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"While pre-clinical study demonstrates that prolonged rapamycin treatment suppresses Akt and PKB signaling due to the destabilization of mTORC2 in some types of cultured cancer cells, 172 the results from recent clinical trials provide evidence about PI3K-Akt activation in patient tumors treated with rapamycin or the rapamycin analog RAD001, XREF_BIBR, XREF_BIBR Thus, Dr. Rosen 's group demonstrated that mTOR inhibition with RAD001 treatment induced IRS-1 expression and Akt activation in patient tumors."