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Cancer Cell. 2011 Aug 16;20(2):173-86. doi: 10.1016/j.ccr.2011.07.013.

Identification of PHLPP1 as a tumor suppressor reveals the role of feedback activation in PTEN-mutant prostate cancer progression.

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  • 1Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.

Abstract

Hyperactivation of the PI 3-kinase/AKT pathway is a driving force of many cancers. Here we identify the AKT-inactivating phosphatase PHLPP1 as a prostate tumor suppressor. We show that Phlpp1-loss causes neoplasia and, on partial Pten-loss, carcinoma in mouse prostate. This genetic setting initially triggers a growth suppressive response via p53 and the Phlpp2 ortholog, and reveals spontaneous Trp53 inactivation as a condition for full-blown disease. Surprisingly, the codeletion of PTEN and PHLPP1 in patient samples is highly restricted to metastatic disease and tightly correlated to deletion of TP53 and PHLPP2. These data establish a conceptual framework for progression of PTEN mutant prostate cancer to life-threatening disease.

Copyright © 2011 Elsevier Inc. All rights reserved.

PMID:
21840483
[PubMed - indexed for MEDLINE]
PMCID:
PMC3176728
Free PMC Article

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