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Disabling Skp2 gene helps shut down cancer growth
Date:3/17/2010

er, research conducted in mouse models with faulty or inactive tumor suppressor networks showed that Skp2 deficiency and oncogenic signaling elicit a senescence response that restricts formation of tumors.

Novel Findings Point to New Therapeutic Approaches

Lin said these studies suggest that in the future Skp2 might be an effective therapeutic target for tumors with deregulated Akt signaling due to the loss or inactivation of Pten functions. Pten, which is commonly lost in human cancers, acts as a tumor suppressor gene by suppressing Akt signaling. Skp2 and Pten loss are believed to cooperate in triggering cellular senescence to restrict invasive prostate cancer.

"We now want to examine whether Skp2 is required in other tumor model systems, such as a HER2 model, to determine whether it is globally required for an oncogenic event," said Lin, who previously was affiliated with Memorial Sloan-Kettering Cancer Center's Department of Pathology and Cancer Biology and Genetics program and continued his research at M. D. Anderson. "We are testing whether Skp2 might be widely used for different types of cancer or perhaps used to trigger this newly described cellular senescence program."

The researchers also are working to develop a Skp2-specific small molecule inhibitor to establish that the protein is indeed an important therapeutic target in cancer treatment. They believe that Skp2-based therapy might also be used as a general cancer treatment that could be combined with existing cancer therapies.


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Contact: Scott Merville
smerville@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert  

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