An oncogenic role for alternative NF-κB signaling in DLBCL revealed upon deregulated BCL6 expression
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Baochun Zhang Dinis Calado Zhe Wang Sebastian Fröhler Karl Köchert Yu Qian Sergei B Koralov Marc Schmidt-Supprian Yoshiteru Sasaki Christine Unitt Scott Rodig Wei Chen Riccardo Dalla-Favera Frederick W Alt Laura Pasqualucci Klaus RajewskyAbstract
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-κB activity, a role for oncogenic lesions that activate the alternative NF-κB pathway in DLBCL has remained elusive. Here, we show that deletion/mutation of TRAF3, a negative regulator of the alternative NF-κB 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-κB pathway cooperates with BCL6 deregulation in DLBCL development. This work demonstrates a key oncogenic role for the alternative NF-κB pathway in DLBCL development.
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Journal Cell Reports
Volume 11
Issue number 5
Pages 715-726
Available online
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Publisher website (DOI) 10.1016/j.celrep.2015.03.059
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Europe PubMed Central 25921526
Pubmed 25921526
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