%0 Journal Article %1 Sander.2012 %A Sander, Sandrine %A Calado, Dinis P. %A Srinivasan, Lakshmi %A Köchert, Karl %A Zhang, Baochun %A Rosolowski, Maciej %A Rodig, Scott J. %A Holzmann, Karlheinz %A Stilgenbauer, Stephan %A Siebert, Reiner %A Bullinger, Lars %A Rajewsky, Klaus %D 2012 %J Cancer cell %K Animals B-Lymphocytes/enzymology/pathology Base_Sequence Burkitt_Lymphoma/enzymology/genetics/pathology Cell_Line,_Tumor Cell_Transformation,_Neoplastic/genetics/metabolism/pathology Enzyme_Activation Gene_Expression_Regulation,_Neoplastic Germinal_Center/enzymology/pathology Humans Mice Mice,_Inbred_C57BL Molecular_Sequence_Data Phosphatidylinositol_3-Kinases/genetics/metabolism Proto-Oncogene_Proteins_c-myc/genetics/metabolism Signal_Transduction/genetics %N 2 %P 167–179 %T Synergy between PI3K signaling and MYC in Burkitt lymphomagenesis %V 22 %X 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.

@article{Sander.2012, 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.}, added-at = {2014-10-13T18:24:59.000+0200}, author = {Sander, Sandrine and Calado, Dinis P. and Srinivasan, Lakshmi and Köchert, Karl and Zhang, Baochun and Rosolowski, Maciej and Rodig, Scott J. and Holzmann, Karlheinz and Stilgenbauer, Stephan and Siebert, Reiner and Bullinger, Lars and Rajewsky, Klaus}, biburl = {https://www.bibsonomy.org/bibtex/24bc6bdb33d4ac110d67ea36df56c3956/drtester}, interhash = {dece206a1dcae25d6bcae4ff09a83ca5}, intrahash = {4bc6bdb33d4ac110d67ea36df56c3956}, journal = {Cancer cell}, keywords = {Animals B-Lymphocytes/enzymology/pathology Base_Sequence Burkitt_Lymphoma/enzymology/genetics/pathology Cell_Line,_Tumor Cell_Transformation,_Neoplastic/genetics/metabolism/pathology Enzyme_Activation Gene_Expression_Regulation,_Neoplastic Germinal_Center/enzymology/pathology Humans Mice Mice,_Inbred_C57BL Molecular_Sequence_Data Phosphatidylinositol_3-Kinases/genetics/metabolism Proto-Oncogene_Proteins_c-myc/genetics/metabolism Signal_Transduction/genetics}, number = 2, pages = {167–179}, timestamp = {2014-10-13T18:24:59.000+0200}, title = {Synergy between PI3K signaling and MYC in Burkitt lymphomagenesis}, volume = 22, year = 2012 }