Federico Gulluni

TL;DR: The impact of class I catalytic subunit mutations on AKT-mediated cellular processes that control crucial mechanisms in tumor development are elucidated, exploiting the potential benefits of PI3K signaling inhibitors in clinical use.

TL;DR: It is shown that formation of PI(3,4)P2 by class II phosphatidylinositol-3-kinase C2α (PI(3)K C2 α) spatiotemporally controls clathrin-mediated endocytosis and unravels a novel discrete function of PI (3, 4)P 2 in a central cell physiological process.

TL;DR: It is reported that PI3K-C2α is enriched in the pericentriolar recycling endocytic compartment (PRE) at the base of the primary cilium, where it regulates the formation of a PtdIns3P pool at the PRE required for Rab11 and Shh pathway activation.

TL;DR: Individual PIK3CA mutations are discussed as predictors of sensitivity and resistance to targeted therapies, leading to use of novel PI3K/mTOR/AKT inhibitors to a more “personalized” treatment.

TL;DR: It is shown that a partial or complete loss of Inpp4b morphs benign thyroid adenoma lesions in Pten heterozygous mice into lethal and metastatic follicular-like thyroid cancer (FTC) and is identified as a novel tumor suppressor in FTC oncogenesis and metastasis through localized regulation of the PI3K-AKT pathway at the endosomes.