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Vol. 96, Issue 8, 4240-4245, April 13, 1999
* Department of Cell Biology, Harvard Medical School, Boston, MA
02115;
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.
Copyright © 1999 by The National Academy of Sciences 0027-8424/99/964240-6$2.00/0
Review
New insights into tumor suppression: PTEN suppresses tumor formation by
restraining the phosphoinositide 3-kinase/AKT pathway
,
and
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
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.
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