Journal
CELL REPORTS
Volume 11, Issue 5, Pages 715-726Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2015.03.059
Keywords
-
Categories
Funding
- National Cancer Institute [P01 CA092625, R01 CA098285, CA172492]
- Leukemia & Lymphoma Society SCOR grant
- European Research Council, ERC Advanced Grant [ERC-AG-LS6]
- Leukemia & Lymphoma Society fellowships
- Dana-Farber Cancer Institute Faculty Startup Funds
- Cancer Research UK
- MRC career development award [MR/J008060/1]
- Cancer Research UK [16857] Funding Source: researchfish
- Medical Research Council [MR/J008060/1] Funding Source: researchfish
- The Francis Crick Institute [10057] Funding Source: researchfish
- MRC [MR/J008060/1] Funding Source: UKRI
Ask authors/readers for more resources
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 similar to 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available