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

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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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2. 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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3. Baecklund E, Natkunam Y, Backlin C, Iliadou A, Askling J, Ekbom A, Feltelius N, Klareskog L, Enblad G, Lossos IS, Levy R, Sundström C, Rosenquist R: Expression of the human germinal-centre-associated lymphoma protein in diffuse large B-cell lymphomas in patients with rheumatoid arthritis. Br J Haematol; 2008 Apr;141(1):69-72
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  • [Title] Expression of the human germinal-centre-associated lymphoma protein in diffuse large B-cell lymphomas in patients with rheumatoid arthritis.
  • Diffuse large B-cell lymphomas (DLBCL) can be subdivided into germinal centre (GC)-like and non-GC-like subtypes by CD10, BCL6 and MUM1/IRF4 status.
  • We previously reported that patients with severe rheumatoid arthritis (RA) are at increased risk of non-GC DLBCL.
  • This study examined a new GC-marker, human germinal-centre-associated lymphoma (HGAL) protein, in RA-DLBCL.
  • Of 111, 38 (34%) DLBCL were HGAL-positive and showed less disseminated disease and a tendency toward improved overall survival compared to HGAL-negative cases.
  • This supports that a majority of RA-DLBCL are of non-GC origin, indicating a specific role for activated peripheral B cells in the pathogenesis of RA-DLBCL.
  • [MeSH-major] Arthritis, Rheumatoid / complications. Biomarkers, Tumor / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Neoplasm Proteins / metabolism


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4. 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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5. 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.


6. Tam W, Gomez M, Chadburn A, Lee JW, Chan WC, Knowles DM: Mutational analysis of PRDM1 indicates a tumor-suppressor role in diffuse large B-cell lymphomas. Blood; 2006 May 15;107(10):4090-100
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  • [Title] Mutational analysis of PRDM1 indicates a tumor-suppressor role in diffuse large B-cell lymphomas.
  • The PR (PRDI-BF1-RIZ) domain zinc finger protein 1 (PRDM1) is a transcription repressor with a pivotal role in plasma-cell differentiation.
  • We identified clonal inactivating mutations in PRDM1 in the diffuse large B-cell lymphoma (DLBCL) cell line OCI-Ly3 and in 8 of 35 de novo clinical DLBCL samples.
  • This study identifies PRDM1 inactivation as a recurrent genetic defect in DLBCL cells and establishes PRDM1 as a potential tumor suppressor gene in DLBCL.
  • Moreover, it implies inhibition of terminal differentiation as a pathogenetic pathway in DLBCL, particularly for the activated B-cell-like DLBCL.
  • [MeSH-major] Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Non-Hodgkin / genetics. Repressor Proteins / genetics. Transcription Factors / genetics
  • [MeSH-minor] Amino Acid Sequence. Base Sequence. Cell Line, Tumor. Cell Nucleus / genetics. DNA Primers. Exons. Genes, Tumor Suppressor. Humans. Introns. Molecular Sequence Data. Polymerase Chain Reaction

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  • (PMID = 16424392.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Repressor Proteins; 0 / Transcription Factors; 138415-26-6 / PRDM1 protein, human
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7. Berglund M, Thunberg U, Amini RM, Book M, Roos G, Erlanson M, Linderoth J, Dictor M, Jerkeman M, Cavallin-Ståhl E, Sundström C, Rehn-Eriksson S, Backlin C, Hagberg H, Rosenquist R, Enblad G: Evaluation of immunophenotype in diffuse large B-cell lymphoma and its impact on prognosis. Mod Pathol; 2005 Aug;18(8):1113-20
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  • [Title] Evaluation of immunophenotype in diffuse large B-cell lymphoma and its impact on prognosis.
  • Diffuse large B-cell lymphoma (DLBCL) has been shown to be comprised of at least two prognostic entities, depending on its resemblance to normal germinal center or activated B cells, using global gene expression profiling.
  • Also, the expression patterns of bcl-6, CD10 and IRF-4 (also known as MUM1) have been suggested as alternative means of identifying the germinal- and nongerminal center (activated B-cell like) groups.
  • In the present study, we evaluated by immunohistochemistry the expression patterns of CD10, bcl-6, IRF-4 and bcl-2 in a large material of 161 DLBCL patients.
  • Positive staining for bcl-6 or CD10 predicted for superior survival, while expression of IRF-4 alone showed no association with prognosis.
  • Furthermore, expression of bcl-2 was associated with worse event-free survival and overall survival.
  • Here we confirm the prognostic importance of determining the germinal- or nongerminal center phenotype in patients with DLBCL.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology

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  • (PMID = 15920553.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Interferon Regulatory Factors; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-bcl-6; 0 / Transcription Factors; 0 / interferon regulatory factor-4; EC 3.4.24.11 / Neprilysin
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8. Koens L, Vermeer MH, Willemze R, Jansen PM: IgM expression on paraffin sections distinguishes primary cutaneous large B-cell lymphoma, leg type from primary cutaneous follicle center lymphoma. Am J Surg Pathol; 2010 Jul;34(7):1043-8
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  • [Title] IgM expression on paraffin sections distinguishes primary cutaneous large B-cell lymphoma, leg type from primary cutaneous follicle center lymphoma.
  • In the World Health Organization (WHO) 2008 classification 2 main types of primary cutaneous large B-cell lymphomas (PCLBCLs) are distinguished: primary cutaneous follicle center lymphoma (PCFCL) and primary cutaneous large B-cell lymphoma, leg type (PCBCL-LT).
  • Expression profiling studies have shown higher RNA expression of the IgM heavy chain in PCBCL-LT compared with PCFCL.
  • To find out whether this difference could also be demonstrated at the protein level, we performed immunohistochemical staining for B-cell receptor heavy and light chains on skin biopsies from 53 patients with PCFCL and 40 patients with PCBCL-LT.
  • Analogous to other nodal and extranodal large B-cell lymphomas, expression of IgM in PCLBCL seems to be related to an activated B cell-like phenotype.
  • Finally, the expression of IgM (and IgD) in this type of lymphoma might imply defective class switch recombination.
  • [MeSH-major] Immunoglobulin M / metabolism. Lymphoma, Follicular / diagnosis. Lymphoma, Large B-Cell, Diffuse / diagnosis. Skin Neoplasms / diagnosis


9. 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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10. 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
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  • [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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11. 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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12. 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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13. Raoux D, Duband S, Forest F, Trombert B, Chambonnière ML, Dumollard JM, Khaddage A, Gentil-Perret A, Péoc'h M: Primary central nervous system lymphoma: immunohistochemical profile and prognostic significance. Neuropathology; 2010 Jun;30(3):232-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary central nervous system lymphoma: immunohistochemical profile and prognostic significance.
  • Primary central nervous system lymphoma (PCNSL) is a rare subtype of non-Hodgkin lymphoma (NHL) with extranodal location affecting only the CNS, meninges and eye, without visceral or lymph node involvement.
  • Most PCNSL cases are diffuse large B-cell lymphomas (DLBCLs).
  • However, it differs from nodal DLBCL in that it has a worse prognosis.
  • Two prognostic algorithms were then prepared using a panel of immunohistochemical markers (CD10, Bcl6, MUM1/IRF-4, and Bcl2), thus categorizing DLBCL into two subgroups, GCB (germinal centre B-cell-like) or non-GCB, and into Group 1 or Group 2.
  • 74.3% of our PCNSLs were of a non-GCB phenotype, corresponding to an activated postgerminal origin.
  • The recent discovery of a specific "transcriptional signature" of PCNSL, marking them out of DLBCL could account for the irrelevance of such prognostic classifications to PCNSL.
  • [MeSH-major] Central Nervous System Neoplasms / chemistry. Central Nervous System Neoplasms / immunology. Lymphoma, B-Cell / chemistry. Lymphoma, B-Cell / immunology. Lymphoma, Non-Hodgkin / chemistry. Lymphoma, Non-Hodgkin / immunology

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  • (PMID = 19925562.001).
  • [ISSN] 1440-1789
  • [Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology
  • [ISO-abbreviation] Neuropathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Australia
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14. 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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  • [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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15. Delsol G: [Molecular abnormalities in lymphomas]. Bull Cancer; 2010 Nov;97(11):1347-64
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  • Several techniques are available to detect these molecular anomalies: conventional cytogenetic analysis, multicolor FISH, CGH array or gene expression profiling using DNA microarrays.
  • In some lymphomas, genetic abnormalities are responsible for the expression of an abnormal protein (e.g. tyrosine-kinase, transcription factor) detectable by immunohistochemistry.
  • In the present review, molecular abnormalities observed in the most frequent B, T or NK cell lymphomas are discussed.
  • In the broad spectrum of diffuse large B-cell lymphomas microarray analysis shows mostly two subgroups of tumors, one with gene expression signature corresponding to germinal center B-cell-like (GCB: CD10+, BCL6 [B-Cell Lymphoma 6]+, centerine+, MUM1-) and a subgroup expressing an activated B-cell-like signature (ABC: CD10-, BCL6-, centerine-, MUM1+).
  • Among other B-cell lymphomas with well characterized molecular abnormalies are follicular lymphoma (BCL2 deregulation), MALT lymphoma (Mucosa Associated Lymphoid Tissue) [API2-MALT1 (mucosa-associated-lymphoid-tissue-lymphoma-translocation-gene1) fusion protein or deregulation BCL10, MALT1, FOXP1.
  • MALT1 transcription factors], mantle cell lymphoma (cycline D1 [CCND1] overexpression) and Burkitt lymphoma (c-Myc expression).
  • Except for ALK (anaplastic lymphoma kinase)-positive anaplastic large cell lymphoma, well characterized molecular anomalies are rare in lymphomas developed from T or NK cells.
  • Peripheral T cell lymphomas not otherwise specified are a heterogeneous group of tumors with frequent but not recurrent molecular abnormalities.
  • Gene profiling analysis shows that the expression of several genes is deregulated including PDGFRA (platelet-derived growth factor receptor) gene, encoding a receptor with tyrosine kinase activity.
  • In angio-immunoblastic T-cell lymphomas molecular abnormalities are found in follicular helper T-cell (TFH) that express some distinctive markers such as CD10, PD-1, CXCR5 and the CXCL13 chemokine.
  • ALK-positive anaplastic large cell lymphoma is a paradigme of T-cell lymphoma since it is associated with an X-ALK oncogenic fusion protein due to a translocation involving ALK gene at 2p23.
  • Helicobacter pylori in MALT lymphoma) in lymphomagenesis.
  • [MeSH-major] Gene Amplification / genetics. Genes, Tumor Suppressor. Lymphoma / genetics. Mutation / genetics. Translocation, Genetic / genetics
  • [MeSH-minor] Gene Deletion. Gene Expression Regulation, Neoplastic / genetics. Genetic Techniques. Humans. Lymphoma, B-Cell / genetics. Lymphoma, B-Cell / metabolism. Lymphoma, T-Cell / genetics. Lymphoma, T-Cell / metabolism. Neoplasm Proteins / metabolism


16. Li D, Mi C, Zhao Y, Wang YL, Ma Y, Li YY, Xiang MH: [Primary diffuse large B-cell lymphoma of testis: a clinicopathologic study of 14 cases]. Zhonghua Bing Li Xue Za Zhi; 2007 Jul;36(7):461-5
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  • [Title] [Primary diffuse large B-cell lymphoma of testis: a clinicopathologic study of 14 cases].
  • OBJECTIVE: To study the clinicopathologic features, immunohistochemical findings and prognosis of primary diffuse large B-cell lymphoma (DLBCL) of testis.
  • METHODS: Fourteen cases of primary DLBCL of testis, diagnosed according to the 2001 World Health Organization staging standards for hematopoietic and lymphoid tumors, were retrospectively studied.
  • Histologically, the lymphoma cells of all cases showed a centroblastic appearance.
  • One case belonged to the germinal center B cell-like subtype on immunohistochemical study, while the remaining 13 cases were classified as non-germinal center B cell-like subtype.
  • CONCLUSIONS: Most cases with primary DLBCL of testis were of peripheral activated B-cell origin.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology. Testicular Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD20 / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Diagnosis, Differential. Doxorubicin / therapeutic use. Follow-Up Studies. Gene Expression Regulation, Neoplastic. Germinoma / drug therapy. Germinoma / metabolism. Germinoma / pathology. Germinoma / surgery. Humans. Male. Middle Aged. Neprilysin / metabolism. Orchiectomy. Prednisone / therapeutic use. Proto-Oncogene Proteins c-bcl-2 / metabolism. Retrospective Studies. Seminoma / pathology. Survival Rate. Tumor Suppressor Protein p53 / metabolism. Vincristine / therapeutic use

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  • (PMID = 17845759.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD20; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 3.4.24.11 / Neprilysin; VB0R961HZT / Prednisone; CHOP protocol
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17. 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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18. Camilleri-Broët S, Crinière E, Broët P, Delwail V, Mokhtari K, Moreau A, Kujas M, Raphaël M, Iraqi W, Sautès-Fridman C, Colombat P, Hoang-Xuan K, Martin A: A uniform activated B-cell-like immunophenotype might explain the poor prognosis of primary central nervous system lymphomas: analysis of 83 cases. Blood; 2006 Jan 1;107(1):190-6
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  • [Title] A uniform activated B-cell-like immunophenotype might explain the poor prognosis of primary central nervous system lymphomas: analysis of 83 cases.
  • Most primary central nervous system lymphomas (PCNSLs) in immunocompetent patients are diffuse large B-cell lymphomas (DLBCLs), characterized by poor prognosis, compared with systemic forms.
  • A germinal center B-cell-like (GCB) origin of PCNSL was hypothesized on the basis of BCL-6 expression and ongoing mutational activity.
  • Our goal herein was to determine, for 83 PCNSLs, the percentages of GCB and activated B-cell-like (ABC) phenotypes and their prognostic significance.
  • Among the 82 patients with complete information, 79 (96.3%) were classified as ABC; 42 (51.2%) expressed BCL-6+ MUM1+, suggesting an "activated GCB" origin; 33 (40.2%) were exclusively MUM1+, and the remaining 4 (4.9%) were negative for all markers tested.
  • These findings provide new insights into interpreting the poor PCNSL prognostic, which may, in part, be due to biologic aggressiveness associated with its activated B-cell-like pattern.
  • We postulate assigning PCNSL a histogenetic "time-slot," overlapping late GC and early post-GC, that could explain the predominant ABC phenotype observed.
  • [MeSH-major] B-Lymphocytes / pathology. Central Nervous System Neoplasms / pathology. Germinal Center / pathology. Lymphocyte Activation. Lymphoma, B-Cell / pathology

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  • (PMID = 16150948.001).
  • [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 / Antigens, Neoplasm
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19. 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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20. 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
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  • [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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21. Dierlamm J, Murga Penas EM, Bentink S, Wessendorf S, Berger H, Hummel M, Klapper W, Lenze D, Rosenwald A, Haralambieva E, Ott G, Cogliatti SB, Möller P, Schwaenen C, Stein H, Löffler M, Spang R, Trümper L, Siebert R, Deutsche Krebshilfe Network Project "Molecular Mechanisms in Malignant Lymphomas": Gain of chromosome region 18q21 including the MALT1 gene is associated with the activated B-cell-like gene expression subtype and increased BCL2 gene dosage and protein expression in diffuse large B-cell lymphoma. Haematologica; 2008 May;93(5):688-96
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  • [Title] Gain of chromosome region 18q21 including the MALT1 gene is associated with the activated B-cell-like gene expression subtype and increased BCL2 gene dosage and protein expression in diffuse large B-cell lymphoma.
  • BACKGROUND: The aim of this study was to determine the impact of a gain of the MALT1 gene on gene expression and clinical parameters in diffuse large B-cell lymphoma.
  • DESIGN AND METHODS: We analyzed 116 cases of diffuse large B-cell lymphoma by fluorescence in situ hybridization, array-based comparative genomic hybridization, and transcriptional profiling.
  • Cases with 18q21/MALT1 gain more frequently showed an activated B-cell-like (ABC) gene expression signature (65%) than a germinal center B-cell-like (GCB) one (23%) (p<0.001).
  • Ninety-eight genes including MALT1, BCL2, and some selected nuclear factor-kappaB target genes were differentially expressed between the two genetic groups of diffuse large B-cell lymphoma.
  • By global testing of each chromosome, we identified 33 genes, all located on chromosome 18q, which were differentially expressed between the two genetic groups independently of the ABC/GCB status.
  • CONCLUSIONS: In diffuse large B-cell lymphoma, gain of 18q21 including MALT1 is significantly associated with differential expression of genes located on 18q, the ABC gene expression subtype, increased BCL2 gene and protein expression and might indicate an unfavorable prognosis.
  • [MeSH-major] B-Lymphocytes / cytology. Caspases / genetics. Chromosomes, Human, Pair 18. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / metabolism. Neoplasm Proteins / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism
  • [MeSH-minor] Aged. Female. Gene Expression Profiling. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Nucleic Acid Hybridization. Prognosis. Transcription, Genetic

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  • [CommentIn] Haematologica. 2008 May;93(5):641-5 [18450732.001]
  • (PMID = 18367485.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; EC 3.4.22.- / Caspases; EC 3.4.22.- / MALT1 protein, human
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22. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunophenotyping of diffuse large B-cell lymphoma (DLBCL) defines multiple sub-groups of germinal centre-like tumours displaying different survival characteristics.
  • Diffuse large B-cell lymphoma (DLBCL) forms a heterogeneous collection of aggressive non-Hodgkin's Lymphoma in which three principle classes of neoplasia have been defined according to gene expression and immunophenotyping studies.
  • A series of 155 DLBCL treated uniformly with anthracycline therapy in clinical trials, were stratified upon the basis of common biomarker expression with combination immunophenotype being related to patient overall survival.
  • Stratification of tumours with respect to combined expression profiles of the three biological markers (CD10, Bcl-6 and MUM-1) revealed six groups showing significant differences in survival (p=0.014).
  • The greatest difference resided between distinct populations of germinal centre (GC) cell tumours; the first being CD10-, Bcl-6+, MUM-1- and the second CD10+ Bcl-6+ MUM-1+ (p=0.002).
  • Of the three groups presenting a non-GC or activated B cell (NGC/ABC) phenotype, only one (CD10-, Bcl-6+ and MUM-1+) presented short-term median survival (27 months) comparable with poor prognosis GC sub-populations.
  • Within the remaining ABC tumour groups (CD10- Bcl-6- MUM-1- and CD10- Bcl-6- MUM-1+) patients presented intermediate median survival times of 54 and 58 months, respectively.
  • The first of these comprised two patient sub-populations with GC-like tumours together with one sub-population of NGC/ABC, the second two sub-populations of ABC-like tumours, and the final a single group of GC-like tumours associated with optimal long-term survival.
  • [MeSH-major] Biomarkers, Tumor / analysis. Lymphoma, Large B-Cell, Diffuse / metabolism. Lymphoma, Large B-Cell, Diffuse / mortality

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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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23. Borovecki A, Korać P, Nola M, Ivanković D, Jaksić B, Dominis M: Prognostic significance of B-cell differentiation genes encoding proteins in diffuse large B-cell lymphoma and follicular lymphoma grade 3. Croat Med J; 2008 Oct;49(5):625-35
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  • [Title] Prognostic significance of B-cell differentiation genes encoding proteins in diffuse large B-cell lymphoma and follicular lymphoma grade 3.
  • AIM: To define prognostic significance of B-cell differentiation genes encoding proteins and BCL2 and BCL6 gene abnormalities in diffuse large B-cell lymphoma and follicular lymphoma grade 3 with >75% follicular growth pattern.
  • METHODS: In 53 patients with diffuse large B-cell lymphoma and 20 patients with follicular lymphoma grade 3 with >75% follicular growth pattern the following was performed:.
  • 1) determination of protein expression of BCL6, CD10, MUM1/IRF4, CD138, and BCL2 by immunohistochemistry;.
  • 2) subclassification into germinal center B-cell-like (GCB) and activated B-cell-like (ABC) groups according to the results of protein expression;.
  • 3) detection of t(14;18)(q32;q21)/IgH-BCL2 and BCL6 abnormalities by fluorescent in situ hybridization in diffuse large B-cell lymphoma and follicular lymphoma grade 3 with >75% follicular growth pattern as well as in GCB and ABC groups; and 4) assessment of the influence of the analyzed characteristics and clinical prognostic factors on overall survival.
  • RESULTS: Only BCL6 expression was more frequently found in follicular lymphoma grade 3 with >75% follicular growth pattern than in diffuse large B-cell lymphoma (P=0.030).
  • There were no differences in BCL2 and BCL6 gene abnormalities between diffuse large B-cell lymphoma and follicular lymphoma grade 3 with >75% follicular growth pattern.
  • Diffuse large B-cell lymphoma and follicular lymphoma grade 3 with >75% follicular growth pattern patients were equally distributed in GCB and ABC groups. t(14;18)(q32;q21) was more frequently recorded in GCB group, and t(14;18)(q32;q21) with BCL2 additional signals or only BCL2 and IgH additional signals in ABC group (P=0.004).
  • The GCB and ABC groups showed no difference in BCL6 gene abnormalities.
  • There was no overall survival difference between the diffuse large B-cell lymphoma and follicular lymphoma grade 3 with >75% follicular growth pattern patients, however, GCB group had longer overall survival than ABC group (P=0.047).
  • Multivariate analysis showed that BCL6, CD10, and BCL2 expression, BCL2 and BCL6 abnormalities, and International Prognostic Index were not significantly related to overall survival.
  • CONCLUSION: Diffuse large B-cell lymphoma and follicular lymphoma grade 3 with >75% follicular growth pattern patients have very similar characteristics and their prognosis is more influenced by protein expression of B-cell differentiation stage genes than by tumor cells growth pattern, BCL2 and BCL6 abnormalities, and International Prognostic Index.
  • [MeSH-major] Biomarkers, Tumor / genetics. DNA-Binding Proteins / genetics. Interleukin-6 / genetics. Lymphoma, Follicular / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Gene Expression Regulation, Neoplastic. Genetic Markers. Humans. Immunohistochemistry. Male. Middle Aged. Neprilysin / genetics. Predictive Value of Tests. Prognosis. Syndecan-1 / genetics

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  • (PMID = 18925696.001).
  • [ISSN] 1332-8166
  • [Journal-full-title] Croatian medical journal
  • [ISO-abbreviation] Croat. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Croatia
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Genetic Markers; 0 / Interleukin-6; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Syndecan-1; EC 3.4.24.11 / Neprilysin
  • [Other-IDs] NLM/ PMC2582355
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24. 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
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  • [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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  • (PMID = 17335572.001).
  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1828714
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25. Dorfman DM, Hornick JL, Shahsafaei A, Freeman GJ: The phosphatidylserine receptors, T cell immunoglobulin mucin proteins 3 and 4, are markers of histiocytic sarcoma and other histiocytic and dendritic cell neoplasms. Hum Pathol; 2010 Oct;41(10):1486-94
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  • [Title] The phosphatidylserine receptors, T cell immunoglobulin mucin proteins 3 and 4, are markers of histiocytic sarcoma and other histiocytic and dendritic cell neoplasms.
  • The T cell immunoglobulin mucin (TIM) proteins are a family of cell surface phosphatidyserine receptors that are important for the recognition and phagocytosis of apoptotic cells.
  • Because TIM-4 is expressed by macrophages and dendritic cells in human tissue, we examined its expression in a range of histiocytic and dendritic cell neoplasms and found moderate to strong immunohistochemical staining in cases of juvenile xanthogranuloma and histiocytic sarcoma, and lower level staining in interdigitating dendritic cell sarcoma, Langerhans cell histiocytosis, acute monocytic leukemia (leukemia cutis), and blastic plasmacytoid dendritic cell neoplasm (hematodermic tumor).
  • TIM-3 was first described on activated T(H)1 cells but was recently shown to also be a phosphatidylserine receptor and mediate phagocytosis.
  • We found that it, like TIM-4, is expressed in a range of histiocytic and dendritic cell neoplasms, typically with strong immunohistochemical staining.
  • Cases of diffuse large B cell lymphoma, anaplastic large cell lymphoma, metastatic malignant melanoma, and metastatic poorly differentiated carcinoma generally exhibited negative to minimal heterogenous staining for TIM-4 and TIM-3.
  • We conclude that histiocytic and dendritic cell neoplasms consistently express TIM-3 and TIM-4 and that these molecules are new markers of neoplasms derived from histiocytic and dendritic cells.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Dendritic Cells / metabolism. Histiocytes / metabolism. Histiocytic Disorders, Malignant / metabolism. Membrane Proteins / metabolism. Receptors, Cell Surface / metabolism

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20656318.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / P01 AI054456; United States / NIAID NIH HHS / AI / P01 AI054456; United States / NIAID NIH HHS / AI / P01 AI054456-01; United States / NIAID NIH HHS / AI / P01 AI054456-02; United States / NIAID NIH HHS / AI / P01 AI054456-03; United States / NIAID NIH HHS / AI / P01 AI054456-04; United States / NIAID NIH HHS / AI / P01 AI054456-05; United States / NIAID NIH HHS / AI / P01 AI054456-06A1; United States / NIAID NIH HHS / AI / P01 AI054456-07; United States / NIAID NIH HHS / AI / R01 AI089955; United States / NIAID NIH HHS / AI / R01 AI089955-01; United States / NIAID NIH HHS / AI / R01 AI089955-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / HAVCR2 protein, human; 0 / Membrane Proteins; 0 / Receptors, Cell Surface; 0 / TIMD4 protein, human; 0 / phosphatidylserine receptor
  • [Other-IDs] NLM/ NIHMS298185; NLM/ PMC3115740
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36. 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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  • [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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37. 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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  • [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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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. 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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  • 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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40. 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
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  • [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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  • [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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41. Li S, Phong M, Lahn M, Brail L, Sutton S, Lin BK, Thornton D, Liao B: Retrospective analysis of protein kinase C-beta (PKC-beta) expression in lymphoid malignancies and its association with survival in diffuse large B-cell lymphomas. Biol Direct; 2007;2:8
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  • [Title] Retrospective analysis of protein kinase C-beta (PKC-beta) expression in lymphoid malignancies and its association with survival in diffuse large B-cell lymphomas.
  • BACKGROUND: Both mechanistic features and recent correlative findings suggest a potential role for protein kinase C-beta (PKC-beta) in tumor pathogenesis, particularly in B-cell malignancies.
  • To evaluate the role of this gene in lymphoid malignancies, we analyzed global gene expression data to quantify PKC-beta expression across diagnostic groups and, when possible, determined correlations between PKC-beta expression and survival.
  • RESULTS: Our analysis showed that the level of PKC-beta expression was highest in chronic lymphocytic leukemia and follicular lymphoma.
  • Within diffuse large-B cell lymphoma (DLBCL), PKC-beta expression was significantly higher in activated B-cell- like subtype than germinal center B-cell- like subtype (P < 0.0001).
  • When analyzed within clinically defined risk groups established by the International Prognostic Index (IPI), PKC-beta expression was lowest in patients with low IPI scores (0-1).
  • Within intermediate- and high-risk IPI groups, elevated PKC-beta expression was associated with worse survival, suggesting that PKC-beta may expand the prognostic value of the IPI.
  • Results of global gene expression analyses of DLBCL samples corroborate previous observations that anti-apoptosis, cell proliferation, and B-cell proliferation signaling pathways are functionally related to PKC-beta.
  • CONCLUSION: We present a first detailed pharmacogenomics report comparing PKC-beta mRNA expression across different lymphoid malignancies and evaluating it as an outcome predictor.
  • Our findings suggest that DLBCL patients with elevated PKC-beta have a worse prognosis, indicating that further evaluation of PKC-beta as a chemotherapeutic target for lymphoid malignancies is warranted.

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  • [ISO-abbreviation] Biol. Direct
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42. Tibiletti MG, Martin V, Bernasconi B, Del Curto B, Pecciarini L, Uccella S, Pruneri G, Ponzoni M, Mazzucchelli L, Martinelli G, Ferreri AJ, Pinotti G, Assanelli A, Scandurra M, Doglioni C, Zucca E, Capella C, Bertoni F: BCL2, BCL6, MYC, MALT 1, and BCL10 rearrangements in nodal diffuse large B-cell lymphomas: a multicenter evaluation of a new set of fluorescent in situ hybridization probes and correlation with clinical outcome. Hum Pathol; 2009 May;40(5):645-52
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  • [Title] BCL2, BCL6, MYC, MALT 1, and BCL10 rearrangements in nodal diffuse large B-cell lymphomas: a multicenter evaluation of a new set of fluorescent in situ hybridization probes and correlation with clinical outcome.
  • Diffuse large B-cell lymphoma is the most common type of non-Hodgkin lymphoma.
  • We analyzed 74 cases of diffuse large B-cell lymphoma using interphase fluorescent in situ hybridization with commercially available probes for split-signal targeting BCL-2, BCL-6, MYC, BCL-10, and MALT-1.
  • When diffuse large B-cell lymphoma cases were subdivided into germinal-center B-cell-like and activated B-cell-like groups, an inverse pattern of BCL-2 and BCL-6 rearrangements was observed.
  • The pattern of cytogenetic abnormalities highlighted the fact not only that diffuse large B-cell lymphoma is a heterogeneous entity but also that even individual cases may contain subclones bearing different chromosomal rearrangements.
  • The fluorescent in situ hybridization analysis with the panel used in this study is useful to detect the heterogeneity of diffuse large B-cell lymphomas and identify alterations with prognostic implications.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Caspases / genetics. In Situ Hybridization, Fluorescence / methods. Lymphoma, Large B-Cell, Diffuse / genetics. Neoplasm Proteins / genetics. Proto-Oncogene Proteins / genetics

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  • [CommentIn] Hum Pathol. 2009 Jul;40(7):1055-6; author reply 1056 [19524106.001]
  • (PMID = 19144384.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / BCL10 protein, human; 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc; EC 3.4.22.- / Caspases; EC 3.4.22.- / MALT1 protein, human
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43. 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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44. Arai E, Shimizu M, Hirose T: A review of 55 cases of cutaneous lymphoid hyperplasia: reassessment of the histopathologic findings leading to reclassification of 4 lesions as cutaneous marginal zone lymphoma and 19 as pseudolymphomatous folliculitis. Hum Pathol; 2005 May;36(5):505-11
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  • [Title] A review of 55 cases of cutaneous lymphoid hyperplasia: reassessment of the histopathologic findings leading to reclassification of 4 lesions as cutaneous marginal zone lymphoma and 19 as pseudolymphomatous folliculitis.
  • To clarify the confusion surrounding the diagnosis of cutaneous lymphoid hyperplasia (CLH) that was formerly described as lymphadenosis benigna cutis, lymphocytoma cutis, or lymphocytic infiltration of Jessner and to assess whether newly recognized diagnoses, such as cutaneous marginal zone lymphoma and pseudolymphomatous folliculitis (PLF), may have been overlooked, we reexamined 55 Japanese cases of nonepidermotropic lymphoproliferative disorder that had previously been diagnosed as "cutaneous pseudolymphoma."
  • As a result of these investigations, we have identified 4 cases of cutaneous marginal zone lymphoma, 19 cases of PLF, 1 case of diffuse large B-cell lymphoma, and 2 cases of solitary nonepidermotropic pseudo-T-cell lymphoma, with the remaining 29 cases being CLH.
  • Cutaneous marginal zone lymphoma, which represented 7.3% of the total, was distinguished from CLH by the presence of patchy or diffuse proliferation of centrocyte-like cells, plasma cells at the periphery of the lymphocytic infiltration, monotypic restriction of the light chains, and gene rearrangement of the immunoglobulin heavy chain.
  • Pseudolymphomatous folliculitis was identified by the presence of activated pilosebaceous units with abundant CD1a-and S-100 protein-positive T-cell-activated dendritic cells.
  • [MeSH-major] Lymphoma / classification. Lymphoma / pathology. Pseudolymphoma / classification. Pseudolymphoma / pathology. Skin Diseases / classification. Skin Diseases / pathology

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  • (PMID = 15948117.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / S100 Proteins
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45. Schenten D, Egert A, Pasparakis M, Rajewsky K: M17, a gene specific for germinal center (GC) B cells and a prognostic marker for GC B-cell lymphomas, is dispensable for the GC reaction in mice. Blood; 2006 Jun 15;107(12):4849-56
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  • [Title] M17, a gene specific for germinal center (GC) B cells and a prognostic marker for GC B-cell lymphomas, is dispensable for the GC reaction in mice.
  • In T-cell-dependent antibody responses, antigen-specific B cells undergo a phase of secondary antibody diversification in germinal centers (GCs).
  • Aberrant SHM or CSR is thought to contribute to the development of GC-derived B-cell malignancies.
  • Diffuse large B-cell lymphomas (DLBCLs) are a heterogeneous group of such GC-derived tumors.
  • Based on their gene expression profile, DLBCLs can be divided into activated B-cell-like and GC-like subgroups.
  • It is also part of the gene expression signature of GC-like DLBCL, and its high expression in DLBCL has been associated with a better clinical prognosis.
  • The mutant animals form normal GCs, undergo efficient CSR and SHM, and mount T-cell-dependent antibody responses similar to wild-type controls.
  • Thus, M17 is dispensable for the GC reaction, and its potential function in the pathogenesis of DLBCL remains elusive.


46. Lu X, Nechushtan H, Ding F, Rosado MF, Singal R, Alizadeh AA, Lossos IS: Distinct IL-4-induced gene expression, proliferation, and intracellular signaling in germinal center B-cell-like and activated B-cell-like diffuse large-cell lymphomas. Blood; 2005 Apr 1;105(7):2924-32
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  • [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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47. 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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  • [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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48. 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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  • [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.


49. Feuring-Buske M, Hartmann EM, Ott G, Reuter H, Buske C, Rosenwald A: [DNA-chips in the diagnosis of hematological malignancies]. Internist (Berl); 2006 Jan;47(1):39-46
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  • In hematological malignancies, gene expression profiling using DNA-microarrays led to the discovery of novel lymphoma and leukemia subgroups.
  • The heterogeneous entity of diffuse large B-cell lymphoma could be subdivided into the germinal center B-cell-like and the activated B-cell-like subtype which differ in pathogenesis and clinical behavior.
  • In leukemia, existing entities defined by morphological, cytogenetic, molecular and immunophenotypic criteria were confirmed on the global gene expression level; in addition, new important molecular subgroups could be identified.
  • In retrospective clinical lymphoma and leukemia studies, robust gene expression signatures were discovered that predict the clinical course at the time of diagnosis.
  • [MeSH-major] Biomarkers, Tumor / analysis. Leukemia / diagnosis. Leukemia / metabolism. Lymphoma / diagnosis. Lymphoma / metabolism. Neoplasm Proteins / analysis. Oligonucleotide Array Sequence Analysis / methods
  • [MeSH-minor] Gene Expression Profiling / methods. Humans

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  • (PMID = 16247632.001).
  • [ISSN] 0020-9554
  • [Journal-full-title] Der Internist
  • [ISO-abbreviation] Internist (Berl)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  • [Number-of-references] 27
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50. 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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  • [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


51. 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
  •  go-up   go-down


52. Bai M, Skyrlas A, Agnantis NJ, Kamina S, Papoudou-Bai A, Kitsoulis P, Kanavaros P: B-cell differentiation, apoptosis and proliferation in diffuse large B-cell lymphomas. Anticancer Res; 2005 Jan-Feb;25(1A):347-62
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  • [Title] B-cell differentiation, apoptosis and proliferation in diffuse large B-cell lymphomas.
  • Diffuse large B-cell lymphomas (DLBCL) represent the most common type of adult non-Hodgkin's lymphomas in Western countries and are characterized by heterogeneous clinical, histological, immunophenotypic and genetic features.
  • Recent investigations using cDNA and oligonucleotide microarrays have identified molecularly distinct groups of DLBCL with respect to the B-cell differentiation gene expression profile: the germinal center (GC) B-cell-like DLBCL, the activated B-cell-like DLBCL and the type 3 DLBCL.
  • The GC B-cell-like DLBCL were characterized by the expression of genes of the normal GC B-cells, the activated B-cell-like DLBCL were characterized by the expression of genes that are normally induced luring in vitro activation of peripheral blood B-cells, while the type 3 DLBCL did not express either set of genes at a high level.
  • Patients with GC B-cell-like DLBCL had more favorable clinical outcome than those with activated B-cell-like or type 3 DLBCL.
  • Immunohistochemical studies have shown that the bc16/CD10/MUM1/CD138 B-cell differentiation immunophenotypes are prognostically relevant and may predict the cDNA classification in a sizable fraction of DLBCL.
  • In the last few years, there has been accumulating molecular and immunohistochemical evidence indicating links between B-cell differentiation gene expression profiles and expression of apoptosis and cell cycle-associated genes in DLBCL.
  • The present review summarizes data with respect to the relationships between B-cell differentiation, apoptosis and proliferation in DLBCL.
  • [MeSH-major] B-Lymphocytes / pathology. Lymphoma, B-Cell / genetics. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Animals. Apoptosis / genetics. Cell Differentiation / genetics. Humans. Oligonucleotide Array Sequence Analysis

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  • (PMID = 15816558.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Greece
  • [Number-of-references] 163
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53. 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


54. 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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  • [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


55. 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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56. Baecklund E, Backlin C, Iliadou A, Granath F, Ekbom A, Amini RM, Feltelius N, Enblad G, Sundström C, Klareskog L, Askling J, Rosenquist R: Characteristics of diffuse large B cell lymphomas in rheumatoid arthritis. Arthritis Rheum; 2006 Dec;54(12):3774-81
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  • [Title] Characteristics of diffuse large B cell lymphomas in rheumatoid arthritis.
  • OBJECTIVE: Patients with rheumatoid arthritis (RA) are at increased risk of malignant lymphomas, with a correlation between RA disease severity and lymphoma risk, most pronounced for diffuse large B cell lymphomas (DLBCLs), which also constitute the majority of RA-associated lymphomas.
  • DLBCLs can be further subdivided into germinal center (GC)-like and non-GC-like subtypes, with different cellular origins and prognoses.
  • This study was undertaken to investigate whether RA displays a specific association with any of the DLBCL subtypes.
  • METHODS: We identified 139 patients with DLBCLs within a population-based case-control study of 378 RA patients with lymphoma.
  • The DLBCLs were examined for CD10, Bcl-6, and interferon regulatory factor 4 expression patterns, subclassified into GC and non-GC subtypes, and then correlated with clinical parameters.
  • These patients more often had an advanced stage of lymphoma at diagnosis and had a worse 5-year overall survival rate (16% versus 33%) compared with patients with the GC subtype.
  • CONCLUSION: These findings suggest that severe RA is particularly associated with the non-GC subtype of DLBCL, and indicate a critical role of activated peripheral B cells as the cells of origin in these lymphomas.
  • [MeSH-major] Arthritis, Rheumatoid / complications. Lymphoma, B-Cell / complications. Lymphoma, Large B-Cell, Diffuse / complications

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  • (PMID = 17133544.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-4; EC 3.4.24.11 / Neprilysin
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57. 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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58. Booman M, Douwes J, Glas AM, de Jong D, Schuuring E, Kluin PM: Primary testicular diffuse large B-cell lymphomas have activated B-cell-like subtype characteristics. J Pathol; 2006 Oct;210(2):163-71
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  • [Title] Primary testicular diffuse large B-cell lymphomas have activated B-cell-like subtype characteristics.
  • Diffuse large B-cell lymphomas (DLBCLs) constitute a heterogeneous group of lymphomas in which germinal centre B-cell-like and activated B-cell-like subtypes can be discerned based on pathology, clinical presentation, and gene expression patterns.
  • In the present study, cDNA microarray analysis, immunohistochemistry for CD10, Bcl6 and MUM1, and somatic hypermutation analysis of the immunoglobulin heavy chain gene rearrangements were used to determine the subtype of primary testicular DLBCL.
  • Immunohistochemistry revealed 14/22 testicular DLBCLs with an activated B-cell-like immunophenotype and 8/22 with an ambiguous immunophenotype co-expressing CD10 and high levels of MUM1. cDNA microarray analysis of these 22 and four additional cases showed a uniform activated B-cell-like gene expression pattern for both immunophenotypes.
  • It is concluded that primary testicular DLBCLs have uniform activated B-cell-like subtype characteristics despite a number of cases showing an ambiguous immunophenotype.
  • [MeSH-major] B-Lymphocytes / immunology. Lymphocyte Activation. Lymphoma, B-Cell / immunology. Lymphoma, Large B-Cell, Diffuse / immunology. Testicular Neoplasms / immunology

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  • (PMID = 16823896.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / DNA, Neoplasm; 0 / Immunoglobulin Variable Region; 0 / Interferon Regulatory Factors; 0 / Neoplasm Proteins; 0 / interferon regulatory factor-4; EC 3.4.24.11 / Neprilysin
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59. Montesinos-Rongen M, Brunn A, Bentink S, Basso K, Lim WK, Klapper W, Schaller C, Reifenberger G, Rubenstein J, Wiestler OD, Spang R, Dalla-Favera R, Siebert R, Deckert M: Gene expression profiling suggests primary central nervous system lymphomas to be derived from a late germinal center B cell. Leukemia; 2008 Feb;22(2):400-5
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  • [Title] Gene expression profiling suggests primary central nervous system lymphomas to be derived from a late germinal center B cell.
  • To characterize the molecular origin of primary lymphomas of the central nervous system (PCNSL), 21 PCNSLs of immunocompetent patients were investigated by microarray-based gene expression profiling.
  • Comparison of the transcriptional profile of PCNSL with various normal and neoplastic B-cell subsets demonstrated PCNSL (i) to display gene expression patterns most closely related to late germinal center B cells, (ii) to display a gene expression profile similar to systemic diffuse large B-cell lymphomas (DLBCLs) and (iii) to be in part assigned to the activated B-cell-like (ABC) or the germinal center B-cell-like (GCB) subtype of DLBCL.
  • [MeSH-major] B-Lymphocytes / pathology. Central Nervous System Neoplasms / genetics. Gene Expression Profiling. Germinal Center / pathology. Lymphoma / genetics
  • [MeSH-minor] Aged. Aged, 80 and over. Female. Humans. Immunocompetence. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology. Male. Microarray Analysis. Middle Aged

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  • (PMID = 17989719.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K23 CA100291
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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60. 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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61. Nyman H, Jerkeman M, Karjalainen-Lindsberg ML, Banham AH, Leppä S: Prognostic impact of activated B-cell focused classification in diffuse large B-cell lymphoma patients treated with R-CHOP. Mod Pathol; 2009 Aug;22(8):1094-101
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  • [Title] Prognostic impact of activated B-cell focused classification in diffuse large B-cell lymphoma patients treated with R-CHOP.
  • Gene expression profiling studies initially enabled diffuse large B-cell lymphoma to be divided into germinal center and activated B-cell-like subtypes, which define high- and low-risk patient groups when treated with chemotherapy.
  • The aim of this study was to determine whether modified immunohistochemical classification of cell of origin focusing on activated B-cell-like markers could be used to predict the outcome of immunochemotherapy-treated diffuse large B-cell lymphoma patients.
  • The expression of CD10, Bcl-6, MUM1/IRF4, Bcl-2, and FOXP1 was determined immunohistochemically from 88 samples of diffuse large B-cell lymphoma patients treated uniformly with R-CHOP.
  • When the modified classification using MUM1/IRF4 and FOXP1 positivities as activated B-cell-like markers was applied to distinguish the patients between the activated B-cell-like and other diffuse large B-cell lymphoma subtypes, a significantly worse outcome was seen for the patients with the activated B-cell-like phenotype (3-year failure-free survival 63 vs 82%, P=0.048, overall survival 69 vs 85%, P=0.110).
  • In conclusion, the data suggest that both the modified activated B-cell-like and Muris classifications define the non-germinal center phenotype as an adverse risk factor in R-CHOP-treated diffuse large B-cell lymphoma patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. B-Lymphocytes / pathology. Lymphoma, Large B-Cell, Diffuse / classification. Lymphoma, Large B-Cell, Diffuse / immunology. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Algorithms. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal, Murine-Derived. Biomarkers, Tumor / analysis. Cyclophosphamide / therapeutic use. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / genetics. Doxorubicin / therapeutic use. Forkhead Transcription Factors / biosynthesis. Forkhead Transcription Factors / genetics. Gene Expression. Gene Expression Profiling. Humans. Immunohistochemistry. Interferon Regulatory Factors / biosynthesis. Interferon Regulatory Factors / genetics. Kaplan-Meier Estimate. Lymphocyte Activation / immunology. Neprilysin / biosynthesis. Neprilysin / genetics. Phenotype. Prednisolone / therapeutic use. Prognosis. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Proto-Oncogene Proteins c-bcl-2 / genetics. Repressor Proteins / biosynthesis. Repressor Proteins / genetics. Rituximab. Vincristine / therapeutic use

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  • (PMID = 19448593.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / FOXP1 protein, human; 0 / Forkhead Transcription Factors; 0 / Interferon Regulatory Factors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Repressor Proteins; 0 / interferon regulatory factor-4; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; EC 3.4.24.11 / Neprilysin; VAP-cyclo protocol
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62. 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
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  • [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


63. 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
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  • [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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64. 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


65. Choi WW, Weisenburger DD, Greiner TC, Piris MA, Banham AH, Delabie J, Braziel RM, Geng H, Iqbal J, Lenz G, Vose JM, Hans CP, Fu K, Smith LM, Li M, Liu Z, Gascoyne RD, Rosenwald A, Ott G, Rimsza LM, Campo E, Jaffe ES, Jaye DL, Staudt LM, Chan WC: A new immunostain algorithm classifies diffuse large B-cell lymphoma into molecular subtypes with high accuracy. Clin Cancer Res; 2009 Sep 1;15(17):5494-502
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  • [Title] A new immunostain algorithm classifies diffuse large B-cell lymphoma into molecular subtypes with high accuracy.
  • PURPOSE: Hans and coworkers previously developed an immunohistochemical algorithm with approximately 80% concordance with the gene expression profiling (GEP) classification of diffuse large B-cell lymphoma (DLBCL) into the germinal center B-cell-like (GCB) and activated B-cell-like (ABC) subtypes.
  • EXPERIMENTAL DESIGN: We studied 84 cases of cyclophosphamide-doxorubicin-vincristine-prednisone (CHOP)-treated DLBCL (47 GCB, 37 ABC) with GCET1, CD10, BCL6, MUM1, FOXP1, BCL2, MTA3, and cyclin D2 immunostains, and compared different combinations of the immunostaining results with the GEP classification.
  • A separate set of 63 DLBCL cases treated with rituximab plus CHOP (37 GCB, 26 ABC) was used to validate the new algorithm.
  • The new algorithm predicted 3-year overall survival of the validation set [GCB (87%) versus ABC (44%); P < 0.001], simulating the predictive power of the GEP classification.
  • For a group of seven primary mediastinal large B-cell lymphoma, the new algorithm is a better prognostic classifier (all "GCB") than the Hans' algorithm (two GCB, five non-GCB).
  • CONCLUSION: Our new algorithm is significantly more accurate than the Hans' algorithm and will facilitate risk stratification of DLBCL patients and future DLBCL research using archival materials.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Immunohistochemistry / methods. Lymphoma, Large B-Cell, Diffuse / classification
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Algorithms. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Female. Gene Expression Profiling. Germinal Center / metabolism. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prednisone / therapeutic use. Vincristine / therapeutic use


66. 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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  • [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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67. 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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68. 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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69. Chen Y, Han T, Iqbal J, Irons R, Chan WC, Zhu X, Fu K: Diffuse large B-cell lymphoma in Chinese patients: immunophenotypic and cytogenetic analyses of 124 cases. Am J Clin Pathol; 2010 Feb;133(2):305-13
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  • [Title] Diffuse large B-cell lymphoma in Chinese patients: immunophenotypic and cytogenetic analyses of 124 cases.
  • In diffuse large B-cell lymphoma (DLBCL), BCL2 expression usually correlates with the t(14;18) (q32;q21) in germinal center B-cell (GCB) subtype and with gain/amplification of chromosome 18q21 in the activated B cell-like subtype.
  • We studied 124 Chinese DLBCL cases using immunohistochemical, conventional cytogenetics, and interphase fluorescence in situ hybridization analyses.
  • A cohort of 114 well-characterized DLBCL cases from Western populations was also analyzed for comparison.
  • BCL2 expression was associated with gain of chromosome 18/18q in the Chinese and Western cohorts.
  • More interestingly, BCL2 expression was associated with gain of chromosome 3/3q in Chinese DLBCL cases, whereas this association was less significant in Western cases.
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 18. Chromosomes, Human, Pair 3. Gene Amplification. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / immunology. Translocation, Genetic

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  • (PMID = 20093241.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.24.11 / Neprilysin
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70. 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
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  • 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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71. Kemmerling R, Stintzing S, Mühlmann J, Dietze O, Neureiter D: Primary testicular lymphoma: a strictly homogeneous hematological disease? Oncol Rep; 2010 May;23(5):1261-7
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  • [Title] Primary testicular lymphoma: a strictly homogeneous hematological disease?
  • Primary testicular lymphomas display mostly aggressive diffuse large cell B-cell lymphomas, which could be further subclassified into germinal center B-cell-like and an activated B-cell phenotype via immunohistochemistry.
  • We found 18 cases of primary testicular lymphoma diagnosed in elderly patients showing no side predilection and having an aggressive clinical behavior with short overall survival independent of treatment.
  • The lymphomas could for the most be classified into diffuse large cell B-cell lymphomas [15/18 (83.3%)] showing a non-significant prevalence of activated B cell phenotype [9/15 (60%)] compared to the germinal centre phenotype [6/15 (40%)].
  • Two of the cases were mantle cell lymphomas consisting of the infrequent pleomorphic subtype.
  • Primary testicular lymphomas are for the most DLBCL, but subtype classification reveal molecular heterogeneity inside this lymphoma entity.
  • [MeSH-major] Biomarkers, Tumor / analysis. Lymphoma, Large B-Cell, Diffuse / chemistry. Lymphoma, Mantle-Cell / chemistry. Testicular Neoplasms / chemistry

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  • (PMID = 20372839.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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72. Liu YH, Li L, Liu G, Zhuang HG, Luo DL, Luo XL, Xu J: [Gene expression profiling of diffuse large B-cell lymphoma in China]. Zhonghua Bing Li Xue Za Zhi; 2007 Feb;36(2):79-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Gene expression profiling of diffuse large B-cell lymphoma in China].
  • OBJECTIVE: Gene expression profiling of diffuse large B-cell lymphoma (DLBCL) of different immunophenotypes.
  • METHODS: The study included 156 cases of DLBCL, which were subclassified by immunohistochemistry including CD10, bcl-6 and MUM1.
  • Affymetrix U133 plus2.0 oligonucleotide microarrays were used to obtain differential gene expression profiling of 9 DLBCL (3 representative cases from each immunophenotypical group) and 3 tonsils.
  • RESULTS: The immunohistochemistry subclassified 156 cases of DLBCL into 3 groups: CD10(+) and/or bcl-6(+), MUM1(-) (group 1); CD10(+) and/or bcl-6(+), MUM1(+) (group 2); CD10(-) and bcl-6(-), MUM1(+) (group 3).
  • By gene expression array, 9 lymphomas and 3 tonsils were clustered in an unsupervised fashion into 4 groups (A, B, C and D), which were in accordance with the immunophenotypical groups (group 1, 2, 3 and normal).
  • A total of 81 genes were markedly decreased and 86 genes were over-expressed in all DLBCL groups.
  • Although Group B lymphomas showed mixed immunophenotypical features of both germinal center B-cell-like DLBCL (Group A) and activated B-cell-like lymphomas (Group C), gene profile clustering showed that Group B was dissimilar to Group A or Group C, with 45 over-expressed and 27 uniquely expressed genes.
  • CONCLUSIONS: Gene expression profiling indicates that DLBCL can be subgrouped at the molecular level and can be identified by immunophenotyping.
  • The gene expression profile of Group B lymphomas suggests that factors other than the cell-of-origin may contribute to the pathogenesis of DLBCL.
  • [MeSH-major] Gene Expression Profiling. Immunophenotyping / methods. Lymphoma, Large B-Cell, Diffuse / genetics

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  • (PMID = 17493379.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Interferon Regulatory Factors; 0 / Proto-Oncogene Proteins c-bcl-6; 0 / interferon regulatory factor-4; EC 3.4.24.11 / Neprilysin
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73. Kluiver J, Poppema S, de Jong D, Blokzijl T, Harms G, Jacobs S, Kroesen BJ, van den Berg A: BIC and miR-155 are highly expressed in Hodgkin, primary mediastinal and diffuse large B cell lymphomas. J Pathol; 2005 Oct;207(2):243-9
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  • [Title] BIC and miR-155 are highly expressed in Hodgkin, primary mediastinal and diffuse large B cell lymphomas.
  • In a previous study we demonstrated high expression of the non-coding BIC gene in the vast majority of Hodgkin's lymphomas (HLs).
  • We therefore analysed HL cell lines and tissue samples to determine whether miR-155 is also expressed in HL.
  • However, in diffuse large B cell lymphoma (DLBCL) and primary mediastinal B cell lymphoma (PMBL), significant percentages of positive tumour cells were observed in 12/18 and 8/8 cases.
  • A higher proportion of tumour cells were positive for BIC in DLBCL with activated B cell-like phenotype than in DLBCL with germinal centre B cell-like phenotype.
  • Differential BIC expression was confirmed by qRT-PCR analysis.
  • Northern blot analysis showed expression of miR-155 in all DLBCL and PMBL derived cell lines and tissue samples analysed.
  • In summary, we demonstrate expression of primary microRNA BIC and its derivative miR-155 in HL, PMBL and DLBCL.
  • [MeSH-major] Lymphoma / genetics. Mediastinal Neoplasms / genetics. MicroRNAs / genetics. Receptors, Antigen, B-Cell / genetics
  • [MeSH-minor] Cell Line, Tumor. Hodgkin Disease / genetics. Humans. Immunohistochemistry / methods. In Situ Hybridization / methods. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. RNA, Neoplasm / genetics. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • [Copyright] Copyright (c) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 16041695.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / RNA, Neoplasm; 0 / Receptors, Antigen, B-Cell
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74. 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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  • [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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75. Tsirigotis P, Economopoulos T: Monoclonal antibodies in the treatment of lymphoid malignancies. J Steroid Biochem Mol Biol; 2008 Feb;108(3-5):267-71
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  • Rit is a chimeric mouse/human monoclonal antibody, consisting of the human IgG1 and k constant Fc region, and a mouse variable Fab region specific against the B-cell antigen CD20.
  • Effector cytotoxic cells such as natural killer cells (NK) are activated after binding to the Fc portion of the anti-CD20 molecule.
  • Activated NK cells kill the coated lymphoma cells with the use of granzyme-perforin system.
  • More recently, pre-clinical data support the concept that Rituximab can provoke a vaccination-like effect.
  • The relative contribution of these mechanisms in vivo and in different lymphoma subtypes is not well known and remains to be further evaluated.
  • Among the different histological groups, follicular lymphoma (FL) has been proven to be the most sensitive to Rit when used as a single agent, with overall response rates of 80% and 50% in untreated and previously treated patients, respectively.
  • Similarly, the addition of Rit to standard chemotherapy improves the disease-free and overall survival of patients with diffuse large B-cell lymphoma.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Lymphoma / drug therapy
  • [MeSH-minor] Antibodies, Bispecific / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antigens, CD20 / immunology. Antigens, CD20 / metabolism. Humans. Lymphoma, Follicular / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy. Rituximab

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  • (PMID = 17935974.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Bispecific; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 30
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76. Liu YH, Xu FP, Zhuang HG, Lai KC, Xie D, Luo DL, Li L, Luo XL, Xu J, Zhang MH, Zhang F, Li HM: Clinicopathologic significance of immunophenotypic profiles related to germinal center and activation B-cell differentiation in diffuse large B-cell lymphoma from Chinese patients. Hum Pathol; 2008 Jun;39(6):875-84
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  • [Title] Clinicopathologic significance of immunophenotypic profiles related to germinal center and activation B-cell differentiation in diffuse large B-cell lymphoma from Chinese patients.
  • Diffuse large B-cell lymphoma (DLBCL) can be subdivided into prognostically significant groups with germinal center B-cell-like (GCB), activated B-cell-like (ABC), and type 3 groups.
  • One hundred forty-nine of 163 DLBCLs could then be classified into GCB group (pattern A), activated GCB group (pattern B) and activated non-GCB group (pattern C) according to the expression of CD10, Bcl-6, MUM1, and CD138.
  • Of the 149 cases, 40 (26%) showed pattern A expression and were grouped as GCB group, lower than reported frequency of the studies involving mostly Western population.
  • Compared with cases with pattern A, those with pattern B (activated GCB group) and C (activated non-GCB group) more often presented with more aggressive tumors and a shorter survival time.
  • These results indicate that most of DLBCLs from Chinese patients can be classified into prognostically different groups based on the antigenic expression models using a panel of GCB- and ABC-associated markers.
  • The translocation was significantly associated with expression of Bcl-2 protein.
  • The group with pattern B demonstrated more frequent expression of Ki-67, cyclin D3, geminin, and showed higher proliferative activity than the group with pattern A.
  • These findings suggest that high proliferative activity of tumors with pattern B may be associated with aggressive tumor behavior and poor clinical outcome in patients with DLBCL.
  • [MeSH-major] B-Lymphocytes / immunology. Cell Transformation, Neoplastic. Germinal Center / pathology. Lymph Nodes / pathology. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Cell Proliferation. Child. Child, Preschool. China. Female. Humans. Immunophenotyping. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Survival Rate. Tissue Array Analysis


77. Saad AA, Awed NM, Abdel-Hafeez ZM, Kamal GM, Elsallaly HM, Alloub AI: Prognostic value of immunohistochemical classification of diffuse large B-cell lymphoma into germinal center B-cell and non-germinal center B-cell subtypes. Saudi Med J; 2010 Feb;31(2):135-41
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  • [Title] Prognostic value of immunohistochemical classification of diffuse large B-cell lymphoma into germinal center B-cell and non-germinal center B-cell subtypes.
  • OBJECTIVE: To study the expression of germinal center B-cell (GCB)/activated B-cell like-related proteins to get optimal stratification of diffuse large B-cell lymphoma (DLBCL) patients, and correlate this with the established clinical and laboratory parameters.
  • METHODS: This study was conducted retrospectively on 30 archival paraffin tissue blocks of DLBCL.
  • Each case included in this study was investigated by immunohistochemical reaction for multiple myeloma-1/interferon regulatory factor-4, B-cell/lymphoma 6, and cluster of differentiation10 monoclonal antibodies.
  • CONCLUSION: The subclassification of DLBCL into GCB and non-GCB groups using immunohistochemistry may be useful for identifying those patients whose prognosis is so poor that more aggressive therapy can be given at the time of diagnosis.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / classification

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  • (PMID = 20174727.001).
  • [ISSN] 0379-5284
  • [Journal-full-title] Saudi medical journal
  • [ISO-abbreviation] Saudi Med J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Saudi Arabia
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78. 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
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  • [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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79. 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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80. Lu X, Malumbres R, Shields B, Jiang X, Sarosiek KA, Natkunam Y, Tiganis T, Lossos IS: PTP1B is a negative regulator of interleukin 4-induced STAT6 signaling. Blood; 2008 Nov 15;112(10):4098-108
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  • We demonstrate that IL-4 induces PTP1B mRNA expression in a phosphatidylinositol 3-kinase-dependent manner and enhances PTP1B protein stability to suppress IL-4-induced STAT6 signaling.
  • Finally, we show that PTP1B expression may be preferentially elevated in activated B cell-like diffuse large B-cell lymphomas.
  • [MeSH-minor] Animals. Enzyme Inhibitors / pharmacology. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Enzymologic / genetics. Gene Expression Regulation, Enzymologic / immunology. HeLa Cells. Humans. Inflammation / genetics. Inflammation / immunology. Inflammation / metabolism. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / immunology. Lymphoma, Large B-Cell, Diffuse / metabolism. Mice. Mice, Knockout. Mutation, Missense. Phosphatidylinositol 3-Kinases / genetics. Phosphatidylinositol 3-Kinases / immunology. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation / drug effects. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Messenger / metabolism. STAT5 Transcription Factor / genetics. STAT5 Transcription Factor / immunology. STAT5 Transcription Factor / metabolism. Staurosporine / pharmacology. TYK2 Kinase / genetics. TYK2 Kinase / immunology. TYK2 Kinase / metabolism. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / immunology. Tumor Suppressor Proteins / metabolism

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  • (PMID = 18716132.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109335; United States / NCI NIH HHS / CA / R01 CA122105
  • [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 / Enzyme Inhibitors; 0 / IL4 protein, human; 0 / RNA, Messenger; 0 / STAT5 Transcription Factor; 0 / STAT5A protein, human; 0 / STAT5B protein, human; 0 / STAT6 Transcription Factor; 0 / STAT6 protein, human; 0 / Stat5a protein, mouse; 0 / Stat5b protein, mouse; 0 / Stat6 protein, mouse; 0 / Tumor Suppressor Proteins; 207137-56-2 / Interleukin-4; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.2 / TYK2 Kinase; EC 2.7.10.2 / TYK2 protein, human; EC 2.7.10.2 / Tyk2 protein, mouse; EC 3.1.3.48 / PTPN1 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 1; EC 3.1.3.48 / Ptpn1 protein, mouse; H88EPA0A3N / Staurosporine
  • [Other-IDs] NLM/ PMC2582009
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81. Feuerhake F, Kutok JL, Monti S, Chen W, LaCasce AS, Cattoretti G, Kurtin P, Pinkus GS, de Leval L, Harris NL, Savage KJ, Neuberg D, Habermann TM, Dalla-Favera R, Golub TR, Aster JC, Shipp MA: NFkappaB activity, function, and target-gene signatures in primary mediastinal large B-cell lymphoma and diffuse large B-cell lymphoma subtypes. Blood; 2005 Aug 15;106(4):1392-9
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  • [Title] NFkappaB activity, function, and target-gene signatures in primary mediastinal large B-cell lymphoma and diffuse large B-cell lymphoma subtypes.
  • Primary mediastinal large B-cell lymphoma (MLBCL) shares important clinical and molecular features with classic Hodgkin lymphoma, including nuclear localization of the nuclear factor kappaB (NFkappaB) subunit c-REL (reticuloendotheliosis viral oncogene homolog) in a pilot series.
  • Herein, we analyzed c-REL subcellular localization in additional primary MLBCLs and characterized NFkappaB activity and function in a MLBCL cell line.
  • The new primary MLBCLs had prominent c-REL nuclear staining, and the MLBCL cell line exhibited high levels of NFkappaB binding activity.
  • MLBCL cells expressing a superrepressor form of inhibitor of kappa B alpha signaling (IkappaB alpha) had a markedly higher rate of apoptosis, implicating constitutive NFkappaB activity in MLBCL cell survival.
  • The transcriptional profiles of newly diagnosed primary MLBCLs and diffuse large B-cell lymphomas (DLBCLs) were then used to characterize the NFkappaB target gene signatures of MLBCL and specific DLBCL subtypes.
  • MLBCLs expressed increased levels of NFkappaB targets that promote cell survival and favor antiapoptotic tumor necrosis factor alpha (TNFalpha) signaling.
  • In contrast, activated B cell (ABC)-like DLBCLs had a more restricted, potentially developmentally regulated, NFkappaB target gene signature.
  • Of interest, the newly characterized host response DLBCL subtype had a robust NFkappaB target gene signature that partially overlapped that of primary MLBCL.
  • In this large series of primary MLBCLs and DLBCLs, NFkappaB activation was not associated with amplification of the cREL locus, suggesting alternative pathogenetic mechanisms.
  • [MeSH-major] Gene Expression Regulation, Neoplastic. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Mediastinal Neoplasms / pathology. NF-kappa B / physiology. Proto-Oncogene Proteins c-rel / genetics
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Gene Expression Profiling. Humans

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  • (PMID = 15870177.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Proto-Oncogene Proteins c-rel
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82. Ngo VN, Davis RE, Lamy L, Yu X, Zhao H, Lenz G, Lam LT, Dave S, Yang L, Powell J, Staudt LM: A loss-of-function RNA interference screen for molecular targets in cancer. Nature; 2006 May 4;441(7089):106-10
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  • We used a doxycycline-inducible retroviral vector for the expression of small hairpin RNAs (shRNAs) to construct a library targeting 2,500 human genes.
  • We used retroviral pools from this library to infect cell lines representing two distinct molecular subgroups of diffuse large B-cell lymphoma (DLBCL), termed activated B-cell-like DLBCL and germinal centre B-cell-like DLBCL.
  • We observed that a subset of shRNA vectors was depleted from the transduced cells after three weeks in culture only if shRNA expression was induced.
  • In activated B-cell-like DLBCL cells, but not germinal centre B-cell-like DLBCL cells, shRNAs targeting the NF-kappaB pathway were depleted, in keeping with the essential role of this pathway in the survival of activated B-cell-like DLBCL.
  • This screen uncovered CARD11 as a key upstream signalling component responsible for the constitutive IkappaB kinase activity in activated B-cell-like DLBCL.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / deficiency. Adaptor Proteins, Signal Transducing / genetics. Adaptor Proteins, Signal Transducing / metabolism. Apoptosis Regulatory Proteins / deficiency. Apoptosis Regulatory Proteins / genetics. Apoptosis Regulatory Proteins / metabolism. CARD Signaling Adaptor Proteins. Caspases. Cell Line, Tumor. Cell Proliferation. Cell Survival / genetics. Drug Design. Guanylate Cyclase / deficiency. Guanylate Cyclase / genetics. Guanylate Cyclase / metabolism. Humans. Lymphoma, B-Cell / genetics. Lymphoma, B-Cell / metabolism. Lymphoma, B-Cell / pathology. Lymphoma, B-Cell, Marginal Zone / genetics. Lymphoma, B-Cell, Marginal Zone / metabolism. NF-kappa B / metabolism. Neoplasm Proteins / deficiency. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Substrate Specificity

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  • [CommentIn] Nature. 2006 May 4;441(7089):32-4 [16672958.001]
  • (PMID = 16572121.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE3896
  • [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] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Apoptosis Regulatory Proteins; 0 / BCL10 protein, human; 0 / CARD Signaling Adaptor Proteins; 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
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83. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Microarray-based classification of diffuse large B-cell lymphoma.
  • OBJECTIVE: Hierarchical clusterings of diffuse large B-cell lymphoma (DLBCL) based on gene expression signatures have previously been used to classify DLBCL into Germinal Center B-cell (GCB) and Activated B-cell (ABC) types.
  • To examine if it was feasible to perform a cross-platform validation on the Affymetrix HG-U133A oligonucleotide arrays and improve the classification, we determined the expression profiles of pretreatment, diagnostic samples from 52 primary nodal DLBCL.
  • In this way, three subtypes, including the GCB type (n = 20), the ABC type (n = 25) and an intermediate group, Type-3 (n = 5), were distinguished.
  • The CD10 and Bcl-6 expression as well as t(14;18) translocation were prevalent, but not exclusive to the GCB type.
  • By contrast, MUM1 was only expressed in the ABC and in Type-3 samples.
  • The 5-year survival was similar between the groups, but GCB patients showed a better initial response to CHOP or CHOP-like regimens than the remaining patients and tended to have less advanced disease and lower IPI scores.
  • As a next step, an improved set of classifier genes was generated by analysis of 34 patients that were consistently classified as GCB or ABC in the above analyses.
  • CONCLUSION: We conclude that gene expression profiling with Affymetrix Genechips is efficient to distinguish between GCB and ABC types of DLBCL and that these are likely to represent separate biological entities.
  • The Genechip platform is highly standardised and therefore useful for future prospective investigations to establish the value of gene expression profiling in the clinical management of DLBCL.
  • [MeSH-major] Gene Expression Regulation, Leukemic. Lymphoma, Large B-Cell, Diffuse / classification. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. B-Lymphocytes / pathology. Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 18 / genetics. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / genetics. Female. Gene Expression Profiling. Germinal Center / pathology. Humans. Lymphocyte Activation. Male. Middle Aged. Neprilysin / biosynthesis. Neprilysin / genetics. Translocation, Genetic / genetics

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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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84. Bhattacharyya I, Chehal HK, Cohen DM, Al-Quran SZ: Primary diffuse large B-cell lymphoma of the oral cavity: germinal center classification. Head Neck Pathol; 2010 Sep;4(3):181-91
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  • [Title] Primary diffuse large B-cell lymphoma of the oral cavity: germinal center classification.
  • Primary lymphomas of the oral cavity are rare and the most frequent type is diffuse large B-cell lymphoma (DLBCL).
  • Recently, several reports have highlighted the value of classifying DLBCL into prognostically important subgroups, namely germinal center B-cell like (GCB) and non-germinal center B-cell like (non-GCB) lymphomas based on gene expression profiles and by immunohistochemical expression of CD10, BCL6 and MUM-1.
  • Studies validating this classification have been done for DLBCL of the breast, CNS, testes and GI tract.
  • IHC was performed using antibodies against germinal center markers (CD10, BCL6), activated B-cell markers (MUM1, BCL2) and Ki-67 (proliferation marker).
  • In conclusion, our analysis shows that primary oral DLBCL predominantly belongs to the non-GCB subgroup, which tends to exhibit a poorer prognosis.
  • [MeSH-major] Germinal Center / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Mouth Neoplasms / pathology

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  • (PMID = 20533006.001).
  • [ISSN] 1936-0568
  • [Journal-full-title] Head and neck pathology
  • [ISO-abbreviation] Head Neck Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Interferon Regulatory Factors; 0 / Ki-67 Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / interferon regulatory factor-4; EC 3.4.24.11 / Neprilysin
  • [Other-IDs] NLM/ PMC2923304
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85. 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.