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Vol. 96, Issue 8, 4240-4245, April 13, 1999

Review
New insights into tumor suppression: PTEN suppresses tumor formation by restraining the phosphoinositide 3-kinase/AKT pathway

Lewis C. Cantley*,dagger ,Dagger and Benjamin G. Neel§

* Department of Cell Biology, Harvard Medical School, Boston, MA 02115; dagger  Division of Signal Transduction, Department of Medicine; Beth Israel Deaconess Medical Center, Boston, MA 02215; and § Cancer Biology Program, Division of Hematology-Oncology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215

The most recently discovered PTEN tumor suppressor gene has been found to be defective in a large number of human cancers. In addition, germ-line mutations in PTEN result in the dominantly inherited disease Cowden syndrome, which is characterized by multiple hamartomas and a high proclivity for developing cancer. A series of publications over the past year now suggest a mechanism by which PTEN loss of function results in tumors. PTEN appears to negatively control the phosphoinositide 3-kinase signaling pathway for regulation of cell growth and survival by dephosphorylating the 3 position of phosphoinositides.


Dagger    To whom reprint requests should be addressed at: Harvard Institutes of Medicine, 77 Avenue Louis Pasteur, Room 1024, Boston, MA 02115. e-mail: cantley{at}helix.mgh.harvard.edu.

Copyright © 1999 by The National Academy of Sciences  0027-8424/99/964240-6$2.00/0
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