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Cancer Cell. 2007 Aug;12(2):131-44.

Promiscuous mutations activate the noncanonical NF-kappaB pathway in multiple myeloma.

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1
Comprehensive Cancer Center, Mayo Clinic Arizona, Scottsdale, AZ 85259, USA.

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.

PMID:
17692805
PMCID:
PMC2083698
DOI:
10.1016/j.ccr.2007.07.003
[Indexed for MEDLINE]
Free PMC Article

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