Shen, Rhine R.Zhou, Alicia Y.Kim, EejungO’Connell, Joyce T.Hagerstrand, DanielBeroukhim, RameenHahn, William2015-08-032014Shen, Rhine R., Alicia Y. Zhou, Eejung Kim, Joyce T. O’Connell, Daniel Hagerstrand, Rameen Beroukhim, and William C. Hahn. 2014. “TRAF2 is an NF-κB activating oncogene in epithelial cancers.” Oncogene 34 (2): 209-216. doi:10.1038/onc.2013.543. http://dx.doi.org/10.1038/onc.2013.543.0950-9232http://nrs.harvard.edu/urn-3:HUL.InstRepos:17820652Aberrant NF-κB activation is frequently observed in human cancers. Genome characterization efforts have identified genetic alterations in multiple components of the NF-κB pathway, some of which have been shown to be essential for cancer initiation and tumor maintenance. Here using patient tumors and cancer cell lines, we identify the NF-κB regulator, TRAF2 as an oncogene that is recurrently amplified and rearranged in 15% of human epithelial cancers. Suppression of TRAF2 in cancer cells harboring TRAF2 copy number gain inhibits proliferation, NF-κB activation, anchorage-independent growth and tumorigenesis. Cancer cells that are dependent on TRAF2 also require NF-κB for survival. The phosphorylation of TRAF2 at serine 11 is essential for the survival of cancer cells harboring TRAF2 amplification. Together these observations identify TRAF2 as a frequently amplified oncogene.en-USTRAF2NF-κBcancer9q34 amplificationJournal Article2015-08-0310.1038/onc.2013.543