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Cancers 2015, 7(2), 811-822; doi:10.3390/cancers7020812

Insights into the Molecular Pathogenesis of Activated B-Cell-like Diffuse Large B-Cell Lymphoma and Its Therapeutic Implications

1
Translational Oncology, Department of Medicine A, Albert-Schweitzer Campus 1, University Hospital Münster, 48149 Münster, Germany
2
Cluster of Excellence EXC 1003, Cells in Motion, 48149 Münster, Germany 
Academic Editor: Martin Dreyling
Received: 23 April 2015 / Accepted: 14 May 2015 / Published: 22 May 2015
(This article belongs to the Special Issue Lymphoma)
View Full-Text   |   Download PDF [443 KB, uploaded 22 May 2015]   |  

Abstract

Within the last couple of years, the understanding of the molecular mechanisms that drive the pathogenesis of diffuse large B-cell lymphoma (DLBCL) has significantly improved. Large-scale gene expression profiling studies have led to the discovery of several molecularly defined subtypes that are characterized by specific oncogene addictions and significant differences in their outcome. Next generation sequencing efforts combined with RNA interference screens frequently identify crucial oncogenes that lead to constitutive activation of various signaling pathways that drive lymphomagenesis. This review summarizes our current understanding of the molecular pathogenesis of the activated B-cell-like (ABC) DLBCL subtype that is characterized by poor prognosis. A special emphasis is put on findings that might impact therapeutic strategies of affected patients. View Full-Text
Keywords: ABC DLBCL; NF-B pathway; B-cell receptor signaling; molecular targets ABC DLBCL; NF-B pathway; B-cell receptor signaling; molecular targets
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Lenz, G. Insights into the Molecular Pathogenesis of Activated B-Cell-like Diffuse Large B-Cell Lymphoma and Its Therapeutic Implications. Cancers 2015, 7, 811-822.

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