[Can defective TGF-Beta signaling be an Achilles heel in human cancer?].

Survival signals in cancer cells activate mTOR— the mammalian target of rapamycin. mTOR suppresses TGFβ signals that arrest cell cycle progression in late G 1 —thus activated mTOR prevents cell cycle arrest at a checkpoint mediated by TGFβ. Rapamycin treat‑ ment resurrects TGFβ signals causing G 1 arrest. Defects in TGFβ signaling are common in human cancer, and ironically, cancer cells with defective TGFβ signaling that do not arrest in G 1 , instead undergo apoptosis when treated with rapamycin. Thus, defective TGFβ signaling may represent an Achilles heel for rational therapeutic targeting of cancer cells using rapamycin‑based strategies.