| Literature DB >> 17692805 |
Jonathan J Keats1, Rafael Fonseca, Marta Chesi, Roelandt Schop, Angela Baker, Wee-Joo Chng, Scott Van Wier, Rodger Tiedemann, Chang-Xin Shi, Michael Sebag, Esteban Braggio, Travis Henry, Yuan-Xiao Zhu, Homer Fogle, Tammy Price-Troska, Gregory Ahmann, Catherine Mancini, Leslie A Brents, Shaji Kumar, Philip Greipp, Angela Dispenzieri, Barb Bryant, George Mulligan, Laurakay Bruhn, Michael Barrett, Riccardo Valdez, Jeff Trent, A Keith Stewart, John Carpten, P Leif Bergsagel.
Abstract
Activation of NF-kappaB has been noted in many tumor types, however only rarely has this been linked to an underlying genetic mutation. An integrated analysis of high-density oligonucleotide array CGH and gene expression profiling data from 155 multiple myeloma samples identified a promiscuous array of abnormalities contributing to the dysregulation of NF-kappaB in approximately 20% of patients. We report mutations in ten genes causing the inactivation of TRAF2, TRAF3, CYLD, cIAP1/cIAP2 and activation of NFKB1, NFKB2, CD40, LTBR, TACI, and NIK that result primarily in constitutive activation of the noncanonical NF-kappaB pathway, with the single most common abnormality being inactivation of TRAF3. These results highlight the critical importance of the NF-kappaB pathway in the pathogenesis of multiple myeloma.Entities:
Mesh：
Substances：
Year: 2007 PMID： 17692805 PMCID： PMC2083698 DOI： 10.1016/j.ccr.2007.07.003
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743