@entity2109 ( @entity2109 ) features translocations linking c-myc to an Ig locus. Breakpoints in the H chain locus ( @entity7528 ) stand either close to J(H) or within switch regions and always link c-myc to the 3' @entity7528 locus control region (3' LCR). To test the hypothesis that the 3' LCR alone was sufficient to deregulate c-myc, we generated @entity19 carrying a 3' LCR-driven c-myc transgene and specifically up-regulating c-myc in B cells. Splenic B cells from @entity19 proliferated exaggeratedly in response to various signals had an elevated apoptosis rate but normal B220/IgM/IgD expression. Although all Ig levels were lowered in vivo, class switching and Ig secretion proved normal in vitro. Beginning at the age of 12 wk, @entity19 developed @entity981 with an overall incidence of 80% by 40 wk. @entity981 were B220(+)IgM(+)IgD(+) with the @entity2109 "starry sky" appearance. Gene expression profiles revealed broad alterations in the proliferation program and the Ras-p21 pathway. Our study demonstrates that 3' @entity7528 enhancers alone can deregulate c-myc and initiate the development of @entity706 . The rapid and constant occurrence of @entity706 in this model makes it valuable for the understanding and the potential therapeutic manipulation of c-myc oncogenicity in vivo.

The 3' XXXX locus control region is sufficient to deregulate a c-myc transgene and promote mature B cell malignancies with a predominant Burkitt-like phenotype.

@entity981 :: ('MESH:D054198', 'Disease') :: ['clonal lymphoblastic lymphomas or diffuse anaplastic plasmacytomas', 'Lymphoblastic lymphomas'] @entity706 :: ('MESH:D008223', 'Disease') :: ['lymphoma', 'BL-like lymphomas'] @entity19 :: ('10090', 'Species') :: ['mice', 'transgenic mice'] @entity2109 :: ('MESH:D002051', 'Disease') :: ['Burkitt lymphoma', 'BL'] @entity7528 :: ('111507(Tax:10090)', 'Gene') :: ['IgH']
@entity7528 :: (111507(Tax:10090),Gene) :: ['IgH']
