Journal article

PI3K activation in neural stem cells drives tumorigenesis which can be ameliorated by targeting the cAMP response element binding protein

Paul M Daniel, Gulay Filiz, Daniel V Brown, Michael Christie, Paul M Waring, Yi Zhang, John M Haynes, Colin Pouton, Dustin Flanagan, Elizabeth Vincan, Terrance G Johns, Karen Montgomery, Wayne A Phillips, Theo Mantamadiotis



Background: Hyperactivation of phosphoinositide 3-kinase (PI3K) signaling is common in cancers, but the precise role of the pathway in glioma biology remains to be determined. Some understanding of PI3K signaling mechanisms in brain cancer comes from studies on neural stem/progenitor cells (NSPCs), where signals transmitted via the PI3K pathway cooperate with other intracellular pathways and downstream transcription factors to regulate critical cell functions. Methods: To investigate the role of the PI3K pathway in glioma initiation and development, we generated a mouse model targeting the inducible expression of a PIK3CAH1047A oncogenic mutant and deletion of the PI3K negative regulator, ph..

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Awarded by Department of Pathology, CASS Foundation

Awarded by National Health and Medical Research Council (NHMRC) of Australia

Funding Acknowledgements

This work was supported by the Department of Pathology, CASS Foundation grant 6236. W.A.P. was supported in part by project grant 1080491 from the National Health and Medical Research Council (NHMRC) of Australia.