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Cancer Cell. 2012 Aug 14;22(2):167-79. doi: 10.1016/j.ccr.2012.06.012.

Synergy between PI3K signaling and MYC in Burkitt lymphomagenesis.

Author information

1
Program of Cellular and Molecular Medicine, Children's Hospital, and Immune Disease Institute, Harvard Medical School, Boston, MA 02115, USA.

Abstract

In Burkitt lymphoma (BL), a germinal center B-cell-derived tumor, the pro-apoptotic properties of c-MYC must be counterbalanced. Predicting that survival signals would be delivered by phosphoinositide-3-kinase (PI3K), a major survival determinant in mature B cells, we indeed found that combining constitutive c-MYC expression and PI3K activity in germinal center B cells of the mouse led to BL-like tumors, which fully phenocopy human BL with regard to histology, surface and other markers, and gene expression profile. The tumors also accumulate tertiary mutational events, some of which are recurrent in the human disease. These results and our finding of recurrent PI3K pathway activation in human BL indicate that deregulated c-MYC and PI3K activity cooperate in BL pathogenesis.

PMID:
22897848
PMCID:
PMC3432451
DOI:
10.1016/j.ccr.2012.06.012
[Indexed for MEDLINE]
Free PMC Article

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