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Therapeutic inhibition of the mammalian target of rapamycin (mTOR) has recently demonstrated a 30% to 40% response rate in patients with relapsed mantle cell lymphoma (MCL).1,2 However, the exact mechanisms underlying this clinically significant response rate remain poorly understood. Here, we discuss the potential molecular mechanisms underlying this activity, and how to improve the therapeutic value of mTOR inhibitors by combining them with other agents that may target different molecular pathways.
Addendum to: Yazbeck VY, Buglio D, Georgakis GV, et al. Temsirolimus downregulates p21 without altering cyclin D1 expression and induces autophagy and synergizes with vorinostat in mantle cell lymphoma. Exp Hematol 2008; 36:443-50.
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