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MYC/BCL2 protein coexpression contributes to the inferior survival of activated B-cell subtype of diffuse large B-cell lymphoma and demonstrates high-risk gene expression signatures: a report from The International DLBCL Rituximab-CHOP Consortium Program.

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Date
2013-05
Authors
Hu, Shimin
Xu-Monette, Zijun Y
Tzankov, Alexander
Green, Tina
Wu, Lin
Balasubramanyam, Aarthi
Liu, Wei-min
Visco, Carlo
Li, Yong
Miranda, Roberto N
Montes-Moreno, Santiago
Dybkaer, Karen
Chiu, April
Orazi, Attilio
Zu, Youli
Bhagat, Govind
Richards, Kristy L
Hsi, Eric D
Choi, William WL
Zhao, Xiaoying
van Krieken, J Han
Huang, Qin
Huh, Jooryung
Ai, Weiyun
Ponzoni, Maurilio
Ferreri, Andrés JM
Zhou, Fan
Slack, Graham W
Gascoyne, Randy D
Tu, Meifeng
Variakojis, Daina
Chen, Weina
Go, Ronald S
Piris, Miguel A
Møller, Michael B
Medeiros, L Jeffrey
Young, Ken H
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Abstract
Diffuse large B-cell lymphoma (DLBCL) is stratified into prognostically favorable germinal center B-cell (GCB)-like and unfavorable activated B-cell (ABC)-like subtypes based on gene expression signatures. In this study, we analyzed 893 de novo DLBCL patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone). We show that MYC/BCL2 protein coexpression occurred significantly more commonly in the ABC subtype. Patients with the ABC or GCB subtype of DLBCL had similar prognoses with MYC/BCL2 coexpression and without MYC/BCL2 coexpression. Consistent with the notion that the prognostic difference between the 2 subtypes is attributable to MYC/BCL2 coexpression, there is no difference in gene expression signatures between the 2 subtypes in the absence of MYC/BCL2 coexpression. DLBCL with MYC/BCL2 coexpression demonstrated a signature of marked downregulation of genes encoding extracellular matrix proteins, those involving matrix deposition/remodeling and cell adhesion, and upregulation of proliferation-associated genes. We conclude that MYC/BCL2 coexpression in DLBCL is associated with an aggressive clinical course, is more common in the ABC subtype, and contributes to the overall inferior prognosis of patients with ABC-DLBCL. In conclusion, the data suggest that MYC/BCL2 coexpression, rather than cell-of-origin classification, is a better predictor of prognosis in patients with DLBCL treated with R-CHOP.
Type
Journal article
Subject
B-Lymphocyte Subsets
Humans
Cyclophosphamide
Vincristine
Doxorubicin
Prednisone
Proto-Oncogene Proteins c-myc
Proto-Oncogene Proteins c-bcl-2
Antineoplastic Combined Chemotherapy Protocols
Prognosis
Risk Factors
Survival Analysis
Retrospective Studies
Cohort Studies
Lymphocyte Activation
Gene Expression Regulation, Neoplastic
International Cooperation
Adult
Aged
Aged, 80 and over
Middle Aged
Female
Male
Lymphoma, Large B-Cell, Diffuse
Antibodies, Monoclonal, Murine-Derived
Transcriptome
Rituximab
Permalink
https://hdl.handle.net/10161/19329
Published Version (Please cite this version)
10.1182/blood-2012-10-460063
Publication Info
Hu, Shimin; Xu-Monette, Zijun Y; Tzankov, Alexander; Green, Tina; Wu, Lin; Balasubramanyam, Aarthi; ... Young, Ken H (2013). MYC/BCL2 protein coexpression contributes to the inferior survival of activated B-cell subtype of diffuse large B-cell lymphoma and demonstrates high-risk gene expression signatures: a report from The International DLBCL Rituximab-CHOP Consortium Program. Blood, 121(20). pp. 4021-4250. 10.1182/blood-2012-10-460063. Retrieved from https://hdl.handle.net/10161/19329.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
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Scholars@Duke

Xu-Monette

Zijun Yidan Xu-Monette

Assistant Professor in Pathology
My research efforts have been focused on identifying prognostic and therapeutic biomarkers in B-cell lymphoma. My research interests also include investigation of molecular and immune mechanisms underlying the poor clinical outcomes of lymphoma, the pathogenesis and evolution of drug resistant clones, and development of novel therapies for aggressive B-cell lymphoma.
Young

Ken H Young

Professor of Pathology
I am a clinically-oriented diagnostic physician with clinical expertise in the pathologic diagnosis of hematologic cancers including tumors of the bone marrow, lymphoid tissue, spleen and pre-malignant hematologic conditions. Another area of interest is blood cancer classification with molecular and genetic profiling. In my research program, we focus on molecular mechanisms of tumor progression, cell-of-origin, biomarkers, and novel therapeutic strategies in lymphoma, myeloma and leukemia. In
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