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PTEN, TSC2, and tumorigenesis

e important clinical implications for the way in which tumor arising from such mutations are treated. Dr. Manning adds that "This attenuation of Akt signaling triggered upon loss of the TSC genes has been shown in cell culture experiments to be due to uncontrolled mTOR activity, as the mTOR inhibitor rapamycin can restore Akt activation. Our findings that relieving this feedback mechanism in vivo greatly enhances tumor growth in this mouse model of tuberous sclerosis complex, raises some concern about the use of rapamycin to treat this disease. Pending the results of ongoing clinical trials with rapamycin, these studies suggest that combination therapy with rapamycin and drugs that block receptor activation of Akt could be much more effective at treating TSC."


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Contact: Heather Cosel
coselpie@cshl.edu
Cold Spring Harbor Laboratory
18-Jul-2005


Page: 1 2

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