Public release date: 15-Dec-2003
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Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation

Autophagy active in tumor suppression

Normal cell growth requires well-coordinated balance between synthesis and breakdown. Autophagy is a regulated lysosomal pathway whereby long-lived cellular proteins and cytoplasmic organelles are degraded. The beclin 1 autophagy gene is monoallelically deleted in 40-75% of cases of human sporadic breast, ovarian, and prostate cancer. However, little is known about the role of autophagy in cancer biology. In the December 15 issue of the Journal of Clinical Investigation Beth Levine and colleagues studied a targeted mutant mouse model with a heterozygous disruption of beclin 1 and observed an increase in cellular proliferation and the frequency of spontaneous malignancies and a reduction in autophagy in vivo. The report demonstrates that beclin 1 is a haplo-insufficient tumor-suppressor gene and suggests that autophagy is a novel and important mechanism in the regulation of cell growth and tumor suppression.

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TITLE: Promotion of tumorigenesis by heterozygous disruption of the beclin 1 autophagy gene

AUTHOR CONTACT:
Beth Levine
Columbia University College of Physicians and Surgeons, New York, New York, USA.
Phone: 212-305-7312
Fax: 212-305-7290
E-mail: levine@cancercenter.columbia.edu

View the PDF of this article at: http://www.jci.org/cgi/content/full/113/12/1809

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