期刊
CANCER CELL
卷 12, 期 2, 页码 131-144出版社
CELL PRESS
DOI: 10.1016/j.ccr.2007.07.003
关键词
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资金
- NCI NIH HHS [P01 CA062242, P50 CA100707-010005, R01 CA83724-01, P50 CA100707, P50 CA100707-010004, P50 CA100707-01, R01 CA083724, R01 CA083724-07, P01 CA62242] Funding Source: Medline
- NIA NIH HHS [R01 AG020686-05, R01 AG020686-03, R01 AG020686, R01 AG020686-01A1, R01 AG020686-04, R01 AG020686-02] Funding Source: Medline
Activation of NF-kappa B 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-kappa B 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-kappa B pathway, with the single most common abnormality being inactivation of TRAF3. These results highlight the critical importance of the NF-kappa B pathway in the pathogenesis of multiple myeloma.
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