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JCI online early table of contents: Feb. 8, 2010
Date:2/8/2010

etermined a way to enhance it to suppress prostate tumor development and growth in mice.

Previous work by Pandolfi and colleagues determined that inactivation of the protein Pten leads to a senescence response that opposes tumorigenesis. In this study, Pten-lossinduced cellular senescence (PICS) was found to be distinct from another form of cellular senescence known as oncogene-induced senescence in that it did not cause cellular proliferation and DNA damage. This was important because these two consequences of oncogene-induced senescence mean that enhancing this process for the treatment of cancer is not a viable option. As pharmacological inhibition of PTEN was found to drive senescence and inhibit tumor development and growth in vivo in a human xenograft model of prostate cancer, the authors suggest that enhancing PICS might provide a new approach for cancer prevention and therapy.

TITLE: A novel type of cellular senescence that can be enhanced in mouse models and human tumor xenografts to suppress prostate tumorigenesis

AUTHOR CONTACT:
Pier Paolo Pandolfi
Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Phone: 617.735.2121; Fax: 617.735.2120; E-mail: ppandolf@bidmc.harvard.edu.

View this article at: http://www.jci.org/articles/view/40535?key=9b25621b73ed2877356a


NEPHROLOGY: New approach to treating the kidney disease Alport syndrome?

Alport syndrome is a progressive hereditary kidney disease with no definitive therapy. It is caused by mutations in any of the collagen IV genes (COL4A3, COL4A4, and COL4A5). Motoko Yanagita and colleagues, at Kyoto University Graduate School of Medicine, Japan, have now identified a role for the protein USAG-1 in the development of disease in mice that model Alport syndrome (Col4a3/ mice).
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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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