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1. Lam LT, Davis RE, Ngo VN, Lenz G, Wright G, Xu W, Zhao H, Yu X, Dang L, Staudt LM: Compensatory IKKalpha activation of classical NF-kappaB signaling during IKKbeta inhibition identified by an RNA interference sensitization screen. Proc Natl Acad Sci U S A; 2008 Dec 30;105(52):20798-803
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A subtype of diffuse large B-cell lymphoma (DLBCL), termed activated B-cell-like (ABC) DLBCL, depends on constitutive nuclear factor-kappaB (NF-kappaB) signaling for survival.
  • Small molecule inhibitors of IkappaB kinase beta (IKKbeta), a key regulator of the NF-kappaB pathway, kill ABC DLBCL cells and hold promise for the treatment of this lymphoma type.
  • We conducted an RNA interference genetic screen to investigate potential mechanisms of resistance of ABC DLBCL cells to IKKbeta inhibitors.
  • We screened a library of small hairpin RNAs (shRNAs) targeting 500 protein kinases for shRNAs that would increase the killing of an ABC DLBCL cell line in the presence of a small molecule IKKbeta inhibitor.
  • Two independent shRNAs targeting IKKalpha synergized with the IKKbeta inhibitor to kill three different ABC DLBCL cell lines but were not toxic by themselves.
  • Surprisingly, IKKalpha shRNAs blocked the classical rather than the alternative NF-kappaB pathway in ABC DLBCL cells, as judged by inhibition of IkappaBalpha phosphorylation.
  • These results suggest that therapy for ABC DLBCL may be improved by targeting both IKKalpha and IKKbeta, possibly through CARD11 inhibition.

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  • (PMID = 19104039.001).
  • [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 / 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 / CARD Signaling Adaptor Proteins; 0 / NF-kappa B; 0 / Protein Kinase Inhibitors; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.10 / I-kappa B Kinase; EC 4.6.1.2 / CARD11 protein, human; EC 4.6.1.2 / Guanylate Cyclase
  • [Other-IDs] NLM/ PMC2634958
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2. 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
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  • [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.

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  • (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
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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
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  • [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.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (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
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4. 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
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  • [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.

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  • (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
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5. 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
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  • [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


6. 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
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  • [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.

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  • (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
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7. Vajpayee N, Hussain J, Tolocica I, Hutchison RE, Gajra A: Expression of signal transducer and activator of transcription 3 (STAT3) in primary central nervous system diffuse large B-cell lymphoma: a retrospective analysis of 17 cases. J Neurooncol; 2010 Nov;100(2):249-53
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  • [Title] Expression of signal transducer and activator of transcription 3 (STAT3) in primary central nervous system diffuse large B-cell lymphoma: a retrospective analysis of 17 cases.
  • Most primary central nervous system lymphomas (PCNSL) occurring in immunocompetent patients are diffuse large B-cell lymphomas (DLBCL), characterized by poor prognosis.
  • An activated B-cell (ABC) origin of PCNSL has been postulated based on bcl-6 and MUM-1 expression by majority of these tumors.
  • ABC DLBCL has been functionally subdivided using gene expression profiling and immunohistochemical analysis into STAT3-high and STAT-3 low subsets.
  • A potentially crucial difference between STAT3-high and STAT3-low ABC DLBCL is in the expression of bcl-2 family members.
  • STAT3-high cases are generally bcl-2 low and STAT3-low cases show higher expression of bcl-2.
  • Further mechanisms such as activation of nuclear factor-kappa B (NF-κB) activation seem to be responsible for upregulation of bcl-2 in ABC subtype of DLBCL with an adverse outcome.
  • As deregulation of STAT-3 pathway is known to play a critical role in ABC DLBCL and majority of the PCNSL are of the ABC subtype we studied the immunohistochemical expression of STAT-3 proteins in PCNSL along with other traditional markers (CD10, bcl-6, MUM-1 and bcl-2) in 17 cases of PCNSL occurring in immunocompetent patients.
  • Despite lack of STAT3 expression in all our cases, majority (70%) of the patients with bcl-2 positive PCNSL had an adverse outcome similar to that reported in systemic lymphomas of ABC subtype.
  • Based on our observations we propose that PCNSL represents a distinct subset of ABC diffuse large B-cell lymphomas with low STAT3 expression and perhaps mechanisms other than interaction of STAT-3 and NF-κB pathways may play a role in upregulation of bcl-2 in PCNSL.
  • To the best of our knowledge expression of STAT-3 protein in PCNSL which represents a distinct anatomical subset of ABC DLBCL with a dismal prognosis has not been studied before.
  • [MeSH-major] Central Nervous System Neoplasms / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. STAT3 Transcription Factor / biosynthesis

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  • (PMID = 20446017.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human
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8. 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
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  • [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.

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  • (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
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9. Leich E, Hartmann EM, Burek C, Ott G, Rosenwald A: Diagnostic and prognostic significance of gene expression profiling in lymphomas. APMIS; 2007 Oct;115(10):1135-46
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  • [Title] Diagnostic and prognostic significance of gene expression profiling in lymphomas.
  • Gene expression profiling is a powerful tool to uncover complex molecular networks in cancer and, specifically, in malignant lymphomas.
  • Within diffuse large B-cell lymphomas (DLBCL), two major molecular subtypes, the activated B-cell-like (ABC) and the germinal center B-cell-like (GCB) DLBCL, can be defined.
  • Compared to GCB DLBCL, ABC DLBCL shows a vast difference in gene expression and constitutively expresses NFkappaB and its target genes.
  • In retrospective analyses, the molecular phenotype of ABC DLBCL is associated with inferior survival.
  • Gene expression profiling furthermore allows the molecular separation of Burkitt lymphoma (BL) from DLBCL and reveals a Burkitt-specific signature which is also expressed by a subset of tumors that are currently classified as DLBCL.
  • Whether patients with a DLBCL displaying a Burkitt-specific gene expression signature may benefit from alternative therapeutic approaches will have to be determined in future prospective clinical trials.
  • In follicular lymphoma (FL), two outcome-related signatures, termed Immune response 1 (IR1) and Immune response 2 (IR2), have been identified by gene expression profiling, indicating a significant role of the microenvironment in tumor development and progression.
  • In mantle cell lymphoma (MCL), a gene expression-based proliferation signature of 20 different genes was identified that is able to predict survival of MCL patients in a linear fashion.
  • Future efforts will have to be directed towards the translation of relevant molecular diagnostic and prognostic markers derived from the wealth of gene expression data into clinical tests and towards the development of novel, targeted therapies.
  • [MeSH-major] Gene Expression Profiling. Lymphoma / diagnosis. Lymphoma / genetics
  • [MeSH-minor] Burkitt Lymphoma / diagnosis. Burkitt Lymphoma / genetics. Gene Expression Regulation, Neoplastic. Humans. Lymphoma, B-Cell / diagnosis. Lymphoma, B-Cell / genetics. Lymphoma, Follicular / diagnosis. Lymphoma, Follicular / genetics. Lymphoma, Mantle-Cell / diagnosis. Lymphoma, Mantle-Cell / genetics. Prognosis

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  • (PMID = 18042147.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Denmark
  • [Number-of-references] 70
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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
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  • [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

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  • (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
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11. 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
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  • [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.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • [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
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12. 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
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of 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

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  • (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
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13. 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
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  • [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.

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  • (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
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14. 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
The Lens. Cited by Patents in .

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

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  • (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
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15. Wang XM, Greiner TC, Bibikova M, Pike BL, Siegmund KD, Sinha UK, Müschen M, Jaeger EB, Weisenburger DD, Chan WC, Shibata D, Fan JB, Hacia JG: Identification and functional relevance of de novo DNA methylation in cancerous B-cell populations. J Cell Biochem; 2010 Mar 1;109(4):818-27
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification and functional relevance of de novo DNA methylation in cancerous B-cell populations.
  • To begin to address this issue in B-cells, we used BeadArray assays to survey the methylation status of over 1,500 cancer-related CpG loci in two molecular subtypes of diffuse large B-cell lymphoma (ABC-DLBCL and GCB-DLBCL) and cognate normal B-cell populations.
  • We identified 81 loci that showed frequent de novo DNA methylation in GCB-DLBCL and 67 loci that showed frequent de novo DNA methylation in ABC-DLBCL.
  • All candidate loci in GCB-DLBCL are proximal to genes that are poorly expressed or silent in purified normal germinal center (GC) B-cells.

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  • [Copyright] (c) 2010 Wiley-Liss, Inc.
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  • (PMID = 20069569.001).
  • [ISSN] 1097-4644
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] ENG
  • [Grant] United States / NHGRI NIH HHS / HG / P50-HG002790; United States / NCI NIH HHS / CA / U01 CA084967; United States / NCRR NIH HHS / RR / RR10600-01; United States / NIGMS NIH HHS / GM / GM072477-03; United States / NIGMS NIH HHS / GM / R01 GM072477-04; United States / NCI NIH HHS / CA / U01 CA114778; None / None / / R01 CA137060-01A1; United States / NCI NIH HHS / CA / CA84967; United States / NCI NIH HHS / CA / CA36727; United States / NCI NIH HHS / CA / C06 CA062528; United States / NCI NIH HHS / CA / R21 CA152497; United States / NIGMS NIH HHS / GM / R01 GM072477-05; United States / NIGMS NIH HHS / GM / R01 GM072477-02; United States / NIGMS NIH HHS / GM / GM072477-02; United States / NIGMS NIH HHS / GM / R01 GM072447; None / None / / R01 CA139032-01; United States / NIGMS NIH HHS / GM / GM072477-01A1; United States / NIGMS NIH HHS / GM / R01 GM072477-01A1; United States / NCRR NIH HHS / RR / RR14514-01; United States / NCI NIH HHS / CA / R01 CA139032-01; United States / NCI NIH HHS / CA / P30 CA036727; United States / NCI NIH HHS / CA / R21 CA152497-01; United States / NCI NIH HHS / CA / R01 CA137060-01A1; United States / NIGMS NIH HHS / GM / GM072477-05; None / None / / R21 CA152497-01; United States / NCRR NIH HHS / RR / C06 RR014514; United States / NCI NIH HHS / CA / CA114778; United States / NIGMS NIH HHS / GM / GM072447; United States / NCI NIH HHS / CA / R01 CA139032; United States / NIGMS NIH HHS / GM / R01 GM072477-03; United States / NIGMS NIH HHS / GM / GM072477-04; United States / NCI NIH HHS / CA / CA62528-01; United States / NIGMS NIH HHS / GM / R01 GM072477; United States / NHGRI NIH HHS / HG / P50 HG002790; United States / NCI NIH HHS / CA / R01 CA137060
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Polycomb-Group Proteins; 0 / Repressor Proteins
  • [Other-IDs] NLM/ NIHMS305118; NLM/ PMC3122883
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16. 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
The Lens. Cited by Patents in .

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

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  • (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
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17. 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
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  • [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.

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  • (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
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18. 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
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  • [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


19. 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
The Lens. Cited by Patents in .

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

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  • (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
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20. 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
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  • [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

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  • (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
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21. Staudt LM, Dave S: The biology of human lymphoid malignancies revealed by gene expression profiling. Adv Immunol; 2005;87:163-208
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The biology of human lymphoid malignancies revealed by gene expression profiling.
  • Gene expression profiling provides a quantitative molecular framework for the study of human lymphomas.
  • Diffuse large B-cell lymphoma (DLBCL), for example, consists of three gene expression subgroups, termed germinal center B-cell-like (GCB) DLBCL, activated B-cell-like (ABC) DLBCL, and primary mediastinal B-cell lymphoma (PMBL).
  • These DLBCL subgroups arise from different stages of normal B-cell differentiation, utilize distinct oncogenic mechanisms, and differ in their ability to be cured by chemotherapy.
  • ABC DLBCL and PMBL depend upon constitutive activation of the NF-kappaB pathway for their survival but GCB DLBCL does not, demonstrating that this pathway is a potential therapeutic target for certain DLBCL subgroups.
  • In DLBCL, mantle cell lymphoma, and follicular lymphoma, gene expression profiling has also been used to create gene expression-based models of survival, which have identified the biological characteristics of the tumors that influence their clinical behavior.
  • In mantle cell lymphoma, the length of survival following diagnosis is primarily influenced by the tumor proliferation rate, which can be quantitatively measured by a proliferation gene expression "signature."
  • Based on this accurate measure, the proliferation rate can now be viewed as an integration of several oncogenic lesions that each increase progression from the G1 to the S phase of the cell cycle.
  • In DLBCL and follicular lymphoma, gene expression profiling has revealed that the molecular characteristics of non-malignant tumor-infiltrating immune cells have a major influence on the length of survival.

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  • (PMID = 16102574.001).
  • [ISSN] 0065-2776
  • [Journal-full-title] Advances in immunology
  • [ISO-abbreviation] Adv. Immunol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / SC / Z01 SC004024-18
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 165
  • [Other-IDs] NLM/ NIHMS5150; NLM/ PMC1351148
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22. 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
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  • [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

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  • [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
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23. 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
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  • [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.

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  • [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
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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
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  • [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.

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  • (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
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25. Chin M, Herscovitch M, Zhang N, Waxman DJ, Gilmore TD: Overexpression of an activated REL mutant enhances the transformed state of the human B-lymphoma BJAB cell line and alters its gene expression profile. Oncogene; 2009 May 21;28(20):2100-11
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of an activated REL mutant enhances the transformed state of the human B-lymphoma BJAB cell line and alters its gene expression profile.
  • Overexpression of REL is acutely transforming in chicken lymphoid cells, but has not been shown to transform any mammalian lymphoid cell type.
  • In this report, we show that overexpression of a highly transforming mutant of REL (RELDeltaTAD1) increases the oncogenic properties of the human B-cell lymphoma BJAB cell line, as shown by increased colony formation in soft agar, tumor formation in SCID (severe combined immunodeficient) mice, and adhesion.
  • Overexpression of RELDeltaTAD1 in BJAB cells has transformed the gene expression profile of BJAB cells from that of a germinal center B-cell subtype of diffuse large B-cell lymphoma (DLBCL) (GCB-DLBCL) to that of an activated B-cell subtype (ABC-DLBCL), as evidenced by increased expression of many ABC-defining mRNAs.
  • Upregulated genes in BJAB-RELDeltaTAD1 cells include several NF-kappaB targets that encode proteins previously implicated in B-cell development or oncogenesis, including BCL2, IRF4, CD40 and VCAM1.
  • The cell system we describe here may be valuable for further characterizing the molecular details of REL-induced lymphoma in humans.

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  • (PMID = 19377508.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES007381; United States / NCI NIH HHS / CA / R01 CA047763; United States / NCI NIH HHS / CA / CA047763; United States / NIEHS NIH HHS / ES / ES007381-140019; United States / NCI NIH HHS / CA / R01 CA047763-20; United States / NIEHS NIH HHS / ES / P42 ES007381-150019; United States / NCI NIH HHS / CA / R01 CA047763-19; United States / NIEHS NIH HHS / ES / P42 ES007381-140019; United States / NIEHS NIH HHS / ES / ES007381-150019; United States / NCI NIH HHS / CA / CA047763-19; United States / NIEHS NIH HHS / ES / 5 P42 ES07381
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-rel; 0 / RNA, Messenger
  • [Other-IDs] NLM/ NIHMS101814; NLM/ PMC2796798
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26. Morin RD, Johnson NA, Severson TM, Mungall AJ, An J, Goya R, Paul JE, Boyle M, Woolcock BW, Kuchenbauer F, Yap D, Humphries RK, Griffith OL, Shah S, Zhu H, Kimbara M, Shashkin P, Charlot JF, Tcherpakov M, Corbett R, Tam A, Varhol R, Smailus D, Moksa M, Zhao Y, Delaney A, Qian H, Birol I, Schein J, Moore R, Holt R, Horsman DE, Connors JM, Jones S, Aparicio S, Hirst M, Gascoyne RD, Marra MA: Somatic mutations altering EZH2 (Tyr641) in follicular and diffuse large B-cell lymphomas of germinal-center origin. Nat Genet; 2010 Feb;42(2):181-5
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  • [Title] Somatic mutations altering EZH2 (Tyr641) in follicular and diffuse large B-cell lymphomas of germinal-center origin.
  • Follicular lymphoma (FL) and the GCB subtype of diffuse large B-cell lymphoma (DLBCL) derive from germinal center B cells.
  • Targeted resequencing studies have revealed mutations in various genes encoding proteins in the NF-kappaB pathway that contribute to the activated B-cell (ABC) DLBCL subtype, but thus far few GCB-specific mutations have been identified.
  • These mutations, which result in the replacement of a single tyrosine in the SET domain of the EZH2 protein (Tyr641), occur in 21.7% of GCB DLBCLs and 7.2% of FLs and are absent from ABC DLBCLs.


27. 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
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  • [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

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  • [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
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28. Lenz G, Davis RE, Ngo VN, Lam L, George TC, Wright GW, Dave SS, Zhao H, Xu W, Rosenwald A, Ott G, Muller-Hermelink HK, Gascoyne RD, Connors JM, Rimsza LM, Campo E, Jaffe ES, Delabie J, Smeland EB, Fisher RI, Chan WC, Staudt LM: Oncogenic CARD11 mutations in human diffuse large B cell lymphoma. Science; 2008 Mar 21;319(5870):1676-9
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  • [Title] Oncogenic CARD11 mutations in human diffuse large B cell lymphoma.
  • Diffuse large B cell lymphoma (DLBCL) is the most common form of non-Hodgkin's lymphoma.
  • In the least curable (ABC) subtype of DLBCL, survival of the malignant cells is dependent on constitutive activation of the nuclear factor-kappaB (NF-kappaB) signaling pathway.
  • To determine whether CARD11 contributes to tumorigenesis, we sequenced the CARD11 gene in human DLBCL tumors.
  • We detected missense mutations in 7 of 73 ABC DLBCL biopsies (9.6%), all within exons encoding the coiled-coil domain.
  • Experimental introduction of CARD11 coiled-coil domain mutants into lymphoma cell lines resulted in constitutive NF-kappaB activation and enhanced NF-kappaB activity upon antigen receptor stimulation.
  • These results demonstrate that CARD11 is a bona fide oncogenein DLBCL, providing a genetic rationale for the development of pharmacological inhibitors of the CARD11 pathway for DLBCL therapy.
  • [MeSH-major] Apoptosis Regulatory Proteins / genetics. CARD Signaling Adaptor Proteins / genetics. Guanylate Cyclase / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Mutation, Missense. Oncogenes
  • [MeSH-minor] Amino Acid Sequence. Cell Line, Tumor. Cytoplasm / metabolism. Humans. I-kappa B Kinase / metabolism. Jurkat Cells. Molecular Sequence Data. NF-kappa B. Protein Structure, Tertiary. Receptors, Antigen, B-Cell / physiology. Sequence Analysis, DNA


29. 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
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  • [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.

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  • (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
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30. Hallack Neto AE, Siqueira SA, Dulley FL, Ruiz MA, Chamone DA, Pereira J: p63 protein expression in high risk diffuse large B-cell lymphoma. J Clin Pathol; 2009 Jan;62(1):77-9
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  • [Title] p63 protein expression in high risk diffuse large B-cell lymphoma.
  • The isoforms TAp63 and TAp73 transactivate p53 target genes and induce apoptosis, whereas the isoforms DeltaNp63 and DeltaNp73 lack transactivation and might have dominant-negative effects in p53 family members. p63 is expressed in germinal centre lymphocytes and can be related to the development of the lymphoma, but the prognostic significance of its expression in the survival of patients with diffuse large B-cell lymphoma (DLBCL) remains unclear.
  • AIMS: To determine whether quantitative immunohistochemical (IHC) analysis of p63 protein expression correlates with CD10 antigen, Bcl-6 antigen and IRF4 antigen expression and to determine whether p63 is a surrogate predictor of overall survival in high-intermediate and high risk DLBCL populations.
  • METHODS: CD10, Bcl-6 and IRF4 expression were retrospectively evaluated by IHC in 73 samples of high-intermediate and high risk DLBCL and were used to divide the lymphomas into subgroups of germinal centre B-cell-like (GCB) and activate B-cell-like (ABC) DLBCL.
  • Similarly, p63 expression was evaluated by IHC and the results were compared with subgroups of DLBCL origin and with the survival rates for these patients.
  • RESULTS: p63 was expressed in more than 50% of malignant cells in 11 patients and did not show correlation with subgroups of GCB-like DLBCL or ABC-like DLBCL, but p63(+) patients had better disease-free survival (DFS) than those who were negative (p = 0.01).
  • CONCLUSIONS: p63(+) high-intermediate and high risk DLBCL patients have a better DFS than negative cases.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Trans-Activators / metabolism. Tumor Suppressor Proteins / metabolism

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  • (PMID = 19103865.001).
  • [ISSN] 1472-4146
  • [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
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Interferon Regulatory Factors; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / interferon regulatory factor-4; EC 3.4.24.11 / Neprilysin
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31. 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
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  • [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.

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  • (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
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32. 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
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  • [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

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  • (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
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33. 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
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  • [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

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  • (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
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34. 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
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  • [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

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  • (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
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35. van Galen JC, Muris JJ, Oudejans JJ, Vos W, Giroth CP, Ossenkoppele GJ, Otte AP, Raaphorst FM, Meijer CJ: Expression of the polycomb-group gene BMI1 is related to an unfavourable prognosis in primary nodal DLBCL. J Clin Pathol; 2007 Feb;60(2):167-72
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  • [Title] Expression of the polycomb-group gene BMI1 is related to an unfavourable prognosis in primary nodal DLBCL.
  • BACKGROUND: Clinical outcome in patients with diffuse large B cell lymphomas (DLBCL) is highly variable and poorly predictable.
  • Microarray studies showed that patients with DLBCL with a germinal centre B cell-like (GCB) phenotype have a better prognosis than those with an activated B cell-like (ABC) phenotype.
  • The BMI1 proto-oncogene was identified as one of the genes present in the signature of the ABC type of DLBCL, associated with a poor prognosis.
  • OBJECTIVES:. (1) To investigate, in primary nodal DLBCL, the expression of BMI1 and its association with clinical outcome and DLBCL signature;.
  • (2) to look for an association between BMI1 expression and the expression of its putative downstream targets p14ARF and p16INK4a.
  • RESULTS: BMI1 expression was found to be associated with poor clinical outcome, but not clearly with an ABC-like phenotype of DLBCL.
  • Expression of BMI1 was frequently, but not always, related to low levels of expression of p14ARF and p16INK4a.
  • CONCLUSION: Expression of BMI1 is associated with an unfavourable clinical outcome of primary nodal DLBCL.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Lymphoma, B-Cell / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Nuclear Proteins / metabolism. Proto-Oncogene Proteins / metabolism. Repressor Proteins / metabolism

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  • (PMID = 16837630.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BMI1 protein, human; 0 / Biomarkers, Tumor; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p14ARF; EC 6.3.2.19 / Polycomb Repressive Complex 1
  • [Other-IDs] NLM/ PMC1860630
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36. Dasmahapatra G, Lembersky D, Rahmani M, Kramer L, Friedberg J, Fisher RI, Dent P, Grant S: Bcl-2 antagonists interact synergistically with bortezomib in DLBCL cells in association with JNK activation and induction of ER stress. Cancer Biol Ther; 2009 May;8(9):808-19
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  • [Title] Bcl-2 antagonists interact synergistically with bortezomib in DLBCL cells in association with JNK activation and induction of ER stress.
  • Mechanisms underlying interactions between the proteasome inhibitor bortezomib and small molecule Bcl-2 antagonists were examined in GC- and ABC-type human DLBCL (diffuse lymphocytic B-cell lymphoma) cells.
  • Concomitant or sequential exposure to non- or minimally toxic concentrations of bortezomib or other proteasome inhibitors and either HA14-1 or gossypol resulted in a striking increase in Bax/Bak conformational change/translocation, cytochrome c release, caspase activation and synergistic induction of apoptosis in both GC- and ABC-type cells.
  • Collectively these findings indicate that small molecule Bcl-2 antagonists promote bortezomib-mediated mitochondrial injury and lethality in DLBCL cells in association with enhanced JNK activation and ER stress induction.
  • They also raise the possibility that such a strategy may be effective in different DLBCL sub-types (e.g., GC- or ABC), and in bortezomib-resistant disease.

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  • (PMID = 19270531.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA130805-01A1; United States / NCI NIH HHS / CA / CA100866-06; United States / NCI NIH HHS / CA / CA093738-07; United States / NCI NIH HHS / CA / P50 CA130805-01A1; United States / NCI NIH HHS / CA / R01 CA100866; United States / NCI NIH HHS / CA / R01 CA063753; United States / NCI NIH HHS / CA / R01 CA100866-06; United States / NCI NIH HHS / CA / R01 CA093738; United States / NCI NIH HHS / CA / R01 CA093738-07; United States / NCI NIH HHS / CA / CA 63753; United States / NCI NIH HHS / CA / CA 100866; United States / NCI NIH HHS / CA / P50 CA130805; United States / NCI NIH HHS / CA / 1P50 CA 130805; United States / NCI NIH HHS / CA / CA063753-14; United States / NCI NIH HHS / CA / R01 CA063753-14; United States / NIDDK NIH HHS / DK / R01 DK052825; United States / NCI NIH HHS / CA / CA 93738; United States / NCI NIH HHS / CA / R01 CA150214
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzopyrans; 0 / Boronic Acids; 0 / Enzyme Inhibitors; 0 / Nitriles; 0 / Protease Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / ethyl 2-amino-6-bromo-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate; 69G8BD63PP / Bortezomib; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ NIHMS209958; NLM/ PMC2902989
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37. 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
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  • [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

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  • (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
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38. 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
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  • [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

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  • (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
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39. Andreadis C, Gimotty PA, Wahl P, Hammond R, Houldsworth J, Schuster SJ, Rebbeck TR: Members of the glutathione and ABC-transporter families are associated with clinical outcome in patients with diffuse large B-cell lymphoma. Blood; 2007 Apr 15;109(8):3409-16
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  • [Title] Members of the glutathione and ABC-transporter families are associated with clinical outcome in patients with diffuse large B-cell lymphoma.
  • Standard chemotherapy fails in 40% to 50% of patients with diffuse large B-cell lymphoma (DLBCL).
  • We examined the expression of genes in the glutathione (GSH) and ATP-dependent transporter (ABC) families in 2 independent tissue-based expression microarray datasets obtained prior to therapy from patients with DLBCL.
  • This effect remained statistically significant after controlling for biologic signature, LLMPP cell-of-origin signature, and IPI score, and was confirmed in the validation dataset (n = 39) (HR: 1.7; 95% CI: 1.05-2.8; P = .033).
  • Recursive partitioning identified a group of patients with low-level expression of GPX1 and multidrug resistance 1 (MDR1; ABCB1) without early treatment failures and with superior dOS (P < .001).
  • Overall, our findings suggest an important association of oxidative-stress defense and drug elimination with treatment failure in DLBCL and identify GPX1 and ABCB1 as potentially powerful biomarkers of early failure and disease-specific survival.

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  • (PMID = 17179223.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K12 CA076931; United States / NCI NIH HHS / CA / 5K12 CA 076931
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / Biomarkers, Tumor; 0 / Membrane Transport Proteins; 0 / Organic Anion Transporters; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / glutathione transporter; EC 1.11.1.- / glutathione peroxidase GPX1; EC 1.11.1.9 / Glutathione Peroxidase
  • [Other-IDs] NLM/ PMC1852238
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40. 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
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  • [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

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  • (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
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41. 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
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  • [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

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  • [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
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42. 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
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  • [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

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  • (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
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43. 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
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  • [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

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  • (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
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44. 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
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  • [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.

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  • (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
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45. Gormley RP, Madan R, Dulau AE, Xu D, Tamas EF, Bhattacharyya PK, LeValley A, Xue X, Kumar P, Sparano J, Ramesh KH, Pulijaal V, Cannizzaro L, Walsh D, Ioachim HL, Ratech H: Germinal center and activated b-cell profiles separate Burkitt lymphoma and diffuse large B-cell lymphoma in AIDS and non-AIDS cases. Am J Clin Pathol; 2005 Nov;124(5):790-8
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  • [Title] Germinal center and activated b-cell profiles separate Burkitt lymphoma and diffuse large B-cell lymphoma in AIDS and non-AIDS cases.
  • Morphologic features of Burkitt lymphoma (BL) and diffuse large B-cell lymphoma (DLBCL) overlap.
  • We tested a panel of 8 germinal center (GC) and activated B-cell (ABC) markers for their ability to separate BL and DLBCL.
  • We diagnosed 16 BL and 39 DLBCL cases from 21 patients with AIDS and 34 without AIDS based on traditional morphologic criteria, Ki-67 proliferative index, and c-myc rearrangement (fluorescence in situ hybridization).
  • After immunohistochemically staining tissue microarrays of BL and DLBCL for markers of GC (bcl-6, CD10, cyclin H) and ABC (MUM1, CD138, PAK1, CD44, bcl-2), we scored each case for the percentage of positive cells.
  • For comparison, we plotted the sum of the GC scores and ABC scores for each case as x and y data points.
  • This revealed a high-GC/low-ABC group and a low-GC/high-ABC group that were associated significantly with morphologic diagnosis (P < .001).
  • Protein expression of multiple GC and ABC markers can separate BL and DLBCL.
  • [MeSH-major] B-Lymphocytes / immunology. Burkitt Lymphoma / pathology. Germinal Center / immunology. Lymphoma, AIDS-Related / pathology. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology


46. 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
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  • [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

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  • (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
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47. 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
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  • [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

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  • [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
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48. Lyu MA, Rai D, Ahn KS, Sung B, Cheung LH, Marks JW, Aggarwal BB, Aguiar RC, Gandhi V, Rosenblum MG: The rGel/BLyS fusion toxin inhibits diffuse large B-cell lymphoma growth in vitro and in vivo. Neoplasia; 2010 May;12(5):366-75
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  • [Title] The rGel/BLyS fusion toxin inhibits diffuse large B-cell lymphoma growth in vitro and in vivo.
  • Diffuse large B-cell lymphoma (DLBCL) is an aggressive subtype of B-cell non-Hodgkin lymphoma (NHL) and accounts for 30%to 40%of NHL.
  • Molecules targeting nuclear factor-kappaB (NF-kappaB) are expected to be of therapeutic value in those tumors where NF-kappaB seems to play a unique survival role such as activated B-cell (ABC)-subtype DLBCL.
  • In this study, we examined this fusion toxin for its ability to suppress DLBCL growth in vitro and in vivo. rGel/BLyS was specifically cytotoxic to DLBCL lines expressing all three BLyS receptors and constitutively active NF-kappaB.
  • Importantly, rGel/BLyS significantly inhibited tumor growth (P < .05) in a DLBCL xenograft model.

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  • (PMID = 20454508.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA136411; United States / NCI NIH HHS / CA / CA136411
  • [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 / B-Cell Activating Factor; 0 / I kappa B beta protein; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Recombinant Fusion Proteins; 0 / Ribosome Inactivating Proteins, Type 1; 0 / Toxins, Biological; 75037-46-6 / GEL protein, Gelonium multiflorum
  • [Other-IDs] NLM/ PMC2864474
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49. Rai D, Karanti S, Jung I, Dahia PL, Aguiar RC: Coordinated expression of microRNA-155 and predicted target genes in diffuse large B-cell lymphoma. Cancer Genet Cytogenet; 2008 Feb;181(1):8-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Coordinated expression of microRNA-155 and predicted target genes in diffuse large B-cell lymphoma.
  • MicroRNAs (miRNAs) attenuate gene expression by pairing to the 3'UTR of target transcripts inducing RNA cleavage or translational inhibition.
  • Overexpression of microRNA-155 (miR-155), measured either at the primary (BIC gene) or mature transcript level, was recently described in diffuse large B-cell lymphomas (DLBCL).
  • These studies have been limited in size, however, and have not attempted to link miR-155 expression to that of putative target genes.
  • To start to address these issues, we examined a collection of 22 well-characterized DLBCL cell lines.
  • The expression of miR-155 is heterogeneous in these cell lines and associates with NF-kappaB activity.
  • We found that the expression of the primary miR-155 transcript reliably reflects that of the functional mature miR-155.
  • Because many gene array platforms include probe sets for the primary miR-155 sequences, these findings allowed us to confidently examine large array-based expression datasets of primary DLBCLs in the context of miR-155 levels.
  • Our investigation revealed that miR-155 expression segregates with specific molecular subgroups of DLBCL and it is highest in activated B-cell (ABC)-type lymphomas.
  • These tumors are characterized by constitutive activation of NF-kappaB signals, which supports the data derived from our cell lines.
  • More importantly, using supervised learning algorithms, we identified a robust gene signature driven by the differential expression of miR-155.
  • Our data start to unveil the genome-wide effects of miR-155 expression in DLBCL and indicate the utility of this strategy in the identification and validation of miRNA target genes.

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  • (PMID = 18262046.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA054174; United States / NCI NIH HHS / CA / P30 CA054174-16; United States / NCI NIH HHS / CA / P30 CA54174
  • [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 / Culture Media; 0 / MicroRNAs; 0 / NF-kappa B; 0 / RNA Probes; 0 / RNA, Neoplasm
  • [Other-IDs] NLM/ NIHMS41231; NLM/ PMC2276854
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50. 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
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  • [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

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  • (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
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51. Miles RR, Raphael M, McCarthy K, Wotherspoon A, Lones MA, Terrier-Lacombe MJ, Patte C, Gerrard M, Auperin A, Sposto R, Davenport V, Cairo MS, Perkins SL, SFOP/LMB96/CCG5961/UKCCSG/NHL 9600 Study Group: Pediatric diffuse large B-cell lymphoma demonstrates a high proliferation index, frequent c-Myc protein expression, and a high incidence of germinal center subtype: Report of the French-American-British (FAB) international study group. Pediatr Blood Cancer; 2008 Sep;51(3):369-74
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  • [Title] Pediatric diffuse large B-cell lymphoma demonstrates a high proliferation index, frequent c-Myc protein expression, and a high incidence of germinal center subtype: Report of the French-American-British (FAB) international study group.
  • BACKGROUND: Diffuse large B-cell lymphoma (DLBCL) makes up 10-20% of pediatric non-Hodgkin lymphoma, and these patients have a significantly better prognosis than adults with DLBCL.
  • The difference in prognosis may be related to clinical, phenotypic, and/or biological differences between adult and pediatric DLBCL.
  • In adult DLBCL, the germinal center (GC) phenotype is associated with a better prognosis than the activated B-cell (ABC) phenotype.
  • However, a high proliferative index and expression of Bcl2 and c-Myc protein have all been associated with worse outcomes.
  • While multiple studies have addressed the phenotype and expression patterns of adult DLBCL, relatively little is known about these biological variables in pediatric DLBCL.
  • The goal of this study was to investigate the proliferative index, the relative frequencies of the GC and non-GC subtypes, and the expression of Bcl2 and c-Myc protein in a cohort of children with DLBCL treated in a uniform manner.
  • PROCEDURE: We performed immunohistochemistry (IHC) for MIB1, CD10, Bcl6, MUM1, Bcl2, and c-Myc on DLBCL tissue from children treated uniformly in the FAB LMB96 trial (SFOP LMB96/CCG5961/UKCCSG/NHL 9600).
  • RESULTS: Compared to published adult DLBCL studies, pediatric DLBCL demonstrated moderate to high proliferation rates (83%), increased c-Myc protein expression (84%), decreased Bcl2 protein expression (28%), and an increased frequency of the GC phenotype (75%).
  • CONCLUSIONS: These findings suggest that there are significant biologic differences between pediatric and adult forms of DLBCL, which may contribute to the superior prognosis seen in the pediatric population relative to adult disease.

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
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  • (PMID = 18493992.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA098543-06; None / None / / U10 CA098413-05; United States / NCI NIH HHS / CA / U10 CA098413-05; United States / NCI NIH HHS / CA / U10 CA098543; None / None / / U10 CA098543-06
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MYC protein, human; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc
  • [Other-IDs] NLM/ NIHMS123042; NLM/ PMC2712231
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52. Poulsen CB, Borup R, Borregaard N, Nielsen FC, Møller MB, Ralfkiaer E: Prognostic significance of metallothionein in B-cell lymphomas. Blood; 2006 Nov 15;108(10):3514-9
Genetic Alliance. consumer health - B-Cell Lymphomas.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of metallothionein in B-cell lymphomas.
  • We have investigated metallothionein (MT) I and II mRNA and protein in B-cell lymphomas with particular reference to diffuse large B-cell lymphoma (DLBCL).
  • The mRNA profiling was performed on Affymetrix arrays and showed up-regulated MT mRNA in 15 of 48 DLBCLs, including 12 of 23 activated B-cell (ABC) and 3 of 9 type-3 lesions.
  • In contrast, MT mRNA was low to undetectable in 16 germinal center B-cell (GCB)-type DLBCLs.
  • This was confirmed in 2 independent series, which showed significantly shorter 5-year survival in DLBCL with high versus low MT-IIa levels.
  • By immunohistology, MT was shown to be present in both macrophages and lymphoma cells.
  • In contrast, in 115 DLBCLs, MT labeling of more than 20% lymphoma cells was associated with a significantly poorer 5-year survival, independent of the age, stage, or International Prognostic Index.
  • Taken together, it is suggested that both increased MT mRNA and MT protein expression by more than 20% lymphoma cells constitute independent risk factors in DLBCL.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Metallothionein / analysis. Predictive Value of Tests
  • [MeSH-minor] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / mortality. Prognosis. RNA, Messenger / analysis. Survival Analysis. Treatment Failure. Up-Regulation

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  • (PMID = 16868254.001).
  • [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 / RNA, Messenger; 9038-94-2 / Metallothionein
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53. Lossos IS: BLIMP1 against lymphoma: The verdict is reached. Cancer Cell; 2010 Dec 14;18(6):537-9
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  • [Title] BLIMP1 against lymphoma: The verdict is reached.
  • BLIMP1, a master regulator of plasma-cell differentiation, is implicated in the pathogenesis of Activated B cell (ABC)-like Diffuse Large B cell Lymphoma (DLBCL).
  • In this issue of Cancer Cell, Mandelbaum and colleagues and Calado and colleagues unequivocally demonstrate that BLIMP1 functions as a tumor suppressor and guardian of ABC-like DLBCL lymphomagenesis.

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
  • [CommentOn] Cancer Cell. 2010 Dec 14;18(6):580-9 [21156282.001]
  • [CommentOn] Cancer Cell. 2010 Dec 14;18(6):568-79 [21156281.001]
  • (PMID = 21156275.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
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54. 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
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  • [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.

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  • (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
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55. 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
The Lens. Cited by Patents in .

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

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  • (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
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56. Tagawa H: [Analysis of genomic copy number alterations of malignant lymphomas and its application for diagnosis]. Gan To Kagaku Ryoho; 2007 Jul;34(7):975-82

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We herein report the characteristic genomic alterations of malignant lymphomas including diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL) and adult T cell lymphoma/leukemia (ATLL).
  • The combined use of the array CGH data with gene expression profiling and specific gene rearrangement analyses further delineated the subtype-specific genomic alterations.
  • For instance, we revealed that activated B-cell-like DLBCL is characterized by a gain of chromosome 3, 18q and loss of 9 p21, whereas the germinal center B-cell-like DLBCL is characterized by a gain of 2p15, 7q, and 12q.
  • Among these genomic alterations,we found the 9 p21 loss (p16INK4a locus) to be the most aggressive type of DLBCL.
  • Comparison of genome profiles between acute type and lymphoma types of adult T cell lymphoma also demonstrated that acute and lymphoma types are genomically distinct subtypes, and thus may develop tumors via distinct genetic pathways.
  • Furthermore,we developed a computer algorithm to classify lymphoma diseases or subtypes on the basis of copy number gains and losses.
  • We applied the algorithm to the classifications of DLBCL and MCL diseases and ABC and GCB subtypes.
  • The method correctly classified the DLBCL and MCL diseases at 89%, and ABC and GCB subtypes at 83%.
  • [MeSH-major] Gene Dosage. Gene Expression Profiling. Leukemia-Lymphoma, Adult T-Cell / genetics. Lymphoma, B-Cell / genetics. Lymphoma, Follicular / genetics. Lymphoma, Large B-Cell, Diffuse / genetics
  • [MeSH-minor] Burkitt Lymphoma / diagnosis. Burkitt Lymphoma / genetics. Genome, Human. Humans. Lymphoma, Mantle-Cell / diagnosis. Lymphoma, Mantle-Cell / genetics. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis. Translocation, Genetic

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  • (PMID = 17637530.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 13
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57. Belardo G, Piva R, Santoro MG: Heat stress triggers apoptosis by impairing NF-kappaB survival signaling in malignant B cells. Leukemia; 2010 Jan;24(1):187-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Nuclear factor-kappaB (NF-kappaB) is involved in multiple aspects of oncogenesis and controls cancer cell survival by promoting anti-apoptotic gene expression.
  • In this study we show that heat stress inhibits constitutive NF-kappaB DNA-binding activity in different types of B-cell malignancies, including multiple myeloma, activated B-cell-like (ABC) type of diffuse large B-cell lymphoma (DLBCL) and Burkitt's lymphoma presenting aberrant NF-kappaB regulation.
  • NF-kappaB inhibition by the proteasome inhibitor bortezomib and by short-hairpin RNA (shRNA) interference results in increased sensitivity of HS-Sultan B-cell lymphoma to hyperthermic stress.
  • Altogether, the results indicate that aggressive B-cell malignancies presenting constitutive NF-kappaB activity are sensitive to heat-induced apoptosis, and suggest that aberrant NF-kappaB regulation may be a marker of heat stress sensitivity in cancer cells.
  • [MeSH-major] Apoptosis. Heat-Shock Response. Lymphoma, B-Cell / pathology. NF-kappa B / antagonists & inhibitors. Signal Transduction / physiology
  • [MeSH-minor] Boronic Acids / pharmacology. Bortezomib. Cell Line, Tumor. DNA / metabolism. DNA-Binding Proteins / physiology. Hot Temperature. Humans. Inhibitor of Apoptosis Proteins / antagonists & inhibitors. Protein Biosynthesis. Pyrazines / pharmacology. Transcription Factor RelA / antagonists & inhibitors. Transcription Factors / physiology. Ubiquitin-Protein Ligases

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  • (PMID = 19924145.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / BIRC3 protein, human; 0 / Boronic Acids; 0 / DNA-Binding Proteins; 0 / Inhibitor of Apoptosis Proteins; 0 / NF-kappa B; 0 / Pyrazines; 0 / Transcription Factor RelA; 0 / Transcription Factors; 0 / heat shock transcription factor; 69G8BD63PP / Bortezomib; 9007-49-2 / DNA; EC 6.3.2.19 / Ubiquitin-Protein Ligases
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58. 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
The Lens. Cited by Patents in .

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

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  • (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
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59. Singh RR, Kim JE, Davuluri Y, Drakos E, Cho-Vega JH, Amin HM, Vega F: Hedgehog signaling pathway is activated in diffuse large B-cell lymphoma and contributes to tumor cell survival and proliferation. Leukemia; 2010 May;24(5):1025-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hedgehog signaling pathway is activated in diffuse large B-cell lymphoma and contributes to tumor cell survival and proliferation.
  • Recently, we described that HH signaling proteins are commonly expressed in diffuse large B-cell lymphoma (DLBCL); however, the functional role of HH pathway in DLBCL has not been explored.
  • Here, we assessed the possibility that HH pathway activation contributes to the survival of DLBCL.
  • We found that HH signaling inhibition induces predominantly cell-cycle arrest in DLBCL cells of germinal center (GC) B-cell type, and apoptosis in DLBCL cells of activated B-cell (ABC) type.
  • Apoptosis after HH signaling inhibition in DLBCL cells of ABC type was associated with downregulation of BCL2; however HH inhibition was not associated with BCL2 downregulation in DLBCL of GC type.
  • Functional inhibition of BCL2 significantly increased apoptosis induced by HH inhibition in DLBCL cells of both types.
  • We also showed that DLBCL cells synthesize, secrete and respond to endogenous HH ligands, providing support for the existence of an autocrine HH signaling loop.
  • Our findings provide novel evidence that dysregulation of HH pathway is involved in the biology of DLBCL and have significant therapeutic implications as they identify HH signaling as a potential therapeutic target in DLBCL, in particular for those lymphomas expressing the HH receptor smoothened.
  • [MeSH-major] Cell Proliferation. Gene Expression Regulation, Leukemic. Germinal Center / pathology. Hedgehog Proteins / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Lymphoma, Large B-Cell, Diffuse / pathology. Signal Transduction
  • [MeSH-minor] Apoptosis. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Blotting, Western. Cell Cycle. Cell Survival. Humans. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 20200556.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Hedgehog Proteins; 0 / RNA, Messenger
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60. 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
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Primary diffuse large B-cell lymphoma of 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

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  • (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
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61. 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
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  • [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


62. Fridberg M, Servin A, Anagnostaki L, Linderoth J, Berglund M, Söderberg O, Enblad G, Rosén A, Mustelin T, Jerkeman M, Persson JL, Wingren AG: Protein expression and cellular localization in two prognostic subgroups of diffuse large B-cell lymphoma: higher expression of ZAP70 and PKC-beta II in the non-germinal center group and poor survival in patients deficient in nuclear PTEN. Leuk Lymphoma; 2007 Nov;48(11):2221-32
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  • [Title] Protein expression and cellular localization in two prognostic subgroups of diffuse large B-cell lymphoma: higher expression of ZAP70 and PKC-beta II in the non-germinal center group and poor survival in patients deficient in nuclear PTEN.
  • Patients diagnosed with diffuse large B-cell lymphoma (DLBCL) show varying responses to conventional therapy, and this might be contributed to the differentiation stage of the tumor B-cells.
  • De novo DLBCL cases were divided into two subgroups, the germinal center (GC) group (14/28) and the non-germinal center (non-GC) or activated B-cell (ABC) group (14/28).
  • Also, the subcellular localization of PKC-beta I and II differed in DLBCL cells, with the PKC-beta I isoform being expressed in both the cytoplasm and nucleus, while PKC-beta II was found exclusively in the cytoplasm.
  • In addition, five cell lines of DLBCL origin were analyzed for protein expression and for mRNA levels of PTEN and SHP1.
  • For the first time, we show that ZAP70 is expressed in a higher percentage of tumor cells in the aggressive non-GC subgroup of DLBCL and that PKC-beta I and II are differently distributed in the two prognostic subgroups of de novo DLBCL.
  • [MeSH-major] Cell Nucleus / metabolism. Germinal Center / metabolism. Lymphoma, Large B-Cell, Diffuse / diagnosis. PTEN Phosphohydrolase / metabolism. Protein Kinase C / metabolism. ZAP-70 Protein-Tyrosine Kinase / metabolism

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  • (PMID = 17926183.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Protein Isoforms; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C beta; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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63. Dunphy CH, O'Malley DP, Cheng L, Fodrie TY, Perkins SL, Kaiser-Rogers K: Primary mediastinal B-cell lymphoma: detection of BCL2 gene rearrangements by PCR analysis and FISH. J Hematop; 2008 Sep;1(2):77-84
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  • [Title] Primary mediastinal B-cell lymphoma: detection of BCL2 gene rearrangements by PCR analysis and FISH.
  • Primary mediastinal large B-cell lymphoma (PMBCL) has a characteristic clinical presentation, morphology, and immunophenotype, representing a clinically favorable subgroup of diffuse large B-cell lymphoma (DLBCL).
  • By gene expression profiling (GEP), PMBCL shares features with classical Hodgkin lymphoma (cHL).
  • Of further interest, BCL6 gene mutations and BCL6 and/or MUM1 expression in a number of PMBCLs have supported an activated B-cell (ABC) origin.
  • BCL2 protein expression by IHC analysis was variably detected in 21 out of 24 (strongly, uniformly expressed: 6, including all with a t(14;.

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  • (PMID = 19669206.001).
  • [ISSN] 1868-9256
  • [Journal-full-title] Journal of hematopathology
  • [ISO-abbreviation] J Hematop
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2713480
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64. Zinzani PL, Broccoli A, Stefoni V, Musuraca G, Abruzzese E, De Renzo A, Cantonetti M, Bacci F, Baccarani M, Pileri SA: Immunophenotype and intermediate-high international prognostic index score are prognostic factors for therapy in diffuse large B-cell lymphoma patients. Cancer; 2010 Dec 15;116(24):5667-75
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  • [Title] Immunophenotype and intermediate-high international prognostic index score are prognostic factors for therapy in diffuse large B-cell lymphoma patients.
  • BACKGROUND: The development of gene expression profiling and tissue microarray techniques have provided more information about the heterogeneity of diffuse large B-cell lymphoma (DLBCL), enabling categorization of DLBCL patients into 3 prognostic groups according to cell origin (but independently from the International Prognostic Index [IPI] score): germinal center (GCB), activated B-cell (ABC), and not classified (NC) diffuse large B-cell lymphoma.
  • This study investigated the role of immunohistochemical discrimination between GCB and ABC&NC-DLBCL subtypes in identifying those high-risk patients who may benefit from a more aggressive first-line therapeutic approach.
  • METHODS: From February 2003 to August 2006, 45 newly diagnosed DLBCL patients, with IPI≥2, were considered eligible for this study: 13 had a GCB, 8 an ABC, and 24 a NC-DLBCL.
  • GCB patients received 6 courses of rituximab, cyclophophosphamide, doxorubicin, vinicristine, and prednisone (R-CHOP) chemotherapy, with a subsequent, autologous stem cell transplantation in case of partial response.
  • All ABC and NC-DLBCL patients received 6 R-CHOP cycles and autologous stem cell transplantation.
  • RESULTS: Complete response rate for each treatment arm was 84.6% for GCB and 89.7% for ABC&NC-DLBCL (P = .50), with a continuous complete response rate of 81.8% and 84.6%, respectively (P = .59).
  • Projected 4-year overall survival is 100% for GCB and 82% for ABC&NC patients (P = .12).
  • CONCLUSIONS: The autologous stem cell transplantation consolidation in the ABC&NC-DLBCL subtypes induced the same rate of complete response (and similar progression-free survival rate) compared with GCB-DLBCL.
  • In ABC&NC-DLBCL patients the authors observed a complete response rate of 89.7% vs. 84.6% in the GCB-DLBCL subset, without any significant difference in progression-free survival rate.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Immunohistochemistry. Immunophenotyping. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / therapy
  • [MeSH-minor] Adult. Antibodies, Monoclonal, Murine-Derived / administration & dosage. Combined Modality Therapy. Cyclophosphamide / therapeutic use. Disease-Free Survival. Doxorubicin / therapeutic use. Female. Humans. Male. Middle Aged. Prednisone / therapeutic use. Prognosis. Rituximab. Stem Cell Transplantation. Transplantation, Autologous. Treatment Failure. Vincristine / therapeutic use

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  • [Copyright] Copyright © 2010 American Cancer Society.
  • (PMID = 20737566.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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65. 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
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  • [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.

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  • (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
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66. 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
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  • [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

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  • [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
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67. Wilson WH, Hernandez-Ilizaliturri FJ, Dunleavy K, Little RF, O'Connor OA: Novel disease targets and management approaches for diffuse large B-cell lymphoma. Leuk Lymphoma; 2010 Aug;51 Suppl 1:1-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel disease targets and management approaches for diffuse large B-cell lymphoma.
  • Diffuse large B-cell lymphoma (DLBCL) responds well to treatment with CHOP and the R-CHOP regimen, but a subset of patients still fail to achieve complete or durable responses.
  • Recent advances in gene expression profiling have led to the identification of three different subtypes of DLBCL, and confirmed that patients with the activated B-cell (ABC) disease subtype are less likely to respond well to CHOP-based regimens than those with germinal centre B-cell-type (GCB) disease.
  • This discovery could herald the use of gene expression profiling to aid treatment decisions in DLBCL, and help identify the most effective management strategies for patients.
  • Treatment options for patients with relapsed or refractory DLBCL are limited and several novel agents are being developed to address this unmet clinical need.
  • Novel agents developed to treat plasma cell disorders such as multiple myeloma have shown promising activity in patients with NHL.
  • Indeed, the immunomodulatory agent lenalidomide and the proteasome inhibitors bortezomib and carfilzomib, as single agents or in combination with chemotherapy, have already demonstrated promising activity in patients with the ABC subtype of DLBCL.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / drug therapy
  • [MeSH-minor] Disease Management. Gene Expression Profiling / classification. Humans. Precision Medicine / methods


68. Curry CV, Ewton AA, Olsen RJ, Logan BR, Preti HA, Liu YC, Perkins SL, Chang CC: Prognostic impact of C-REL expression in diffuse large B-cell lymphoma. J Hematop; 2009 Mar;2(1):20-6
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  • [Title] Prognostic impact of C-REL expression in diffuse large B-cell lymphoma.
  • Diffuse large B-cell lymphoma (DLBCL) with a germinal center B-cell (GCB) phenotype is believed to confer a better prognosis than DLBCL with an activated B-cell (ABC) phenotype.
  • Previous studies have suggested that nuclear factor-kappaB (NF-kappaB) activation plays an important role in the ABC subtype of DLBCL, whereas c-REL amplification is associated with the GCB subtype.
  • Using immunohistochemical techniques, we examined 68 newly diagnosed de novo DLBCL cases (median follow-up 44 months, range 1 to 142 months) for the expression of c-REL, BCL-6, CD10, and MUM1/IRF4.
  • Forty-four (65%) cases demonstrated positive c-REL nuclear expression.
  • In general, c-REL nuclear expression did not correlate with GCB vs. non-GCB phenotype, International Prognostic Index score, or OS.
  • However, cases with a GCB phenotype and negative nuclear c-REL demonstrated better OS than cases with a GCB phenotype and positive nuclear c-REL (KMS analysis, p = 0.045, Breslow-Gehan-Wilcoxon test), whereas in cases with non-GCB phenotype, the expression of c-REL did not significantly impact the prognosis.
  • These results suggest that c-REL nuclear expression may be a prognostic factor in DLBCL and it may improve patient risk stratification in combination with GCB/non-GCB phenotyping.

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  • (PMID = 19669219.001).
  • [ISSN] 1868-9256
  • [Journal-full-title] Journal of hematopathology
  • [ISO-abbreviation] J Hematop
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA126752
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Other-IDs] NLM/ PMC2713494
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69. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [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 .
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  • (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
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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

  • [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.

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