Tonks, N. K., Myers, M. P. (December 1999) Structural assets of a tumor suppressor. Science, 286 (5447). pp. 2096-2097. ISSN 0036-8075
Abstract
Inactivation of tumor suppressor genes is one way in which cancer cells circumvent normal growth control. Mutations in the stretch of DNA at q23 on chromosome 10 are among the most commonly observed in human cancer and are particularly prevalent in glioblastomas, advanced prostate cancers, and endometrial carcinomas. Early in 1997, two groups reported the discovery of a new tumor suppressor gene at this locus, which they called PTEN (Phosphatase and Tensin homolog deleted on chromosome Ten) or MMAC (Mutated in Multiple Advanced Cancers) (1, 2). Mutations in PTEN are also recognized as the cause of cancer predisposition syndromes, such as Cowden disease (characterized by an increased risk of breast cancer). Since this discovery, rapid progress has been made in characterizing the PTEN protein and its role in regulating the signaling events that control cell proliferation and survival. The latest chapter in this story, published by Pavletich's group in a recent issue of Cell (3), describes the crystal structure of the PTEN protein and sheds new light on how this phosphatase is regulated.
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