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Also in the March 24 JNCI
Date:3/24/2009

tence of risk reduction for up to 10 years after treatment in this trial reinforces the validity of the original trial findings and is consistent with an emerging new paradigm in cancer prevention, namely, that prevention may be achievable with short-term as opposed to life-long treatment," the authors write. Contact: NCI Press Office, ncipressofficers@mail.nih.gov, 301-496-6641


Overexpression of Fatty Acid Synthase Promotes Prostate Cancer in Mouse Models

Fatty acid synthase (FASN) can act as a prostate cancer oncogene in mouse models.

FASN, a key enzyme in the synthesis of long-chain fatty acids, is overexpressed in prostate cancer, relative to its expression in adjacent normal tissue. Additionally, previous studies showed that inhibition of FASN activity promoted programmed cell death in prostate cancer cell lines.

In the current study, Massimo Loda, M.D., of the Dana-Farber Cancer Institute in Boston, and colleagues overexpressed FASN in a variety of prostate cancer and precancerous cell lines.

Overexpression of FASN increased cell proliferation and substrate-independent growth. When immortalized prostate epithelial cells that expressed both FASN and the androgen receptor were injected into immunodeficient mice, the cells gave rise to invasive cancer. Inhibition of FASN gene expression led to programmed cell death in a prostate cancer cell line grown in culture. FASN expression showed an inverse correlation with the rate of programmed cell death in prostate cancer biopsy samples.

"The experimental evidence we provide on the oncogenic role of FASN in the prostate suggests that pharmacological targeting of FASN might represent an effective treatment for prostate cancer," the authors write.

Contact: Bill Schaller, william_schaller@dfci.harvard.edu, 617-632-5357'/>"/>

Contact: Caroline McNeil
jncimedia@oxfordjournals.org
301-841-1287
Journal of the National Cancer Institute
Source:Eurekalert

Page: 1 2 3 4 5 6

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