Modeling multiple myeloma by AID-dependent conditional activation of MYC.
Efforts to create a mouse model that provides even a phenocopy of human multiple myeloma (MM) have been unsuccessful. In this issue of Cancer Cell, Bergsagel and colleagues describe an apparent solution to this problem by creating a model in which a MYC transgene containing a stop codon and flanking Ig kappa regulatory sequences is activated sporadically in germinal center B cells by AID-dependent somatic hypermutation that reverts the stop codon. Although much remains to be done to fully characterize this model, this approach is likely to impact the creation of sporadic models for other kinds of germinal center B cell tumors.
Kuehl
W Michael
WM
Genetics Branch, National Cancer Institute, Bethesda, MD 20889, USA. wmk@helix.nih.gov <wmk@helix.nih.gov>
D000818:Animals; D003564:Cytidine Deaminase / Q000378:metabolism*; D004195:Disease Models, Animal; D018450:Disease Progression; D018858:Germinal Center / Q000473:pathology; D006801:Humans; D051379:Mice; D009101:Multiple Myeloma / Q000201:enzymology* / Q000276:immunology / Q000473:pathology*; D010265:Paraproteinemias / Q000473:pathology; D010950:Plasma Cells / Q000201:enzymology / Q000473:pathology; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics*; D000098830:AICDA (Activation-Induced Cytidine Deaminase)
D016271:Proto-Oncogene Proteins c-myc; D000098830:AICDA (Activation-Induced Cytidine Deaminase); D003564:Cytidine Deaminase