Pièces de Résistance

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Science  25 Apr 2003:
Vol. 300, Issue 5619, pp. 551
DOI: 10.1126/science.300.5619.551a

Because many chemotherapeutic drugs kill tumor cells by inducing apoptosis (programmed cell death), cellular resistance to apoptosis is thought to be a major factor limiting drug efficacy. Elucidation of the molecular factors that determine whether a tumor will be sensitive or resistant to chemotherapy-induced apoptosis may ultimately enable oncologists to optimize therapies for individual cancer patients.

Complementary laboratory and clinical studies by Bergamaschi et al. and Irwin et al. highlight the interactive role of the tumor suppressor protein p53 and its paralog p73 in the apoptotic response to chemotherapy. Their results reveal that specific mutations in p53, when present in combination with a common allelic variant at codon 72 of p53, can confer resistance to drug-induced apoptosis via inhibition of p73 function. Along with the implications for prediction of chemotherapeutic response, these findings raise the possibility that therapeutic modulation of p73 levels may offset the development of drug resistance in certain human cancers.—PAK

Cancer Cell 3, 387; 403 (2003).

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