressed genes.
  • CONCLUSIONS: Gene expression profiling indicates that DLBCL can be subgrouped at the molecular level and can be identified by immunophenotyping.
  • The gene expression profile of Group B lymphomas suggests that factors other than the cell-of-origin may contribute to the pathogenesis of DLBCL.
  • [MeSH-major] Gene Expression Profiling. Immunophenotyping / methods. Lymphoma, Large B-Cell, Diffuse / genetics

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17493379.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Interferon Regulatory Factors; 0 / Proto-Oncogene Proteins c-bcl-6; 0 / interferon regulatory factor-4; EC 3.4.24.11 / Neprilysin
  •  go-up   go-down


42. Feuerhake F, Kutok JL, Monti S, Chen W, LaCasce AS, Cattoretti G, Kurtin P, Pinkus GS, de Leval L, Harris NL, Savage KJ, Neuberg D, Habermann TM, Dalla-Favera R, Golub TR, Aster JC, Shipp MA: NFkappaB activity, function, and target-gene signatures in primary mediastinal large B-cell lymphoma and diffuse large B-cell lymphoma subtypes. Blood; 2005 Aug 15;106(4):1392-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NFkappaB activity, function, and target-gene signatures in primary mediastinal large B-cell lymphoma and diffuse large B-cell lymphoma subtypes.
  • Primary mediastinal large B-cell lymphoma (MLBCL) shares important clinical and molecular features with classic Hodgkin lymphoma, including nuclear localization of the nuclear factor kappaB (NFkappaB) subunit c-REL (reticuloendotheliosis viral oncogene homolog) in a pilot series.
  • Herein, we analyzed c-REL subcellular localization in additional primary MLBCLs and characterized NFkappaB activity and function in a MLBCL cell line.
  • The new primary MLBCLs had prominent c-REL nuclear staining, and the MLBCL cell line exhibited high levels of NFkappaB binding activity.
  • MLBCL cells expressing a superrepressor form of inhibitor of kappa B alpha signaling (IkappaB alpha) had a markedly higher rate of apoptosis, implicating constitutive NFkappaB activity in MLBCL cell survival.
  • The transcriptional profiles of newly diagnosed primary MLBCLs and diffuse large B-cell lymphomas (DLBCLs) were then used to characterize the NFkappaB target gene signatures of MLBCL and specific DLBCL subtypes.
  • MLBCLs expressed increased levels of NFkappaB targets that promote cell survival and favor antiapoptotic tumor necrosis factor alpha (TNFalpha) signaling.
  • In contrast, activated B cell (ABC)-like DLBCLs had a more restricted, potentially developmentally regulated, NFkappaB target gene signature.
  • Of interest, the newly characterized host response DLBCL subtype had a robust NFkappaB target gene signature that partially overlapped that of primary MLBCL.
  • In this large series of primary MLBCLs and DLBCLs, NFkappaB activation was not associated with amplification of the cREL locus, suggesting alternative pathogenetic mechanisms.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Mediastinal Neoplasms / pathology. NF-kappa B / physiology. Proto-Oncogene Proteins c-rel / genetics
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Gene Expression Profiling. Humans

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15870177.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Proto-Oncogene Proteins c-rel
  •  go-up   go-down


43. Berglund M, Thunberg U, Amini RM, Book M, Roos G, Erlanson M, Linderoth J, Dictor M, Jerkeman M, Cavallin-Ståhl E, Sundström C, Rehn-Eriksson S, Backlin C, Hagberg H, Rosenquist R, Enblad G: Evaluation of immunophenotype in diffuse large B-cell lymphoma and its impact on prognosis. Mod Pathol; 2005 Aug;18(8):1113-20
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of immunophenotype in diffuse large B-cell lymphoma and its impact on prognosis.
  • Diffuse large B-cell lymphoma (DLBCL) has been shown to be comprised of at least two prognostic entities, depending on its resemblance to normal germinal center or activated B cells, using global gene expression profiling.
  • Also, the expression patterns of bcl-6, CD10 and IRF-4 (also known as MUM1) have been suggested as alternative means of identifying the germinal- and nongerminal center (activated B-cell like) groups.
  • In the present study, we evaluated by immunohistochemistry the expression patterns of CD10, bcl-6, IRF-4 and bcl-2 in a large material of 161 DLBCL patients.
  • Positive staining for bcl-6 or CD10 predicted for superior survival, while expression of IRF-4 alone showed no association with prognosis.
  • Furthermore, expression of bcl-2 was associated with worse event-free survival and overall survival.
  • Here we confirm the prognostic importance of determining the germinal- or nongerminal center phenotype in patients with DLBCL.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15920553.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [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 / Interferon Regulatory Factors; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-bcl-6; 0 / Transcription Factors; 0 / interferon regulatory factor-4; EC 3.4.24.11 / Neprilysin
  •  go-up   go-down


44. Iqbal J, Greiner TC, Patel K, Dave BJ, Smith L, Ji J, Wright G, Sanger WG, Pickering DL, Jain S, Horsman DE, Shen Y, Fu K, Weisenburger DD, Hans CP, Campo E, Gascoyne RD, Rosenwald A, Jaffe ES, Delabie J, Rimsza L, Ott G, Müller-Hermelink HK, Connors JM, Vose JM, McKeithan T, Staudt LM, Chan WC, Leukemia/Lymphoma Molecular Profiling Project: Distinctive patterns of BCL6 molecular alterations and their functional consequences in different subgroups of diffuse large B-cell lymphoma. Leukemia; 2007 Nov;21(11):2332-43
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinctive patterns of BCL6 molecular alterations and their functional consequences in different subgroups of diffuse large B-cell lymphoma.
  • Gene expression profiling of diffuse large B-cell lymphoma (DLBCL) has revealed biologically and prognostically distinct subgroups: germinal center B-cell-like (GCB), activated B-cell-like (ABC) and primary mediastinal (PM) DLBCL.
  • The BCL6 gene is often translocated and/or mutated in DLBCL.
  • Therefore, we examined the BCL6 molecular alterations in these DLBCL subgroups, and their impact on BCL6 expression and BCL6 target gene repression.
  • BCL6 translocations at the major breakpoint region (MBR) were detected in 25 (18.8%) of 133 DLBCL cases, with a higher frequency in the PM (33%) and ABC (24%) subgroups than in the GCB (10%) subgroup.
  • Translocations at the alternative breakpoint region (ABR) were detected in five (6.4%) of 78 DLBCL cases, with three cases in ABC and one case each in the GCB and the unclassifiable subgroups.
  • The translocated cases involved IgH and non-IgH partners in about equal frequency and were not associated with different levels of BCL6 mRNA and protein expression.
  • BCL6 mutations were detected in 61% of DLBCL cases, with a significantly higher frequency in the GCB and PM subgroups (>70%) than in the ABC subgroup (44%).
  • The repression of known BCL6 target genes correlated with the level of BCL6 mRNA and protein expression in GCB and ABC subgroups but not with BCL6 translocation and intronic mutations.
  • No clear inverse correlation between BCL6 expression and p53 expression was observed.
  • Patients with higher BCL6 mRNA or protein expression had a significantly better overall survival.

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Genes Chromosomes Cancer. 2000 Jan;27(1):69-75 [10564588.001]
  • [Cites] Blood. 2000 Jan 15;95(2):651-9 [10627476.001]
  • [Cites] Blood. 2000 Feb 15;95(4):1400-5 [10666217.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Immunity. 2000 Aug;13(2):199-212 [10981963.001]
  • [Cites] Blood. 2000 Oct 15;96(8):2907-9 [11023530.001]
  • [Cites] Nat Immunol. 2000 Sep;1(3):214-20 [10973278.001]
  • [Cites] Blood. 2001 Aug 15;98(4):945-51 [11493437.001]
  • [Cites] Int J Oncol. 2002 Jan;20(1):161-5 [11743658.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Oncogene. 2002 Jan 17;21(3):368-76 [11821949.001]
  • [Cites] Leukemia. 2002 Feb;16(2):268-75 [11840294.001]
  • [Cites] Blood. 2002 Apr 1;99(7):2624-5 [11926184.001]
  • [Cites] Am J Pathol. 2002 Apr;160(4):1371-80 [11943722.001]
  • [Cites] Br J Haematol. 2002 May;117(2):322-32 [11972514.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Blood. 2003 Apr 15;101(8):2914-23 [12515714.001]
  • [Cites] J Immunol. 2003 Jul 1;171(1):426-31 [12817026.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1931-2; author reply 1932 [12930733.001]
  • [Cites] J Exp Med. 2003 Sep 15;198(6):851-62 [12975453.001]
  • [Cites] Blood. 2003 Dec 1;102(12):3871-9 [12933571.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Diagn Mol Pathol. 2007 Mar;16(1):32-7 [17471156.001]
  • [Cites] Am J Pathol. 2004 Aug;165(2):481-90 [15277222.001]
  • [Cites] Haematologica. 2004 Sep;89(9):1091-9 [15377470.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 28;101(39):14198-203 [15375218.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jun 1;90(11):5262-6 [8506375.001]
  • [Cites] Science. 1993 Oct 29;262(5134):747-50 [8235596.001]
  • [Cites] Blood. 1994 Jan 1;83(1):26-32 [8274740.001]
  • [Cites] Blood. 1994 May 1;83(9):2423-7 [8167331.001]
  • [Cites] N Engl J Med. 1994 Jul 14;331(2):74-80 [8208268.001]
  • [Cites] Blood. 1995 Jul 1;86(1):45-53 [7795255.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Dec 19;92(26):12520-4 [8618933.001]
  • [Cites] EMBO J. 1995 Dec 15;14(24):6209-17 [8557040.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jul 9;93(14):6947-52 [8692924.001]
  • [Cites] Cancer Res. 1997 Jan 1;57(1):7-12 [8988030.001]
  • [Cites] Science. 1997 Apr 25;276(5312):589-92 [9110977.001]
  • [Cites] Genes Dev. 1998 Jul 1;12(13):1953-61 [9649500.001]
  • [Cites] Ann Oncol. 1998 Jul;9(7):717-20 [9739436.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 29;95(20):11816-21 [9751748.001]
  • [Cites] Blood. 1998 Nov 1;92(9):3152-62 [9787151.001]
  • [Cites] Oncogene. 1998 Oct 1;17(13):1717-22 [9796700.001]
  • [Cites] Nature. 2004 Dec 2;432(7017):635-9 [15577913.001]
  • [Cites] J Immunol. 2005 Jan 1;174(1):205-14 [15611242.001]
  • [Cites] Cancer Cell. 2005 May;7(5):445-55 [15894265.001]
  • [Cites] Leuk Lymphoma. 2005 May;46(5):693-701 [16019506.001]
  • [Cites] Am J Pathol. 2004 Jul;165(1):159-66 [15215171.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3183-90 [16046532.001]
  • [Cites] Leukemia. 2005 Oct;19(10):1824-30 [16094416.001]
  • [Cites] Nat Immunol. 2005 Oct;6(10):1054-60 [16142238.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):301-4 [16075463.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1392-9 [15870177.001]
  • (PMID = 17625604.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA084967; United States / NCI NIH HHS / CA / CA114778-03; United States / NCI NIH HHS / CA / CA84967; United States / NCI NIH HHS / CA / CA36727; United States / NCI NIH HHS / CA / U01 CA114778-01; United States / NCI NIH HHS / CA / CA114778-01; United States / NCI NIH HHS / CA / P30 CA036727; United States / NCI NIH HHS / CA / U01 CA114778-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / DNA-Binding Proteins; 0 / RNA, Messenger
  • [Other-IDs] NLM/ NIHMS39596; NLM/ PMC2366166
  •  go-up   go-down


45. Borovecki A, Korać P, Nola M, Ivanković D, Jaksić B, Dominis M: Prognostic significance of B-cell differentiation genes encoding proteins in diffuse large B-cell lymphoma and follicular lymphoma grade 3. Croat Med J; 2008 Oct;49(5):625-35
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of B-cell differentiation genes encoding proteins in diffuse large B-cell lymphoma and follicular lymphoma grade 3.
  • AIM: To define prognostic significance of B-cell differentiation genes encoding proteins and BCL2 and BCL6 gene abnormalities in diffuse large B-cell lymphoma and follicular lymphoma grade 3 with >75% follicular growth pattern.
  • METHODS: In 53 patients with diffuse large B-cell lymphoma and 20 patients with follicular lymphoma grade 3 with >75% follicular growth pattern the following was performed:.
  • 1) determination of protein expression of BCL6, CD10, MUM1/IRF4, CD138, and BCL2 by immunohistochemistry;.
  • 2) subclassification into germinal center B-cell-like (GCB) and activated B-cell-like (ABC) groups according to the results of protein expression;.
  • 3) detection of t(14;18)(q32;q21)/IgH-BCL2 and BCL6 abnormalities by fluorescent in situ hybridization in diffuse large B-cell lymphoma and follicular lymphoma grade 3 with >75% follicular growth pattern as well as in GCB and ABC groups; and 4) assessment of the influence of the analyzed characteristics and clinical prognostic factors on overall survival.
  • RESULTS: Only BCL6 expression was more frequently found in follicular lymphoma grade 3 with >75% follicular growth pattern than in diffuse large B-cell lymphoma (P=0.030).
  • There were no differences in BCL2 and BCL6 gene abnormalities between diffuse large B-cell lymphoma and follicular lymphoma grade 3 with >75% follicular growth pattern.
  • Diffuse large B-cell lymphoma and follicular lymphoma grade 3 with >75% follicular growth pattern patients were equally distributed in GCB and ABC groups. t(14;18)(q32;q21) was more frequently recorded in GCB group, and t(14;18)(q32;q21) with BCL2 additional signals or only BCL2 and IgH additional signals in ABC group (P=0.004).
  • The GCB and ABC groups showed no difference in BCL6 gene abnormalities.
  • There was no overall survival difference between the diffuse large B-cell lymphoma and follicular lymphoma grade 3 with >75% follicular growth pattern patients, however, GCB group had longer overall survival than ABC group (P=0.047).
  • Multivariate analysis showed that BCL6, CD10, and BCL2 expression, BCL2 and BCL6 abnormalities, and International Prognostic Index were not significantly related to overall survival.
  • CONCLUSION: Diffuse large B-cell lymphoma and follicular lymphoma grade 3 with >75% follicular growth pattern patients have very similar characteristics and their prognosis is more influenced by protein expression of B-cell differentiation stage genes than by tumor cells growth pattern, BCL2 and BCL6 abnormalities, and International Prognostic Index.
  • [MeSH-major] Biomarkers, Tumor / genetics. DNA-Binding Proteins / genetics. Interleukin-6 / genetics. Lymphoma, Follicular / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Gene Expression Regulation, Neoplastic. Genetic Markers. Humans. Immunohistochemistry. Male. Middle Aged. Neprilysin / genetics. Predictive Value of Tests. Prognosis. Syndecan-1 / genetics

  • Genetic Alliance. consumer health - Follicular Lymphoma.
  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Arch Pathol Lab Med. 2004 Aug;128(8):863-8 [15270618.001]
  • [Cites] Blood. 2001 Feb 1;97(3):744-51 [11157493.001]
  • [Cites] Am J Clin Pathol. 2001 Jun;115(6):862-7 [11392883.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1136-43 [11830458.001]
  • [Cites] Cancer Genet Cytogenet. 2002 Jan 15;132(2):125-32 [11850073.001]
  • [Cites] Blood. 2002 Apr 1;99(7):2285-90 [11895757.001]
  • [Cites] Br J Haematol. 2002 May;117(2):322-32 [11972514.001]
  • [Cites] Blood. 2002 May 15;99(10):3806-12 [11986240.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Histopathology. 2002 Nov;41(5):414-20 [12405909.001]
  • [Cites] Histopathology. 2002 Dec;41(6):482-509 [12460202.001]
  • [Cites] Nat Rev Immunol. 2002 Dec;2(12):920-32 [12461565.001]
  • [Cites] Blood. 2003 Jan 1;101(1):78-84 [12393466.001]
  • [Cites] Blood. 2003 Feb 1;101(3):1149-54 [12529293.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):722-8 [12576441.001]
  • [Cites] Blood. 2003 Mar 15;101(6):2363-7 [12424193.001]
  • [Cites] Br J Cancer. 2003 Jul 7;89(1):36-42 [12838297.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Am J Surg Pathol. 2004 Apr;28(4):464-70 [15087665.001]
  • [Cites] Am J Pathol. 2004 Jul;165(1):159-66 [15215171.001]
  • [Cites] Am J Pathol. 2004 Aug;165(2):481-90 [15277222.001]
  • [Cites] J Clin Oncol. 2004 Sep 1;22(17):3498-506 [15337798.001]
  • [Cites] J Clin Oncol. 1989 Nov;7(11):1630-6 [2809679.001]
  • [Cites] N Engl J Med. 1993 Sep 30;329(14):987-94 [8141877.001]
  • [Cites] Nat Genet. 1997 Jun;16(2):161-70 [9171827.001]
  • [Cites] Blood. 2005 Jan 1;105(1):301-7 [15345589.001]
  • [Cites] Int J Hematol. 2005 Jan;81(1):48-57 [15717689.001]
  • [Cites] Haematologica. 2005 Mar;90(3):341-7 [15749666.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2005 Jun;13(2):116-23 [15894922.001]
  • [Cites] Leukemia. 2005 Jun;19(6):1058-63 [15815725.001]
  • [Cites] Am J Surg Pathol. 2005 Aug;29(8):1067-73 [16006802.001]
  • [Cites] Leuk Lymphoma. 2005 May;46(5):693-701 [16019506.001]
  • [Cites] Mod Pathol. 2005 Aug;18(8):1113-20 [15920553.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1164-74 [15855278.001]
  • [Cites] J Clin Oncol. 2005 Sep 10;23(26):6351-7 [16155019.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3183-90 [16046532.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3383-5 [16091454.001]
  • [Cites] J Mol Diagn. 2006 May;8(2):141-51 [16645199.001]
  • [Cites] Hum Pathol. 2006 May;37(5):528-33 [16647949.001]
  • [Cites] J Clin Oncol. 2007 Mar 1;25(7):805-12 [17327602.001]
  • [Cites] Blood. 2007 Jun 1;109(11):4930-5 [17299093.001]
  • [Cites] Blood. 2007 Jul 1;110(1):29-36 [17360935.001]
  • [Cites] Curr Opin Oncol. 2007 Sep;19(5):433-7 [17762566.001]
  • [Cites] Blood. 2000 Mar 15;95(6):2084-92 [10706878.001]
  • (PMID = 18925696.001).
  • [ISSN] 1332-8166
  • [Journal-full-title] Croatian medical journal
  • [ISO-abbreviation] Croat. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Genetic Markers; 0 / Interleukin-6; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Syndecan-1; EC 3.4.24.11 / Neprilysin
  • [Other-IDs] NLM/ PMC2582355
  •  go-up   go-down


46. Lu X, Nechushtan H, Ding F, Rosado MF, Singal R, Alizadeh AA, Lossos IS: Distinct IL-4-induced gene expression, proliferation, and intracellular signaling in germinal center B-cell-like and activated B-cell-like diffuse large-cell lymphomas. Blood; 2005 Apr 1;105(7):2924-32
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distinct IL-4-induced gene expression, proliferation, and intracellular signaling in germinal center B-cell-like and activated B-cell-like diffuse large-cell lymphomas.
  • Diffuse large B-cell lymphomas (DLBCLs) can be subclassified into germinal center B-cell (GCB)-like and activated B-cell (ABC)-like tumors characterized by long and short survival, respectively.
  • In contrast to ABC-like DLBCL, GCB-like tumors exhibit high expression of components of the interleukin 4 (IL-4) signaling pathway and of IL-4 target genes such as BCL6 and HGAL, whose high expression independently predicts better survival.
  • These observations suggest distinct activity of the IL-4 signaling pathway in DLBCL subtypes.
  • Herein, we demonstrate similar IL-4 expression but qualitatively different IL-4 effects on GCB-like and ABC-like DLBCL.
  • In GCB-like DLBCL, IL-4 induces expression of its target genes, activates signal transducers and activators of transcription 6 (STAT6) signaling, and increases cell proliferation.
  • In contrast, in the ABC-like DLBCL, IL-4 activates AKT, decreases cell proliferation by cell cycle arrest, and does not induce gene expression due to aberrant Janus kinase (JAK)-STAT6 signaling attributed to STAT6 dephosphorylation.
  • We found distinct expression profiles of tyrosine phosphatases in DLBCL subtypes and identified putative STAT6 tyrosine phosphatases-protein tyrosine phosphatase nonreceptor type 1 (PTPN1) and PTPN2, whose expression is significantly higher in ABC-like DLBCL.
  • These differences in tyrosine phosphatase expression might underlie distinct expression profiles of some of the IL-4 target genes and could contribute to a different clinical outcome of patients with GCB-like and ABC-like DLBCLs.
  • [MeSH-major] B-Lymphocytes / physiology. Germinal Center / pathology. Interleukin-4 / genetics. Lymphoma, B-Cell / physiopathology. Lymphoma, Large B-Cell, Diffuse / physiopathology. Signal Transduction / immunology
  • [MeSH-minor] Active Transport, Cell Nucleus. Cell Division / immunology. Cell Nucleus / metabolism. Cell Nucleus / pathology. Gene Expression Regulation, Neoplastic. Humans. Oligonucleotide Array Sequence Analysis. Phosphorylation. Protein Tyrosine Phosphatase, Non-Receptor Type 1. Protein Tyrosine Phosphatases / metabolism. STAT6 Transcription Factor. Trans-Activators / metabolism

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15591113.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / STAT6 Transcription Factor; 0 / STAT6 protein, human; 0 / Trans-Activators; 207137-56-2 / Interleukin-4; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 1; EC 3.1.3.48 / Protein Tyrosine Phosphatases
  •  go-up   go-down


47. Baecklund E, Natkunam Y, Backlin C, Iliadou A, Askling J, Ekbom A, Feltelius N, Klareskog L, Enblad G, Lossos IS, Levy R, Sundström C, Rosenquist R: Expression of the human germinal-centre-associated lymphoma protein in diffuse large B-cell lymphomas in patients with rheumatoid arthritis. Br J Haematol; 2008 Apr;141(1):69-72
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of the human germinal-centre-associated lymphoma protein in diffuse large B-cell lymphomas in patients with rheumatoid arthritis.
  • Diffuse large B-cell lymphomas (DLBCL) can be subdivided into germinal centre (GC)-like and non-GC-like subtypes by CD10, BCL6 and MUM1/IRF4 status.
  • We previously reported that patients with severe rheumatoid arthritis (RA) are at increased risk of non-GC DLBCL.
  • This study examined a new GC-marker, human germinal-centre-associated lymphoma (HGAL) protein, in RA-DLBCL.
  • Of 111, 38 (34%) DLBCL were HGAL-positive and showed less disseminated disease and a tendency toward improved overall survival compared to HGAL-negative cases.
  • This supports that a majority of RA-DLBCL are of non-GC origin, indicating a specific role for activated peripheral B cells in the pathogenesis of RA-DLBCL.
  • [MeSH-major] Arthritis, Rheumatoid / complications. Biomarkers, Tumor / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Neoplasm Proteins / metabolism


48. Shaknovich R, Geng H, Johnson NA, Tsikitas L, Cerchietti L, Greally JM, Gascoyne RD, Elemento O, Melnick A: DNA methylation signatures define molecular subtypes of diffuse large B-cell lymphoma. Blood; 2010 Nov 18;116(20):e81-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DNA methylation signatures define molecular subtypes of diffuse large B-cell lymphoma.
  • Expression profiling has shown 2 main and clinically distinct subtypes of diffuse large B-cell lymphomas (DLBCLs): germinal-center B cell-like (GCB) and activated B cell-like (ABC) DLBCLs.
  • Here, we show with the use of an assay that measures DNA methylation levels of 50,000 CpG motifs distributed among more than 14,000 promoters that these 2 DLBCL subtypes are also characterized by distinct epigenetic profiles.
  • DNA methylation and gene expression profiling were performed on a cohort of 69 patients with DLBCL.
  • After assigning ABC or GCB labels with a Bayesian expression classifier trained on an independent dataset, a supervised analysis identified 311 differentially methylated probe sets (263 unique genes) between ABC and GCB DLBCLs.
  • Integrated analysis of methylation and gene expression showed a core tumor necrosis factor-α signaling pathway as the principal differentially perturbed gene network.
  • Sixteen genes overlapped between the core ABC/GCB methylation and expression signatures and encoded important proteins such as IKZF1.
  • This reduced gene set was an accurate predictor of ABC and GCB subtypes.
  • Collectively, the data suggest that epigenetic patterning contributes to the ABC and GCB DLBCL phenotypes and could serve as useful biomarker.

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • SciCrunch. ArrayExpress: Data: Microarray .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 2006 Oct;20(10):1855-62 [16900213.001]
  • [Cites] N Engl J Med. 2010 Apr 15;362(15):1417-29 [20393178.001]
  • [Cites] Leukemia. 2007 Jul;21(7):1532-44 [17495977.001]
  • [Cites] Leukemia. 2007 Nov;21(11):2332-43 [17625604.001]
  • [Cites] Mol Cell. 2007 Oct 26;28(2):337-50 [17964271.001]
  • [Cites] Arch Pathol Lab Med. 2008 Jan;132(1):118-24 [18181663.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1515-23 [17951530.001]
  • [Cites] PLoS One. 2008;3(3):e1882 [18365023.001]
  • [Cites] Neurochem Res. 2008 Jun;33(6):1077-84 [18205044.001]
  • [Cites] Bioinformatics. 2008 May 1;24(9):1161-7 [18353789.001]
  • [Cites] Leukemia. 2008 May;22(5):1035-43 [18288132.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Sep 9;105(36):13520-5 [18765795.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1999;64:71-8 [11232339.001]
  • [Cites] J Neurosci Res. 2001 Apr 15;64(2):121-31 [11288141.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Nat Rev Immunol. 2002 Mar;2(3):162-74 [11913067.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2066-70 [3281160.001]
  • [Cites] Blood. 1993 Oct 1;82(7):2169-74 [8400266.001]
  • [Cites] J Rheumatol. 1995 Sep;22(9):1674-80 [8523344.001]
  • [Cites] Gene. 1997 Aug 11;195(1):67-71 [9300822.001]
  • [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] FEMS Immunol Med Microbiol. 2005 May 1;44(2):113-9 [15866204.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):15785-90 [16243968.001]
  • [Cites] Lancet Oncol. 2006 Jan;7(1):27-38 [16389181.001]
  • [Cites] J Clin Oncol. 2006 Feb 20;24(6):961-8 [16418494.001]
  • [Cites] Immunol Rev. 2006 Apr;210:67-85 [16623765.001]
  • [Cites] N Engl J Med. 2006 Jun 8;354(23):2431-42 [16760443.001]
  • [Cites] Genome Res. 2006 Aug;16(8):1046-55 [16809668.001]
  • [Cites] Blood. 2008 Oct 15;112(8):3425-33 [18544678.001]
  • [Cites] N Engl J Med. 2008 Nov 27;359(22):2313-23 [19038878.001]
  • [Cites] N Engl J Med. 2009 Jan 29;360(5):524-6 [19131438.001]
  • [Cites] Blood. 2009 Mar 12;113(11):2488-97 [19075189.001]
  • [Cites] Immunol Rev. 2009 Mar;228(1):225-40 [19290931.001]
  • [Cites] Cancer Metastasis Rev. 2009 Jun;28(1-2):51-63 [19165420.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2009 Jun;296(6):H1850-8 [19363130.001]
  • [Cites] Nature. 2009 Jun 4;459(7247):717-21 [19412164.001]
  • [Cites] Birth Defects Res C Embryo Today. 2009 Dec;87(4):335-50 [19960550.001]
  • [Cites] Haematologica. 2010 Jan;95(1):96-101 [19797725.001]
  • [Cites] Am J Epidemiol. 2010 Feb 1;171(3):267-76 [20047977.001]
  • [Cites] Nat Genet. 2010 Feb;42(2):181-5 [20081860.001]
  • [Cites] Cancer Res. 2010 Feb 1;70(3):979-87 [20103652.001]
  • [Cites] Methods Mol Biol. 2010;632:191-201 [20217579.001]
  • [Cites] Arch Immunol Ther Exp (Warsz). 2010 Apr;58(2):131-41 [20191326.001]
  • [Cites] Int J Hematol. 2006 Oct;84(3):248-55 [17050200.001]
  • (PMID = 20610814.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA127353; Canada / Canadian Institutes of Health Research / /
  • [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 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2993635
  •  go-up   go-down


49. Xu FP, Liu YH, Luo XL, Zhuang HG, Li L, Luo DL, Xu J, Zhang F, Zhang MH, Du X, Li WY: [Clinicopathologic significance of bcl-6 gene rearrangement and expression in three molecular subgroups of diffuse large B-cell lymphoma]. Zhonghua Bing Li Xue Za Zhi; 2008 Jun;37(6):371-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinicopathologic significance of bcl-6 gene rearrangement and expression in three molecular subgroups of diffuse large B-cell lymphoma].
  • OBJECTIVE: To investigate the role of bcl-6 gene rearrangement and bcl-6 expression in three molecular subgroups of diffuse large B-cell lymphoma (DLBCL) and its clinicopathological significance.
  • METHODS: Tissue microarray including 163 newly diagnosed DLBCL was constructed.
  • Fluorescence in situ hybridization (FISH) was performed to detect the bcl-6 gene rearrangement and immunohistochemistry (EnVision method) was used to evaluate the expression of bcl-6, Ki-67, cyclin D3, Geminin and P27(Kip1) proteins in DLBCL.
  • RESULTS: One hundred and forty nine of 163 cases were further classified into three molecular subgroups: 40 cases of germinal center B-cell-like (GCB) type, 75 cases of activated non-germinal center B-cell-like (ABC) type, 34 cases of Type 3.
  • The bcl-6 gene rearrangement was more frequently seen in the ABC subgroup (22/62, 35.5%) than in GCB (6/31, 19.4%) and Type 3 subgroups (5/25, 20.0%, P=0.16).
  • The correlation of bcl-6 gene rearrangement and expression of its encoded protein was further analyzed.
  • Most of DLBCL (26/33, 78.8%) with bcl-6 gene rearrangement presented with overexpression of its encoded protein, which was higher than those without bcl-6 gene rearrangement (53/84, 62.4%, P=0.088).
  • DLBCL with bcl-6 gene rearrangement (24/33, 72.7%) more frequently expressed cyclin D3, and had a higher proliferative activity than those without bcl-6 gene rearrangement (37/81, 45.7% , P=0.009).
  • Twenty-nine of 33 (87.9%) cases of DLBCL with bcl-6 gene rearrangement presented with advanced stage (Ann Arbor stage III/IV), which was higher than those without bcl-6 gene rearrangement (65/85, 76.5% , P=0.167).
  • Univariate Cox proportional hazards regression analysis showed that bcl-6 gene rearrangement was associated with an increased relative risk (at 1.842) of death in DLBCL cases compared with those without bcl-6 gene rearrangement.
  • CONCLUSION: Overexpression of bcl-6 protein caused by bcl-6 gene rearrangement may play some important roles in the development and/or progression of a subset of DLBCL.
  • [MeSH-major] Cyclin D3 / genetics. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Proto-Oncogene Proteins c-bcl-6 / genetics

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19031715.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cyclin D3; 0 / Proto-Oncogene Proteins c-bcl-6
  •  go-up   go-down


50. Liu YH, Xu FP, Zhuang HG, Lai KC, Xie D, Luo DL, Li L, Luo XL, Xu J, Zhang MH, Zhang F, Li HM: Clinicopathologic significance of immunophenotypic profiles related to germinal center and activation B-cell differentiation in diffuse large B-cell lymphoma from Chinese patients. Hum Pathol; 2008 Jun;39(6):875-84
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinicopathologic significance of immunophenotypic profiles related to germinal center and activation B-cell differentiation in diffuse large B-cell lymphoma from Chinese patients.
  • Diffuse large B-cell lymphoma (DLBCL) can be subdivided into prognostically significant groups with germinal center B-cell-like (GCB), activated B-cell-like (ABC), and type 3 groups.
  • One hundred forty-nine of 163 DLBCLs could then be classified into GCB group (pattern A), activated GCB group (pattern B) and activated non-GCB group (pattern C) according to the expression of CD10, Bcl-6, MUM1, and CD138.
  • Of the 149 cases, 40 (26%) showed pattern A expression and were grouped as GCB group, lower than reported frequency of the studies involving mostly Western population.
  • Compared with cases with pattern A, those with pattern B (activated GCB group) and C (activated non-GCB group) more often presented with more aggressive tumors and a shorter survival time.
  • These results indicate that most of DLBCLs from Chinese patients can be classified into prognostically different groups based on the antigenic expression models using a panel of GCB- and ABC-associated markers.
  • The translocation was significantly associated with expression of Bcl-2 protein.
  • The group with pattern B demonstrated more frequent expression of Ki-67, cyclin D3, geminin, and showed higher proliferative activity than the group with pattern A.
  • These findings suggest that high proliferative activity of tumors with pattern B may be associated with aggressive tumor behavior and poor clinical outcome in patients with DLBCL.
  • [MeSH-major] B-Lymphocytes / immunology. Cell Transformation, Neoplastic. Germinal Center / pathology. Lymph Nodes / pathology. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Cell Proliferation. Child. Child, Preschool. China. Female. Humans. Immunophenotyping. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Survival Rate. Tissue Array Analysis


51. Hallack Neto AE, Siqueira SA, Dulley FL, Chauobah A, Belesso M, Saboia R, Ruiz MA, Chamone DA, Pereira J: Bcl-2 protein frequency in patients with high-risk diffuse large B-cell lymphoma. Sao Paulo Med J; 2010 Jan;128(1):14-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bcl-2 protein frequency in patients with high-risk diffuse large B-cell lymphoma.
  • CONTEXT AND OBJECTIVE: Gene expression and immunohistochemical profiling of diffuse large B-cell lymphoma (DLBCL) have revealed important prognostic subgroups: germinal center B-cell-like (GCB-like) DLBCL and activated B cell-like (ABC-like) DLBCL.
  • Although few reports on high-risk DLBCL are available, the prognosis for the GCB-like subgroup has been shown to be better than that of the ABC-like subgroup.
  • The role of Bcl-2 as a predictor of survival in DLBCL cases is unclear and its expression varies between the two subgroups of DLBCL.
  • In this study, we analyzed the frequency and prognostic impact of Bcl-2 protein expression in high-risk DLBCL cases.
  • DESIGN AND SETTING: Retrospective cohort study among DLBCL patients treated at Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo (HC-FMUSP).
  • METHODS: The prognostic impact of the expression of the proteins CD10, Bcl-6, MUM1 (multiple myeloma oncogene-1) and Bcl-2 on high-risk DLBCL cases was evaluated by means of immunohistochemistry.
  • RESULTS: Twenty-four cases (32.9%) were GCB-like and 49 (67.1%) were ABC-like, with no difference regarding complete remission, disease-free survival or overall survival rates.
  • Twenty-seven patients (37%) showed Bcl-2 expression, which was the only independent factor predicting a worse prognosis for overall survival according to multivariate analysis.
  • CONCLUSION: Bcl-2 protein was expressed in 37% of the high-risk DLBCL patients, without any difference between the ABC-like DLBCL and GCB-like DLBCL cases.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] Adolescent. Adult. Chi-Square Distribution. Cohort Studies. DNA-Binding Proteins / metabolism. Disease-Free Survival. Female. Gene Expression. Germinal Center / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Myeloma Proteins / metabolism. Neprilysin / metabolism. Prognosis. Retrospective Studies. Young Adult

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Sao Paulo Med J. 2011 Jan 6;129(1):54; author reply 54 [21437512.001]
  • (PMID = 20512275.001).
  • [ISSN] 1806-9460
  • [Journal-full-title] São Paulo medical journal = Revista paulista de medicina
  • [ISO-abbreviation] Sao Paulo Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Myeloma Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / multiple myeloma M-proteins; EC 3.4.24.11 / Neprilysin
  •  go-up   go-down


52. Brown PJ, Ashe SL, Leich E, Burek C, Barrans S, Fenton JA, Jack AS, Pulford K, Rosenwald A, Banham AH: Potentially oncogenic B-cell activation-induced smaller isoforms of FOXP1 are highly expressed in the activated B cell-like subtype of DLBCL. Blood; 2008 Mar 1;111(5):2816-24
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Potentially oncogenic B-cell activation-induced smaller isoforms of FOXP1 are highly expressed in the activated B cell-like subtype of DLBCL.
  • The FOXP1 forkhead transcription factor is targeted by recurrent chromosome translocations in several subtypes of B-cell non-Hodgkin lymphomas, where high-level FOXP1 protein expression has been linked to a poor prognosis.
  • Western blotting studies of diffuse large B-cell lymphoma (DLBCL) cell lines unexpectedly identified the atypical high-level expression of 2 smaller, 60 to 65 kDa, FOXP1 isoforms in all 5 of those with the activated B cell (ABC)-like DLBCL subtype and in a subgroup of primary DLBCL.
  • The anti-FOXP1 (JC12) monoclonal antibody cannot distinguish FOXP1 isoforms by immunohistochemistry, a finding that may be clinically relevant as high-level expression of the full-length FOXP1 protein was observed in some germinal center-derived DLBCLs.
  • ABC-like DLBCL-derived cell lines were observed to express 2 novel, alternatively spliced FOXP1 mRNA isoforms, encoding N-terminally truncated proteins.
  • These transcripts and the smaller protein isoforms were induced as a consequence of normal B-cell activation, which thus represents an additional mechanism for up-regulating FOXP1 expression in lymphomas.
  • The expression of potentially oncogenic smaller FOXP1 isoforms may resolve the previously contradictory findings that FOXP1 represents a favorable prognostic marker in breast cancer and an adverse risk factor in B-cell lymphomas.
  • [MeSH-major] B-Lymphocytes / immunology. Forkhead Transcription Factors / immunology. Lymphocyte Activation / immunology. Lymphoma, Large B-Cell, Diffuse / classification. Lymphoma, Large B-Cell, Diffuse / immunology. Repressor Proteins / immunology
  • [MeSH-minor] Alternative Splicing / genetics. Antibodies, Monoclonal. Biopsy. Blotting, Western. Cell Line, Tumor. Exons / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Peroxidases / metabolism. Protein Isoforms / genetics. Protein Isoforms / immunology

  • Cellosaurus - a cell line knowledge resource. culture/stock collections - HLY-1 (CVCL_H207) .
  • The Lens. Cited by Patents in .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18077790.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / FOXP1 protein, human; 0 / Forkhead Transcription Factors; 0 / Protein Isoforms; 0 / Repressor Proteins; EC 1.11.1.- / Peroxidases
  •  go-up   go-down


53. Bhattacharyya I, Chehal HK, Cohen DM, Al-Quran SZ: Primary diffuse large B-cell lymphoma of the oral cavity: germinal center classification. Head Neck Pathol; 2010 Sep;4(3):181-91
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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 oral cavity: germinal center classification.
  • Primary lymphomas of the oral cavity are rare and the most frequent type is diffuse large B-cell lymphoma (DLBCL).
  • Recently, several reports have highlighted the value of classifying DLBCL into prognostically important subgroups, namely germinal center B-cell like (GCB) and non-germinal center B-cell like (non-GCB) lymphomas based on gene expression profiles and by immunohistochemical expression of CD10, BCL6 and MUM-1.
  • Studies validating this classification have been done for DLBCL of the breast, CNS, testes and GI tract.
  • IHC was performed using antibodies against germinal center markers (CD10, BCL6), activated B-cell markers (MUM1, BCL2) and Ki-67 (proliferation marker).
  • In conclusion, our analysis shows that primary oral DLBCL predominantly belongs to the non-GCB subgroup, which tends to exhibit a poorer prognosis.
  • [MeSH-major] Germinal Center / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Mouth Neoplasms / pathology

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • MedlinePlus Health Information. consumer health - Oral Cancer.
  • COS Scholar Universe. author profiles.
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Semin Oncol. 1998 Aug;25(4):483-91 [9728598.001]
  • [Cites] Am J Clin Pathol. 1999 Jan;111(1):117-22 [9894462.001]
  • [Cites] J Clin Oncol. 1999 Jan;17(1):423-9 [10458261.001]
  • [Cites] Virchows Arch. 2004 Dec;445(6):545-51 [15517363.001]
  • [Cites] Mod Pathol. 2005 Mar;18(3):398-405 [15492762.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2005 Mar;99(3):303-10 [15716836.001]
  • [Cites] Cancer. 2006 Jan 15;106(2):247-57 [16342164.001]
  • [Cites] Mod Pathol. 2006 Dec;19(12):1521-7 [16998463.001]
  • [Cites] J Clin Oncol. 2008 Jan 20;26(3):447-54 [18086797.001]
  • [Cites] Hematology. 2009 Apr;14(2):84-9 [19298719.001]
  • [Cites] Cancer Sci. 2009 Oct;100(10):1842-7 [19656156.001]
  • [Cites] Mod Pathol. 2010 Feb;23(2):235-43 [19935644.001]
  • [Cites] Blood. 2000 Jan 15;95(2):651-9 [10627476.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1797-803 [10688840.001]
  • [Cites] Blood. 2000 Mar 15;95(6):2084-92 [10706878.001]
  • [Cites] Am J Surg Pathol. 2000 Jun;24(6):846-52 [10843287.001]
  • [Cites] Immunity. 2000 Aug;13(2):199-212 [10981963.001]
  • [Cites] Mod Pathol. 2000 Nov;13(11):1244-52 [11106083.001]
  • [Cites] Mod Pathol. 2001 Feb;14(2):105-10 [11235901.001]
  • [Cites] Curr Opin Oncol. 2001 Sep;13(5):325-34 [11555708.001]
  • [Cites] Leuk Lymphoma. 2001 Sep-Oct;42(5):1089-98 [11697626.001]
  • [Cites] Nat Med. 2002 Jan;8(1):68-74 [11786909.001]
  • [Cites] Hum Pathol. 2002 Feb;33(2):153-7 [11957138.001]
  • [Cites] Br J Haematol. 2002 May;117(2):322-32 [11972514.001]
  • [Cites] N Engl J Med. 1987 Nov 5;317(19):1185-9 [3657890.001]
  • [Cites] J Pathol. 1988 Mar;154(3):223-35 [2450981.001]
  • [Cites] J Clin Pathol. 1989 Nov;42(11):1194-200 [2531171.001]
  • [Cites] Am J Pathol. 1990 Aug;137(2):225-32 [2201196.001]
  • [Cites] Cancer. 1990 Sep 15;66(6):1190-7 [2205355.001]
  • [Cites] N Engl J Med. 1993 Apr 8;328(14):1002-6 [7680764.001]
  • [Cites] Cancer. 1993 Jul 1;72(1):231-6 [8508412.001]
  • [Cites] N Engl J Med. 1993 Sep 30;329(14):987-94 [8141877.001]
  • [Cites] Science. 1993 Oct 29;262(5134):747-50 [8235596.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Mod Pathol. 2002 Aug;15(8):807-16 [12181265.001]
  • [Cites] Mod Pathol. 2002 Dec;15(12):1366-73 [12481019.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):722-8 [12576441.001]
  • [Cites] Clin Cancer Res. 2003 Mar;9(3):1063-9 [12631608.001]
  • [Cites] Am J Surg Pathol. 2003 Sep;27(9):1269-77 [12960812.001]
  • [Cites] Histopathology. 2003 Dec;43(6):509-28 [14636252.001]
  • [Cites] J Clin Oncol. 2004 Sep 1;22(17):3498-506 [15337798.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):5948-55 [15342373.001]
  • [Cites] J Clin Oncol. 1987 Mar;5(3):407-12 [3819806.001]
  • [Cites] Ann Intern Med. 1987 Jul;107(1):25-30 [3296898.001]
  • [Cites] Eur J Cancer B Oral Oncol. 1994;30B(2):121-5 [8032301.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1361-92 [8068936.001]
  • [Cites] Am J Pathol. 1996 May;148(5):1543-55 [8623923.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996 Aug;82(2):173-8 [8863307.001]
  • (PMID = 20533006.001).
  • [ISSN] 1936-0568
  • [Journal-full-title] Head and neck pathology
  • [ISO-abbreviation] Head Neck Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Interferon Regulatory Factors; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / interferon regulatory factor-4; EC 3.4.24.11 / Neprilysin
  • [Other-IDs] NLM/ PMC2923304
  •  go-up   go-down


54. Muris JJ, Ylstra B, Cillessen SA, Ossenkoppele GJ, Kluin-Nelemans JC, Eijk PP, Nota B, Tijssen M, de Boer WP, van de Wiel M, van den Ijssel PR, Jansen P, de Bruin PC, van Krieken JH, Meijer GA, Meijer CJ, Oudejans JJ: Profiling of apoptosis genes allows for clinical stratification of primary nodal diffuse large B-cell lymphomas. Br J Haematol; 2007 Jan;136(1):38-47
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Profiling of apoptosis genes allows for clinical stratification of primary nodal diffuse large B-cell lymphomas.
  • Intrinsic resistance of lymphoma cells to apoptosis is a probable mechanism causing chemotherapy resistance and eventual fatal outcome in patients with diffuse large B cell lymphomas (DLBCL).
  • We investigated whether microarray expression profiling of apoptosis related genes predicts clinical outcome in 46 patients with primary nodal DLBCL.
  • Unsupervised cluster analysis using genes involved in apoptosis (n = 246) resulted in three separate DLBCL groups partly overlapping with germinal centre B-lymphocytes versus activated B-cells like phenotype.
  • One group with poor clinical outcome was characterised by high expression levels of pro-and anti-apoptotic genes involved in the intrinsic apoptosis pathway.
  • The third group showing a favourable outcome was characterised by low expression levels of genes characteristic for both other groups.
  • Our results suggest that chemotherapy refractory DLBCL are characterised either by an intense cellular cytotoxic immune response or by constitutive activation of the intrinsic mediated apoptosis pathway with concomitant downstream inhibition of this apoptosis pathway.
  • Consequently, strategies neutralising the function of apoptosis-inhibiting proteins might be effective as alternative treatment modality in part of chemotherapy refractory DLBCL.
  • [MeSH-major] Gene Expression Profiling. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Oligonucleotide Array Sequence Analysis

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17062006.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.4.21.- / Granzymes
  •  go-up   go-down


55. Baecklund E, Backlin C, Iliadou A, Granath F, Ekbom A, Amini RM, Feltelius N, Enblad G, Sundström C, Klareskog L, Askling J, Rosenquist R: Characteristics of diffuse large B cell lymphomas in rheumatoid arthritis. Arthritis Rheum; 2006 Dec;54(12):3774-81
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characteristics of diffuse large B cell lymphomas in rheumatoid arthritis.
  • OBJECTIVE: Patients with rheumatoid arthritis (RA) are at increased risk of malignant lymphomas, with a correlation between RA disease severity and lymphoma risk, most pronounced for diffuse large B cell lymphomas (DLBCLs), which also constitute the majority of RA-associated lymphomas.
  • DLBCLs can be further subdivided into germinal center (GC)-like and non-GC-like subtypes, with different cellular origins and prognoses.
  • This study was undertaken to investigate whether RA displays a specific association with any of the DLBCL subtypes.
  • METHODS: We identified 139 patients with DLBCLs within a population-based case-control study of 378 RA patients with lymphoma.
  • The DLBCLs were examined for CD10, Bcl-6, and interferon regulatory factor 4 expression patterns, subclassified into GC and non-GC subtypes, and then correlated with clinical parameters.
  • These patients more often had an advanced stage of lymphoma at diagnosis and had a worse 5-year overall survival rate (16% versus 33%) compared with patients with the GC subtype.
  • CONCLUSION: These findings suggest that severe RA is particularly associated with the non-GC subtype of DLBCL, and indicate a critical role of activated peripheral B cells as the cells of origin in these lymphomas.
  • [MeSH-major] Arthritis, Rheumatoid / complications. Lymphoma, B-Cell / complications. Lymphoma, Large B-Cell, Diffuse / complications

  • Genetic Alliance. consumer health - Arthritis.
  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • Genetic Alliance. consumer health - Rheumatoid arthritis.
  • MedlinePlus Health Information. consumer health - Rheumatoid Arthritis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17133544.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-4; EC 3.4.24.11 / Neprilysin
  •  go-up   go-down


56. Pavan A, Spina M, Canzonieri V, Sansonno S, Toffoli G, De Re V: Recent prognostic factors in diffuse large B-cell lymphoma indicate NF-kappaB pathway as a target for new therapeutic strategies. Leuk Lymphoma; 2008 Nov;49(11):2048-58
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Recent prognostic factors in diffuse large B-cell lymphoma indicate NF-kappaB pathway as a target for new therapeutic strategies.
  • The diffuse large B-cell lymphoma (DLBCL) is the most common type of lymphoid cancer.
  • DLBCL classification identified three principle subgroups.
  • The first one, named germinal centre B cell-like (GCB), responds to both CHOP and R-CHOP treatment and it is mainly characterised by the expression of markers like Bcl-6 and CD10.
  • The second, the activated B-cell like (ABC), has a worse prognosis in comparison with GCB, and is mainly characterised by the expression of IRF-4, PRDM1 and NF-kappaB.
  • The third one, mediastinal large B-cell lymphoma (PMBCL) is an uncommon subtype characteristically found in young females.
  • Gene expression profiling suggests that this disease resembles Hodgkin lymphoma more than other types of DLBCL.
  • However, the clinical significance of this finding is still unknown, because both ABC and GCB DLBCL show a significant improvement of overall survival after R-CHOP treatment.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / drug therapy. NF-kappa B / drug effects

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19021048.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B
  • [Number-of-references] 60
  •  go-up   go-down


57. Lyu MA, Sung B, Cheung LH, Marks JW, Aggarwal BB, Aguiar RC, Rosenblum MG: The rGel/BLyS fusion toxin inhibits STAT3 signaling via down-regulation of interleukin-6 receptor in diffuse large B-cell lymphoma. Biochem Pharmacol; 2010 Nov 1;80(9):1335-42
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The rGel/BLyS fusion toxin inhibits STAT3 signaling via down-regulation of interleukin-6 receptor in diffuse large B-cell lymphoma.
  • In this study, we examined this fusion toxin for its ability to impact STAT3 signaling in diffuse large B-cell lymphoma (DLBCL).
  • The activated B cell-like DLBCL lines were found to express higher levels of interleukin-6 receptor (IL-6R) and STAT3 than did the germinal center B cell-like DLBCL lines.
  • Treatment of DLBCL cells with rGel/BLyS resulted in down-regulation of IL-6R and inhibited STAT3 phosphorylation, STAT3-DNA binding activity, and IL-6-inducible STAT3 reporter gene activity.
  • Inhibition of IL-6R-mediated STAT3 signaling by rGel/BLyS led to growth inhibition, triggered accumulation of cells in the sub-G(1) phase of the cell cycle, and induced apoptosis.
  • Our results indicate that rGel/BLyS is an excellent candidate for the treatment of aggressive DLBCL which is resistant to conventional chemotherapeutic regimens and STAT3 signaling pathway may be an attractive therapeutic target for non-Hodgkin's lymphoma.
  • [MeSH-major] B-Cell Activating Factor / pharmacology. Lymphoma, Large B-Cell, Diffuse / drug therapy. Receptors, Interleukin-6 / antagonists & inhibitors. Recombinant Fusion Proteins / pharmacology. Ribosome Inactivating Proteins, Type 1 / pharmacology. STAT3 Transcription Factor / antagonists & inhibitors. Signal Transduction / drug effects
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. DNA / metabolism. Down-Regulation. G1 Phase / drug effects. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Phosphorylation. Protein-Tyrosine Kinases / metabolism. Proto-Oncogene Proteins c-akt / metabolism

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20654581.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / B-Cell Activating Factor; 0 / Intracellular Signaling Peptides and Proteins; 0 / Receptors, Interleukin-6; 0 / Recombinant Fusion Proteins; 0 / Ribosome Inactivating Proteins, Type 1; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 75037-46-6 / GEL protein, Gelonium multiflorum; 9007-49-2 / DNA; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Syk kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  •  go-up   go-down


58. Oschlies I, Klapper W, Zimmermann M, Krams M, Wacker HH, Burkhardt B, Harder L, Siebert R, Reiter A, Parwaresch R: Diffuse large B-cell lymphoma in pediatric patients belongs predominantly to the germinal-center type B-cell lymphomas: a clinicopathologic analysis of cases included in the German BFM (Berlin-Frankfurt-Munster) Multicenter Trial. Blood; 2006 May 15;107(10):4047-52
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diffuse large B-cell lymphoma in pediatric patients belongs predominantly to the germinal-center type B-cell lymphomas: a clinicopathologic analysis of cases included in the German BFM (Berlin-Frankfurt-Munster) Multicenter Trial.
  • Diffuse large B-cell lymphoma (DLBCL) in adults is a heterogeneous disease.
  • Biologic subgroups of DLBCL with a favorable prognosis (germinal center B-cell-like, GCB) and with a poor prognosis (activated B-cell-like, ABC) have been defined by gene expression profiling and can be distinguished by immunohistochemistry.
  • In contrast to their adult counterparts, children with DLBCL have an excellent prognosis.
  • We analyzed 63 cases of DLBCL in pediatric patients by immunohistochemistry and fluorescence in situ hybridization (FISH) and found a striking predominance of a GCB subtype, which might explain the good clinical outcome in these lymphomas.
  • Interestingly, FISH applied to 50 of these cases, as well as conventional cytogenetics available in 3 cases, revealed absence of the translocation t(14;18) involving the BCL2 gene, which is present in about 15% of adult GCB subtype DLBCL.
  • Our data indicate that pediatric DLBCL differs from adult DLBCL and might comprise a biologically unique subgroup of DLBCL from which important insights into the pathogenesis and biology of this disease might be gained.
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 18. Leukemia, Lymphoid / classification. Lymphoma, B-Cell / classification. Translocation, Genetic


59. Kojima Y, Tsurumi H, Goto N, Shimizu M, Kasahara S, Yamada T, Kanemura N, Hara T, Sawada M, Saio M, Yamada T, Takahashi T, Tomita E, Takami T, Moriwaki H: Fas and Fas ligand expression on germinal center type-diffuse large B-cell lymphoma is associated with the clinical outcome. Eur J Haematol; 2006 Jun;76(6):465-72
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fas and Fas ligand expression on germinal center type-diffuse large B-cell lymphoma is associated with the clinical outcome.
  • In recent years, diffuse large B-cell lymphoma (DLBCL) has been classified by DNA microarray analysis into the germinal center B-cell-like (GC) type, the activated B-cell-like (ABC) type and type 3.
  • The protein Fas induces apoptosis of lymphocytes by binding with the Fas ligand (FasL), and escape from such apoptosis is considered to lead to malignant transformation of the cells and unrestricted growth of lymphoma.
  • We proposed a hypothesis that Fas/FasL expression could be possibly related with a better survival of GC type DLBCL and evaluated 69 DLBCL cases immunohistochemically with CD10, Bcl-6, MUM1, Fas and FasL.
  • Among markers as given above, positive CD10 was the most significant prognostic factor for overall survival in total DLBCL (P < 0.05).
  • Hence, Fas or FasL expression might contribute to a better prognosis of this type of DLBCL.
  • [MeSH-major] Antigens, CD95 / biosynthesis. Lymphoma, Large B-Cell, Diffuse / metabolism. Membrane Glycoproteins / biosynthesis. Neoplasm Proteins / biosynthesis. Tumor Necrosis Factors / biosynthesis

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISOLONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16494623.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Interferon Regulatory Factors; 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / Tumor Necrosis Factors; 0 / interferon regulatory factor-4; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; EC 1.1.1.27 / L-Lactate Dehydrogenase; VAP-cyclo protocol; VEP-THP protocol
  •  go-up   go-down


60. Li D, Mi C, Zhao Y, Wang YL, Ma Y, Li YY, Xiang MH: [Primary diffuse large B-cell lymphoma of testis: a clinicopathologic study of 14 cases]. Zhonghua Bing Li Xue Za Zhi; 2007 Jul;36(7):461-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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 testis: a clinicopathologic study of 14 cases].
  • OBJECTIVE: To study the clinicopathologic features, immunohistochemical findings and prognosis of primary diffuse large B-cell lymphoma (DLBCL) of testis.
  • METHODS: Fourteen cases of primary DLBCL of testis, diagnosed according to the 2001 World Health Organization staging standards for hematopoietic and lymphoid tumors, were retrospectively studied.
  • Histologically, the lymphoma cells of all cases showed a centroblastic appearance.
  • One case belonged to the germinal center B cell-like subtype on immunohistochemical study, while the remaining 13 cases were classified as non-germinal center B cell-like subtype.
  • CONCLUSIONS: Most cases with primary DLBCL of testis were of peripheral activated B-cell origin.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology. Testicular Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD20 / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Diagnosis, Differential. Doxorubicin / therapeutic use. Follow-Up Studies. Gene Expression Regulation, Neoplastic. Germinoma / drug therapy. Germinoma / metabolism. Germinoma / pathology. Germinoma / surgery. Humans. Male. Middle Aged. Neprilysin / metabolism. Orchiectomy. Prednisone / therapeutic use. Proto-Oncogene Proteins c-bcl-2 / metabolism. Retrospective Studies. Seminoma / pathology. Survival Rate. Tumor Suppressor Protein p53 / metabolism. Vincristine / therapeutic use

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • MedlinePlus Health Information. consumer health - Testicular Cancer.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17845759.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 3.4.24.11 / Neprilysin; VB0R961HZT / Prednisone; CHOP protocol
  •  go-up   go-down


61. Choi WW, Weisenburger DD, Greiner TC, Piris MA, Banham AH, Delabie J, Braziel RM, Geng H, Iqbal J, Lenz G, Vose JM, Hans CP, Fu K, Smith LM, Li M, Liu Z, Gascoyne RD, Rosenwald A, Ott G, Rimsza LM, Campo E, Jaffe ES, Jaye DL, Staudt LM, Chan WC: A new immunostain algorithm classifies diffuse large B-cell lymphoma into molecular subtypes with high accuracy. Clin Cancer Res; 2009 Sep 1;15(17):5494-502
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A new immunostain algorithm classifies diffuse large B-cell lymphoma into molecular subtypes with high accuracy.
  • PURPOSE: Hans and coworkers previously developed an immunohistochemical algorithm with approximately 80% concordance with the gene expression profiling (GEP) classification of diffuse large B-cell lymphoma (DLBCL) into the germinal center B-cell-like (GCB) and activated B-cell-like (ABC) subtypes.
  • EXPERIMENTAL DESIGN: We studied 84 cases of cyclophosphamide-doxorubicin-vincristine-prednisone (CHOP)-treated DLBCL (47 GCB, 37 ABC) with GCET1, CD10, BCL6, MUM1, FOXP1, BCL2, MTA3, and cyclin D2 immunostains, and compared different combinations of the immunostaining results with the GEP classification.
  • A separate set of 63 DLBCL cases treated with rituximab plus CHOP (37 GCB, 26 ABC) was used to validate the new algorithm.
  • The new algorithm predicted 3-year overall survival of the validation set [GCB (87%) versus ABC (44%); P < 0.001], simulating the predictive power of the GEP classification.
  • For a group of seven primary mediastinal large B-cell lymphoma, the new algorithm is a better prognostic classifier (all "GCB") than the Hans' algorithm (two GCB, five non-GCB).
  • CONCLUSION: Our new algorithm is significantly more accurate than the Hans' algorithm and will facilitate risk stratification of DLBCL patients and future DLBCL research using archival materials.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Immunohistochemistry / methods. Lymphoma, Large B-Cell, Diffuse / classification
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Algorithms. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Female. Gene Expression Profiling. Germinal Center / metabolism. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prednisone / therapeutic use. Vincristine / therapeutic use


62. Shia AK, Gan GG, Jairaman S, Peh SC: High frequency of germinal centre derivation in diffuse large B cell lymphoma from Asian patients. J Clin Pathol; 2005 Sep;58(9):962-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High frequency of germinal centre derivation in diffuse large B cell lymphoma from Asian patients.
  • BACKGROUND: Recent reports have divided diffuse large B cell lymphoma (DLBCL) into germinal centre B cell-like and activated B cell-like subgroups with implicated differences in prognosis.
  • AIMS: To delineate the germinal centre B cell derivation group from an Asian series of DLBCLs.
  • METHODS: Fifty four cases were analysed by polymerase chain reaction to detect the t(14;18) translocation and immunohistochemistry for BCL2, CD10, BCL6, and E2F1 expression.
  • There was a significant association between bcl2 gene rearrangement and the expression of both BCL2 and CD10.
  • Using the minimally acceptable criteria of t(14;18) rearrangement and/or CD10 expression, 26 of 54 cases were probably germinal centre derived, in agreement with other reports.
  • CONCLUSIONS: It may be possible to stratify patients for treatment using markers for specific lineages of B cell differentiation.
  • [MeSH-major] Germinal Center / pathology. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 2000 May;14(5):898-904 [10803523.001]
  • [Cites] Hum Pathol. 1999 Jul;30(7):803-8 [10414499.001]
  • [Cites] Mod Pathol. 2000 Nov;13(11):1219-31 [11106080.001]
  • [Cites] Histopathology. 2001 May;38(5):458-65 [11422484.001]
  • [Cites] Am J Clin Pathol. 2001 Aug;116(2):183-90 [11488064.001]
  • [Cites] Blood. 2001 Aug 15;98(4):945-51 [11493437.001]
  • [Cites] Histopathology. 2001 Aug;39(2):156-62 [11493332.001]
  • [Cites] Hum Pathol. 2001 Sep;32(9):954-62 [11567225.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Histopathology. 2002 Nov;41(5):414-20 [12405909.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):15018-23 [12407182.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2002 Dec;10(4):322-6 [12607600.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Leuk Lymphoma. 2001 Sep-Oct;42(5):1089-98 [11697626.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1136-43 [11830458.001]
  • [Cites] Blood. 2002 Apr 1;99(7):2285-90 [11895757.001]
  • [Cites] Br J Haematol. 2002 May;117(2):322-32 [11972514.001]
  • [Cites] Am J Pathol. 1990 Aug;137(2):225-32 [2201196.001]
  • [Cites] Blood. 1991 Dec 15;78(12):3275-80 [1742487.001]
  • [Cites] Ann Oncol. 1994;5 Suppl 1:55-60 [8172819.001]
  • [Cites] Blood. 1994 Sep 1;84(5):1361-92 [8068936.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Dec 19;92(26):12520-4 [8618933.001]
  • [Cites] Blood. 1996 Aug 1;88(3):1046-51 [8704213.001]
  • [Cites] J Pathol. 1996 Jun;179(2):145-50 [8758205.001]
  • [Cites] Blood. 1997 Jul 1;90(1):244-51 [9207459.001]
  • [Cites] Leukemia. 1997 Dec;11(12):2175-87 [9447838.001]
  • [Cites] Mod Pathol. 1998 May;11(5):457-63 [9619599.001]
  • [Cites] Arch Pathol Lab Med. 1998 Jun;122(6):539-44 [9625422.001]
  • [Cites] Genes Dev. 1998 Aug 1;12(15):2245-62 [9694791.001]
  • [Cites] Ann Oncol. 1998 Jul;9(7):717-20 [9739436.001]
  • [Cites] Blood. 1998 Nov 1;92(9):3152-62 [9787151.001]
  • [Cites] Am J Surg Pathol. 2000 Jun;24(6):846-52 [10843287.001]
  • (PMID = 16126878.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1770829
  •  go-up   go-down


63. Bidère N, Ngo VN, Lee J, Collins C, Zheng L, Wan F, Davis RE, Lenz G, Anderson DE, Arnoult D, Vazquez A, Sakai K, Zhang J, Meng Z, Veenstra TD, Staudt LM, Lenardo MJ: Casein kinase 1alpha governs antigen-receptor-induced NF-kappaB activation and human lymphoma cell survival. Nature; 2009 Mar 5;458(7234):92-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Casein kinase 1alpha governs antigen-receptor-induced NF-kappaB activation and human lymphoma cell survival.
  • The transcription factor NF-kappaB is required for lymphocyte activation and proliferation as well as the survival of certain lymphoma types.
  • We conducted parallel screens involving a mass spectrometry analysis of CARMA1 binding partners and an RNA interference screen for growth inhibition of the CBM-dependent 'activated B-cell-like' (ABC) subtype of diffuse large B-cell lymphoma (DLBCL).
  • CK1alpha dynamically associates with the CBM complex on T-cell-receptor (TCR) engagement to participate in cytokine production and lymphocyte proliferation.
  • ABC DLBCL cells required CK1alpha for constitutive NF-kappaB activity, indicating that CK1alpha functions as a conditionally essential malignancy gene-a member of a new class of potential cancer therapeutic targets.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Nature. 2008 Jul 10;454(7201):226-31 [18568025.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Cell. 2002 Mar 22;108(6):837-47 [11955436.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Nat Immunol. 2002 Sep;3(9):830-5 [12154356.001]
  • [Cites] Nat Immunol. 2002 Sep;3(9):836-43 [12154360.001]
  • [Cites] Immunity. 2003 Jun;18(6):763-75 [12818158.001]
  • [Cites] Curr Biol. 2003 Jul 15;13(14):1247-51 [12867037.001]
  • [Cites] Curr Biol. 2003 Jul 15;13(14):1252-8 [12867038.001]
  • [Cites] Nat Immunol. 2003 Nov;4(11):1057-64 [14586424.001]
  • [Cites] Immunity. 2003 Nov;19(5):749-58 [14614861.001]
  • [Cites] Science. 2003 Nov 28;302(5650):1581-4 [14576442.001]
  • [Cites] Nature. 1999 Sep 23;401(6751):345-50 [10517632.001]
  • [Cites] Science. 2005 Mar 4;307(5714):1465-8 [15746428.001]
  • [Cites] J Exp Med. 2005 Nov 21;202(10):1423-31 [16301747.001]
  • [Cites] Nature. 2005 Dec 8;438(7069):867-72 [16341016.001]
  • [Cites] Immunity. 2005 Dec;23(6):561-74 [16356855.001]
  • [Cites] Immunity. 2005 Dec;23(6):575-85 [16356856.001]
  • [Cites] Genes Dev. 2006 Feb 15;20(4):399-410 [16481469.001]
  • [Cites] Nature. 2006 May 4;441(7089):106-10 [16572121.001]
  • [Cites] Mol Cell. 2006 Jul 7;23(1):13-23 [16818229.001]
  • [Cites] Curr Biol. 2006 Aug 22;16(16):1666-71 [16920630.001]
  • [Cites] Sci STKE. 2006 Oct 17;2006(357):re13 [17047224.001]
  • [Cites] Immunity. 2006 Nov;25(5):701-15 [17098202.001]
  • [Cites] EMBO J. 2007 Apr 4;26(7):1794-805 [17363905.001]
  • [Cites] Cell. 2007 Sep 21;130(6):986-8 [17889643.001]
  • [Cites] EMBO J. 2007 Nov 14;26(22):4634-45 [17948050.001]
  • [Cites] Cell. 2007 Nov 30;131(5):927-39 [18045535.001]
  • [Cites] Science. 2008 Mar 21;319(5870):1676-9 [18323416.001]
  • [Cites] Cell. 2001 Jan 12;104(1):33-42 [11163238.001]
  • (PMID = 19118383.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / / NIH0011349228; United States / PHS HHS / / NIH0011349228; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / BCL10 protein, human; 0 / CARD Signaling Adaptor Proteins; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Receptors, Antigen; EC 2.7.11.1 / Casein Kinases; EC 2.7.11.10 / I-kappa B Kinase; EC 3.4.22.- / Caspases; EC 3.4.22.- / MALT1 protein, human; EC 4.6.1.2 / CARD11 protein, human; EC 4.6.1.2 / Guanylate Cyclase
  • [Other-IDs] NLM/ NIHMS88410; NLM/ PMC2688735
  •  go-up   go-down


64. Jabłońska J, Jesionek-Kupnicka D: Usefulness of immunohistochemistry in identification of prognostically important subgroups (GCB and ABC) in a heterogeneous group of diffuse large B-cell lymphomas--a review article. Pol J Pathol; 2008;59(3):121-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Usefulness of immunohistochemistry in identification of prognostically important subgroups (GCB and ABC) in a heterogeneous group of diffuse large B-cell lymphomas--a review article.
  • Although diffuse large B cell lymphomas (DLBCL) are considered in the WHO classification a specific histopathological type, their diversity in the clinical features, morphology and molecular aberrations strongly suggest that these tumors represent a heterogeneous group of neoplasms rather than a single clinicopathological entity.
  • Although it has been proven that gene expression profiling using cDNA microarrays could identify prognostically important subgroup of DLBCL: germinal center B-cell (GCB)-like DLBCL and activated B-cell (ABC)-like DLBCL, this method is impractical as a clinical tool.
  • Employing various immunohistochemical antibodies, such as CD10, CD138, anti-Bcl-2, anti-Bcl-6, MUM1 and anti-p53, several groups have aimed at subclassifying DLBCL into the GCB and ABC subgroups with comparable differences in clinical behavior.
  • This review summarizes these data and indicates their impact on DLBCL classification.
  • [MeSH-major] Biomarkers, Tumor / analysis. Immunohistochemistry. Lymphoma, Large B-Cell, Diffuse / classification. Lymphoma, Large B-Cell, Diffuse / diagnosis

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19097355.001).
  • [ISSN] 1233-9687
  • [Journal-full-title] Polish journal of pathology : official journal of the Polish Society of Pathologists
  • [ISO-abbreviation] Pol J Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 41
  •  go-up   go-down


65. Kluiver J, Poppema S, de Jong D, Blokzijl T, Harms G, Jacobs S, Kroesen BJ, van den Berg A: BIC and miR-155 are highly expressed in Hodgkin, primary mediastinal and diffuse large B cell lymphomas. J Pathol; 2005 Oct;207(2):243-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BIC and miR-155 are highly expressed in Hodgkin, primary mediastinal and diffuse large B cell lymphomas.
  • In a previous study we demonstrated high expression of the non-coding BIC gene in the vast majority of Hodgkin's lymphomas (HLs).
  • We therefore analysed HL cell lines and tissue samples to determine whether miR-155 is also expressed in HL.
  • However, in diffuse large B cell lymphoma (DLBCL) and primary mediastinal B cell lymphoma (PMBL), significant percentages of positive tumour cells were observed in 12/18 and 8/8 cases.
  • A higher proportion of tumour cells were positive for BIC in DLBCL with activated B cell-like phenotype than in DLBCL with germinal centre B cell-like phenotype.
  • Differential BIC expression was confirmed by qRT-PCR analysis.
  • Northern blot analysis showed expression of miR-155 in all DLBCL and PMBL derived cell lines and tissue samples analysed.
  • In summary, we demonstrate expression of primary microRNA BIC and its derivative miR-155 in HL, PMBL and DLBCL.
  • [MeSH-major] Lymphoma / genetics. Mediastinal Neoplasms / genetics. MicroRNAs / genetics. Receptors, Antigen, B-Cell / genetics
  • [MeSH-minor] Cell Line, Tumor. Hodgkin Disease / genetics. Humans. Immunohistochemistry / methods. In Situ Hybridization / methods. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • MedlinePlus Health Information. consumer health - Lymphoma.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 16041695.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Neoplasm; 0 / Receptors, Antigen, B-Cell
  •  go-up   go-down


66. Koens L, Vermeer MH, Willemze R, Jansen PM: IgM expression on paraffin sections distinguishes primary cutaneous large B-cell lymphoma, leg type from primary cutaneous follicle center lymphoma. Am J Surg Pathol; 2010 Jul;34(7):1043-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IgM expression on paraffin sections distinguishes primary cutaneous large B-cell lymphoma, leg type from primary cutaneous follicle center lymphoma.
  • In the World Health Organization (WHO) 2008 classification 2 main types of primary cutaneous large B-cell lymphomas (PCLBCLs) are distinguished: primary cutaneous follicle center lymphoma (PCFCL) and primary cutaneous large B-cell lymphoma, leg type (PCBCL-LT).
  • Expression profiling studies have shown higher RNA expression of the IgM heavy chain in PCBCL-LT compared with PCFCL.
  • To find out whether this difference could also be demonstrated at the protein level, we performed immunohistochemical staining for B-cell receptor heavy and light chains on skin biopsies from 53 patients with PCFCL and 40 patients with PCBCL-LT.
  • Analogous to other nodal and extranodal large B-cell lymphomas, expression of IgM in PCLBCL seems to be related to an activated B cell-like phenotype.
  • Finally, the expression of IgM (and IgD) in this type of lymphoma might imply defective class switch recombination.
  • [MeSH-major] Immunoglobulin M / metabolism. Lymphoma, Follicular / diagnosis. Lymphoma, Large B-Cell, Diffuse / diagnosis. Skin Neoplasms / diagnosis


67. van Galen JC, Muris JJ, Giroth CP, Vos W, Ossenkoppele GJ, Meijer CJ, Oudejans JJ: Expression of TNF-receptor associated factor 2 correlates with poor progression-free survival time in ABC-like primary nodal diffuse large B-cell lymphomas. Histopathology; 2008 Apr;52(5):578-84
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of TNF-receptor associated factor 2 correlates with poor progression-free survival time in ABC-like primary nodal diffuse large B-cell lymphomas.
  • AIMS: Tumour necrosis factor (TNF)-receptor associated factor 2 (TRAF2) is an adaptor molecule involved in nuclear factor (NF)-kappaB activation, which is characteristic of in vitro activated B-cell (ABC)-like diffuse large B-cell lymphomas (DLBCL) and may result in expression of anti-apoptotic genes and poor response to chemotherapy.
  • The aim was to determine whether TRAF2 is preferentially expressed in ABC-like DLBCL, and whether expression correlates with clinical outcome.
  • METHODS AND RESULTS: TRAF2 was expressed in nine of 20 tested ABC-like DLBCLs and in only one of 13 tested germinal centre B-lymphocyte (GCB)-like DLBCLs.
  • High TRAF2 expression was correlated with high International Prognostic Index at time of presentation, high chance of relapse and short progression-free survival time in 44 tested DLBCLs.
  • Furthermore, when analysis was restricted to ABC-like DLBCL only, TRAF2 expression was significantly associated with poor progression-free survival time.
  • CONCLUSIONS: TRAF2 might be involved in activation of NF-kappaB in a subset of ABC-like DLBCL, and its expression is associated with a particularly poor outcome in primary nodal DLBCL patients.
  • Because of its possible effect on to chemotherapy resistance, resistance, TRAF2 might be an attractive candidate as a molecular target for TRAF2+ DLBCL.
  • [MeSH-major] B-Lymphocytes / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. TNF Receptor-Associated Factor 2 / metabolism

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18312353.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / TNF Receptor-Associated Factor 2; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
  •  go-up   go-down


68. Tam W, Gomez M, Chadburn A, Lee JW, Chan WC, Knowles DM: Mutational analysis of PRDM1 indicates a tumor-suppressor role in diffuse large B-cell lymphomas. Blood; 2006 May 15;107(10):4090-100
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutational analysis of PRDM1 indicates a tumor-suppressor role in diffuse large B-cell lymphomas.
  • The PR (PRDI-BF1-RIZ) domain zinc finger protein 1 (PRDM1) is a transcription repressor with a pivotal role in plasma-cell differentiation.
  • We identified clonal inactivating mutations in PRDM1 in the diffuse large B-cell lymphoma (DLBCL) cell line OCI-Ly3 and in 8 of 35 de novo clinical DLBCL samples.
  • This study identifies PRDM1 inactivation as a recurrent genetic defect in DLBCL cells and establishes PRDM1 as a potential tumor suppressor gene in DLBCL.
  • Moreover, it implies inhibition of terminal differentiation as a pathogenetic pathway in DLBCL, particularly for the activated B-cell-like DLBCL.
  • [MeSH-major] Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Non-Hodgkin / genetics. Repressor Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Amino Acid Sequence. Base Sequence. Cell Line, Tumor. Cell Nucleus / genetics. DNA Primers. Exons. Genes, Tumor Suppressor. Humans. Introns. Molecular Sequence Data. Polymerase Chain Reaction

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16424392.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Repressor Proteins; 0 / Transcription Factors; 138415-26-6 / PRDM1 protein, human
  •  go-up   go-down


69. Oh YH, Park CK: Prognostic evaluation of nodal diffuse large B cell lymphoma by immunohistochemical profiles with emphasis on CD138 expression as a poor prognostic factor. J Korean Med Sci; 2006 Jun;21(3):397-405
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic evaluation of nodal diffuse large B cell lymphoma by immunohistochemical profiles with emphasis on CD138 expression as a poor prognostic factor.
  • Recently diffuse large B cell lymphoma (DLBCLs) was reported to be subdivided into germinal center B-cell-like (GCB) and activated B-cell-like (ABC) subgroups by using cDNA microarray and immunohistochemical markers.
  • By multivariate analysis, CD138 expression alone was considered as an independent risk factor (p=0.031).
  • In summary, our results add to the registration of prognostic implications for previously reported DLBCL subgroups.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, B-Cell / diagnosis. Lymphoma, B-Cell / metabolism. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / metabolism. Syndecan-1 / biosynthesis

  • Genetic Alliance. consumer health - Large B cell diffuse lymphoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pathol Int. 1999 Dec;49(12):1043-52 [10632924.001]
  • [Cites] J Clin Oncol. 2005 Apr 20;23(12):2797-804 [15728226.001]
  • [Cites] Blood. 2000 Mar 15;95(6):2084-92 [10706878.001]
  • [Cites] Leukemia. 2000 Mar;14(3):449-56 [10720141.001]
  • [Cites] Am J Surg Pathol. 2000 Jun;24(6):846-52 [10843287.001]
  • [Cites] Am J Surg Pathol. 2000 Dec;24(12):1641-9 [11117785.001]
  • [Cites] Am J Clin Pathol. 2001 Apr;115(4):582-8 [11293907.001]
  • [Cites] Histopathology. 2001 Aug;39(2):156-62 [11493332.001]
  • [Cites] Curr Opin Oncol. 2001 Sep;13(5):325-34 [11555708.001]
  • [Cites] Leuk Lymphoma. 2001 Sep-Oct;42(5):1099-106 [11697627.001]
  • [Cites] Blood. 2002 Jan 15;99(2):409-26 [11781220.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1136-43 [11830458.001]
  • [Cites] Mod Pathol. 2002 Apr;15(4):413-9 [11950915.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Arch Pathol Lab Med. 2002 Aug;126(8):956-60 [12171495.001]
  • [Cites] Histopathology. 2002 Dec;41(6):482-509 [12460202.001]
  • [Cites] Mod Pathol. 2002 Dec;15(12):1366-73 [12481019.001]
  • [Cites] Blood. 2003 Jan 1;101(1):78-84 [12393466.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):722-8 [12576441.001]
  • [Cites] Histopathology. 2003 Sep;43(3):209-19 [12940773.001]
  • [Cites] Leukemia. 2003 Oct;17(10):1948-60 [14513044.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Br J Haematol. 2004 Jan;124(2):151-9 [14687024.001]
  • [Cites] Am J Surg Pathol. 2004 Apr;28(4):464-70 [15087665.001]
  • [Cites] Am J Surg Pathol. 2004 Jun;28(6):736-47 [15166665.001]
  • [Cites] Blood. 1995 Jul 1;86(1):45-53 [7795255.001]
  • [Cites] Blood. 1997 Jun 1;89(11):3909-18 [9166827.001]
  • [Cites] Blood. 1998 Oct 1;92(7):2220-8 [9746758.001]
  • [Cites] Blood. 1998 Nov 1;92(9):3152-62 [9787151.001]
  • [Cites] Virchows Arch. 2004 Dec;445(6):545-51 [15517363.001]
  • [Cites] Histopathology. 2005 Mar;46(3):328-33 [15720419.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • (PMID = 16778379.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Syndecan-1; 0 / Syndecans; EC 3.4.24.11 / Neprilysin
  • [Other-IDs] NLM/ PMC2729941
  •  go-up   go-down


70. Abd El All H: Smooth muscle actin and s100p on non germinal centre diffuse large B cell lymphoma are adverse prognostic factors: pilot study. Diagn Pathol; 2007;2:9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Smooth muscle actin and s100p on non germinal centre diffuse large B cell lymphoma are adverse prognostic factors: pilot study.
  • INTRODUCTION: The expression of smooth muscle actin (SMA) and s100p has been identified on an aggressive retro-orbital diffuse large B cell lymphoma (DLBCL) 1.
  • AIM: To assess the prognostic significance of immunohistochemical (IHC) expression of SMA and s100p on DLBCL.
  • MATERIALS AND METHODS: Twenty nine cases diagnosed as DLBCL were first classified into germinal centre (GC) B cell like and non GC origin either activated B cells (ABC) or type 3 based on their immunoreactivity for CD10, bcl-6 and Mum-1.
  • RESULTS: Eleven cases (37.93%) positive for CD10 and/or bcl-6 were classified as GC B cell like subtype, 7 cases positive only for Mum-1 as ABC subtype (24.14%), and 11 cases double positive or negative for bcl-6 and Mum-1 were considered as type 3 (37.93%).
  • Nuclear and cytoplasmic SMA and s100p were expressed in 58.62% and 51.72% of cases respectively and were strongly associated with the non GC like phenotype (p < 0.001 for SMA and p < 0.01 for s100p).
  • CONCLUSION: SMA and s100p are expressed on non GC DLBCL and appear to be adverse prognostic factors.
  • Future large studies evaluating their significance will be valuable to assess the different subgroups in clinical context.
  • Lastly, this expression may lead to misdiagnosis of non hematopoeitic neoplasm if lymphoid markers are not included in the IHC panel.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Blood. 2000 Mar 15;95(6):2084-92 [10706878.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Annu Rev Biochem. 2002;71:755-81 [12045110.001]
  • [Cites] Blood. 2002 Jan 15;99(2):409-26 [11781220.001]
  • [Cites] Histopathology. 2001 Nov;39(5):476-81 [11737305.001]
  • [Cites] Am J Surg Pathol. 2000 Jun;24(6):846-52 [10843287.001]
  • [Cites] Histopathology. 2002 Dec;41(6):482-509 [12460202.001]
  • [Cites] Arch Pathol Lab Med. 2003 Jan;127(1):19-22 [12521361.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Aug 27;321(3):623-30 [15358152.001]
  • [Cites] Histopathology. 2005 Mar;46(3):328-33 [15720419.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3183-90 [16046532.001]
  • [Cites] Traffic. 2005 Oct;6(10):847-57 [16138899.001]
  • [Cites] J Clin Oncol. 2006 Feb 20;24(6):961-8 [16418494.001]
  • [Cites] Biomarkers. 2006 May-Jun;11(3):262-9 [16760135.001]
  • [Cites] J Immunol. 1991 Aug 15;147(4):1139-46 [1907989.001]
  • [Cites] Blood. 1991 Oct 1;78(7):1803-13 [1912567.001]
  • [Cites] Proc Natl Acad Sci U S A. 1978 Sep;75(9):4484-8 [309133.001]
  • [Cites] Hum Pathol. 1987 Jul;18(7):756-9 [3596594.001]
  • [Cites] Am J Clin Pathol. 1985 Jan;83(1):69-72 [3881010.001]
  • [Cites] Immunol Lett. 1983;7(2):81-4 [6228523.001]
  • [Cites] Cancer Res. 1983 Oct;43(10):4966-73 [6349796.001]
  • [Cites] Blood. 1982 Mar;59(3):536-41 [6977383.001]
  • [Cites] Biochem J. 1982 Dec 1;207(3):535-9 [7165706.001]
  • [Cites] Cancer Lett. 1998 Apr 10;126(1):75-81 [9563651.001]
  • [Cites] EMBO J. 1997 Aug 1;16(15):4650-6 [9303309.001]
  • [Cites] Blood. 1997 Jun 15;89(12):4501-13 [9192774.001]
  • [Cites] Arch Pathol Lab Med. 1993 Oct;117(10):1053-5 [8215831.001]
  • [Cites] Blood. 1994 Mar 15;83(6):1460-6 [8123837.001]
  • (PMID = 17335572.001).
  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1828714
  •  go-up   go-down


71. Cai YD, Huang T, Feng KY, Hu L, Xie L: A unified 35-gene signature for both subtype classification and survival prediction in diffuse large B-cell lymphomas. PLoS One; 2010;5(9):e12726
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A unified 35-gene signature for both subtype classification and survival prediction in diffuse large B-cell lymphomas.
  • In this paper, expression levels of genes are used for both cancer subtype classification and survival prediction.
  • We considered 350 diffuse large B-cell lymphoma (DLBCL) subjects, taken from four groups of patients (activated B-cell-like subtype dead, activated B-cell-like subtype alive, germinal center B-cell-like subtype dead, and germinal center B-cell-like subtype alive).
  • As classification features, we used 11,271 gene expression levels of each subject.
  • These four groups were combined in different ways for subtype prediction and survival prediction, specifically, the activated versus the germinal center and the alive versus the dead.
  • [MeSH-major] Biomarkers, Tumor / genetics. Gene Expression Regulation, Neoplastic. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology

  • Genetic Alliance. consumer health - B-Cell Lymphomas.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] PLoS One. 2010;5(7):e11900 [20689580.001]
  • [Cites] Immunity. 2000 Aug;13(2):199-212 [10981963.001]
  • [Cites] Blood. 2001 Aug 15;98(4):945-51 [11493437.001]
  • [Cites] Jpn J Cancer Res. 2001 Dec;92(12):1300-4 [11749695.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Oncogene. 2002 Nov 21;21(53):8186-91 [12444555.001]
  • [Cites] Oncol Rep. 2003 Mar-Apr;10(2):333-8 [12579268.001]
  • [Cites] Int J Hematol. 2003 May;77(4):321-9 [12774918.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] Hum Mol Genet. 2003 Sep 15;12(18):2349-58 [12915480.001]
  • [Cites] J Biol Chem. 2003 Sep 12;278(37):35775-80 [12837748.001]
  • [Cites] J Exp Med. 2003 Sep 15;198(6):851-62 [12975453.001]
  • [Cites] J Biol Chem. 2003 Nov 14;278(46):45358-67 [12954615.001]
  • [Cites] N Engl J Med. 2004 Apr 29;350(18):1828-37 [15115829.001]
  • [Cites] Genes Chromosomes Cancer. 2004 Jul;40(3):218-28 [15139001.001]
  • [Cites] Nucleic Acids Res. 2004;32(18):5368-78 [15477387.001]
  • [Cites] Blood. 1997 Jun 1;89(11):3909-18 [9166827.001]
  • [Cites] Biochim Biophys Acta. 1998 Nov 8;1442(2-3):274-85 [9804974.001]
  • [Cites] Blood. 2005 Mar 1;105(5):1851-61 [15550490.001]
  • [Cites] Mol Cell Endocrinol. 2005 May 12;235(1-2):51-61 [15866427.001]
  • [Cites] Mod Pathol. 2005 Aug;18(8):1113-20 [15920553.001]
  • [Cites] IEEE Trans Pattern Anal Mach Intell. 2005 Aug;27(8):1226-38 [16119262.001]
  • [Cites] Prostate. 2005 Nov 1;65(3):276-86 [16015593.001]
  • [Cites] Breast Cancer Res Treat. 2005 Nov;94(1):11-6 [16172792.001]
  • [Cites] Mol Cell Biol. 2006 Mar;26(5):1770-85 [16478997.001]
  • [Cites] Immunol Rev. 2006 Apr;210:67-85 [16623765.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Sep 29;348(3):1034-7 [16899225.001]
  • [Cites] Bioinformatics. 2006 Dec 1;22(23):2926-33 [17000751.001]
  • [Cites] Biotechnol Lett. 2006 Dec;28(24):2057-63 [17028776.001]
  • [Cites] Ann Oncol. 2007 May;18(5):931-9 [17395602.001]
  • [Cites] Mamm Genome. 2007 May;18(5):300-9 [17557176.001]
  • [Cites] Cell Physiol Biochem. 2007;20(6):977-86 [17982280.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Sep 9;105(36):13520-5 [18765795.001]
  • [Cites] J Transl Med. 2008;6:44 [18691426.001]
  • [Cites] Am J Physiol Cell Physiol. 2008 Oct;295(4):C944-53 [18667602.001]
  • [Cites] N Engl J Med. 2008 Nov 27;359(22):2313-23 [19038878.001]
  • [Cites] Oncogene. 2009 Apr 9;28(14):1714-24 [19252524.001]
  • [Cites] J Surg Res. 2009 May 1;153(1):17-22 [18675992.001]
  • [Cites] PLoS One. 2009;4(12):e8126 [19956587.001]
  • [Cites] PLoS One. 2010;5(6):e10972 [20532046.001]
  • [Cites] J Biol Chem. 2000 Mar 31;275(13):9797-804 [10734134.001]
  • (PMID = 20856936.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC2938343
  •  go-up   go-down


72. Li S, Phong M, Lahn M, Brail L, Sutton S, Lin BK, Thornton D, Liao B: Retrospective analysis of protein kinase C-beta (PKC-beta) expression in lymphoid malignancies and its association with survival in diffuse large B-cell lymphomas. Biol Direct; 2007;2:8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Retrospective analysis of protein kinase C-beta (PKC-beta) expression in lymphoid malignancies and its association with survival in diffuse large B-cell lymphomas.
  • BACKGROUND: Both mechanistic features and recent correlative findings suggest a potential role for protein kinase C-beta (PKC-beta) in tumor pathogenesis, particularly in B-cell malignancies.
  • To evaluate the role of this gene in lymphoid malignancies, we analyzed global gene expression data to quantify PKC-beta expression across diagnostic groups and, when possible, determined correlations between PKC-beta expression and survival.
  • RESULTS: Our analysis showed that the level of PKC-beta expression was highest in chronic lymphocytic leukemia and follicular lymphoma.
  • Within diffuse large-B cell lymphoma (DLBCL), PKC-beta expression was significantly higher in activated B-cell- like subtype than germinal center B-cell- like subtype (P < 0.0001).
  • When analyzed within clinically defined risk groups established by the International Prognostic Index (IPI), PKC-beta expression was lowest in patients with low IPI scores (0-1).
  • Within intermediate- and high-risk IPI groups, elevated PKC-beta expression was associated with worse survival, suggesting that PKC-beta may expand the prognostic value of the IPI.
  • Results of global gene expression analyses of DLBCL samples corroborate previous observations that anti-apoptosis, cell proliferation, and B-cell proliferation signaling pathways are functionally related to PKC-beta.
  • CONCLUSION: We present a first detailed pharmacogenomics report comparing PKC-beta mRNA expression across different lymphoid malignancies and evaluating it as an outcome predictor.
  • Our findings suggest that DLBCL patients with elevated PKC-beta have a worse prognosis, indicating that further evaluation of PKC-beta as a chemotherapeutic target for lymphoid malignancies is warranted.

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address: