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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

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

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.[1]

References

  1. Promiscuous mutations activate the noncanonical NF-kappaB pathway in multiple myeloma. Keats, J.J., Fonseca, R., Chesi, M., Schop, R., Baker, A., Chng, W.J., Van Wier, S., Tiedemann, R., Shi, C.X., Sebag, M., Braggio, E., Henry, T., Zhu, Y.X., Fogle, H., Price-Troska, T., Ahmann, G., Mancini, C., Brents, L.A., Kumar, S., Greipp, P., Dispenzieri, A., Bryant, B., Mulligan, G., Bruhn, L., Barrett, M., Valdez, R., Trent, J., Stewart, A.K., Carpten, J., Bergsagel, P.L. Cancer. Cell (2007) [Pubmed]
 
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