| Literature DB >> 16453012 |
Megan Cully1, Han You, Arnold J Levine, Tak W Mak.
Abstract
The tumour-suppressor phosphatase with tensin homology (PTEN) is the most important negative regulator of the cell-survival signalling pathway initiated by phosphatidylinositol 3-kinase (PI3K). Although PTEN is mutated or deleted in many tumours, deregulation of the PI3K-PTEN network also occurs through other mechanisms. Crosstalk between the PI3K pathways and other tumorigenic signalling pathways, such as those that involve Ras, p53, TOR (target of rapamycin) or DJ1, can contribute to this deregulation. How does the PI3K pathway integrate signals from numerous sources, and how can this information be used in the rational design of cancer therapies?Entities:
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Year: 2006 PMID： 16453012 DOI： 10.1038/nrc1819
Source DB: PubMed Journal: Nat Rev Cancer ISSN： 1474-175X Impact factor: 60.716