Article
A senescence program controlled by p53 and p16INK4a contributes to the outcome of cancer therapy.
Cell - 3 May 2002
Schmitt Clemens A, Fridman Jordan S, Yang Meng, Lee Soyoung, Baranov Eugene, Hoffman Robert M, Lowe Scott W
Abstract excerpt
p53 and INK4a/ARF mutations promote tumorigenesis and drug resistance, in part, by disabling apoptosis. We show that primary murine lymphomas also respond to chemotherapy by engaging a senescence program controlled by p53 and p16(INK4a). Hence, tumors with p53 or INK4a/ARF mutations-but not those lacking ARF alone-respond poorly to cyclophosphamide therapy in vivo. Moreover, tumors harboring a Bcl2-mediated...
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