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Cancers 2017, 9(4), 30;

PI3K Signaling in Tissue Hyper-Proliferation: From Overgrowth Syndromes to Kidney Cysts

Department of Molecular Biotechnology and Health Sciences, University of Torino, Torino 10126, Italy
Department of Public Health and Pediatrics, University of Torino, Torino 10126, Italy
These authors equally contributed to this work.
Author to whom correspondence should be addressed.
Academic Editor: Marco Falasca
Received: 22 February 2017 / Revised: 24 March 2017 / Accepted: 27 March 2017 / Published: 29 March 2017
(This article belongs to the Special Issue PI3K/PDK1/Akt Pathways in Cancer)
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The members of the PhosphoInositide-3 Kinase (PI3K) protein family are well-known regulators of proliferative signals. By the generation of lipid second messengers, they mediate the activation of AKT/PKB (AKT) and mammalian Target Of Rapamycin (mTOR) pathways. Although mutations in the PI3K/AKT/mTOR pathway are highly characterized in cancer, recent evidence indicates that alterations in the proliferative signals are major drivers of other diseases such as overgrowth disorders and polycystic kidney disease. In this review, we briefly summarize the role of the PI3K/AKT/mTOR pathway in cell proliferation by comparing the effect of alterations in PI3K enzymes in different tissues. In particular, we discuss the most recent findings on how the same pathway may lead to different biological effects, due to the convergence and cooperation of different signaling cascades. View Full-Text
Keywords: PI3K; mTOR; proliferation; overgrowth syndrome; polycystic kidney disease PI3K; mTOR; proliferation; overgrowth syndrome; polycystic kidney disease
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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De Santis, M.C.; Sala, V.; Martini, M.; Ferrero, G.B.; Hirsch, E. PI3K Signaling in Tissue Hyper-Proliferation: From Overgrowth Syndromes to Kidney Cysts. Cancers 2017, 9, 30.

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