Helmholtz Gemeinschaft


An oncogenic role for alternative NF-κB signaling in DLBCL revealed upon deregulated BCL6 expression

[img] PDF - Requires a PDF viewer such as GSview, Xpdf or Adobe Acrobat Reader

Item Type:Article
Title:An oncogenic role for alternative NF-κB signaling in DLBCL revealed upon deregulated BCL6 expression
Creators Name:Zhang, B. and Calado, D.P. and Wang, Z. and Froehler, S. and Koechert, K. and Qian, Y. and Koralov, S.B. and Schmidt-Supprian, M. and Sasaki, Y. and Unitt, C. and Rodig, S. and Chen, W. and Dalla-Favera, R. and Alt, F.W. and Pasqualucci, L. and Rajewsky, K.
Abstract:Diffuse large B cell lymphoma (DLBCL) is a complex disease comprising diverse subtypes and genetic profiles. Possibly because of the prevalence of genetic alterations activating canonical NF-{kappa}B activity, a role for oncogenic lesions that activate the alternative NF-{kappa}B pathway in DLBCL has remained elusive. Here, we show that deletion/mutation of TRAF3, a negative regulator of the alternative NF-{kappa}B pathway, occurs in ∼15% of DLBCLs and that it often coexists with BCL6 translocation, which prevents terminal B cell differentiation. Accordingly, in a mouse model constitutive activation of the alternative NF-{kappa}B pathway cooperates with BCL6 deregulation in DLBCL development. This work demonstrates a key oncogenic role for the alternative NF-{kappa}B pathway in DLBCL development.
Keywords:B-Lymphocytes, Cell Differentiation, Cell Survival, Diffuse Large B-Cell Lymphoma, DNA-Binding Proteins, Knockout Mice, Neoplastic Gene Expression Regulation, NF-{kappa} B, Protein-Serine-Threonine Kinases, Signal Transduction, TNF Receptor-Associated Factor 3, Tumor Cell Line, Animals, Mice
Source:Cell Reports
Publisher:Cell Press / Elsevier
Page Range:715-726
Date:5 May 2015
Official Publication:https://doi.org/10.1016/j.celrep.2015.03.059
PubMed:View item in PubMed

Repository Staff Only: item control page


Downloads per month over past year

Open Access
MDC Library