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| Item Type: | Article |
|---|---|
| Title: | An oncogenic role for alternative NF-κB signaling in DLBCL revealed upon deregulated BCL6 expression |
| Creators Name: | Zhang, B., Calado, D.P., Wang, Z., Froehler, S., Koechert, K., Qian, Y., Koralov, S.B., Schmidt-Supprian, M., Sasaki, Y., Unitt, C., Rodig, S., Chen, W., Dalla-Favera, R., Alt, F.W., 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 |
| ISSN: | 2211-1247 |
| Publisher: | Cell Press / Elsevier |
| Volume: | 11 |
| Number: | 5 |
| 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 |
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