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Synergy between PI3K signaling and MYC in Burkitt lymphomagenesis

Official URL:https://doi.org/10.1016/j.ccr.2012.06.012
PubMed:View item in PubMed
Creators Name:Sander, S. and Calado, D.P. and Srinivasan, L. and Koechert, K. and Zhang, B. and Rosolowski, M. and Rodig, S.J. and Holzmann, K. and Stilgenbauer, S. and Siebert, R. and Bullinger, L. and Rajewsky, K.
Journal Title:Cancer Cell
Journal Abbreviation:Cancer Cell
Page Range:167-179
Date:14 August 2012
Keywords:B-Lymphocytes, Base Sequence, Burkitt Lymphoma, Enzyme Activation, Germinal Center, Inbred C57BL Mice, Molecular Sequence Data, Neoplastic Cell Transformation, Neoplastic Gene Expression Regulation, Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-myc, Signal Transduction, Tumor Cell Line, Animals, Mice
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.
Publisher:Cell Press / Elsevier (U.S.A.)
Item Type:Article

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