A chemical inhibitor of p53 that protects mice from the side effects of cancer therapy.

@article{Komarov1999ACI,
  title={A chemical inhibitor of p53 that protects mice from the side effects of cancer therapy.},
  author={Pavel G. Komarov and E A Komarova and Roman V Kondratov and K Christov-Tselkov and John Sayler Coon and M. V. Chernov and Andrei V Gudkov},
  journal={Science},
  year={1999},
  volume={285 5434},
  pages={
          1733-7
        }
}
Chemotherapy and radiation therapy for cancer often have severe side effects that limit their efficacy. Because these effects are in part determined by p53-mediated apoptosis, temporary suppression of p53 has been suggested as a therapeutic strategy to prevent damage of normal tissues during treatment of p53-deficient tumors. To test this possibility, a small molecule was isolated for its ability to reversibly block p53-dependent transcriptional activation and apoptosis. This compound… Expand
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Comparison of p53 wild type and p53-deficient mice indicates that p53, in fact, determines massive apoptosis occurring shortly after gamma irradiation in radiosensitive tissues, which makes p53 a potential target for therapeutic suppression with the purpose of rescuing normal tissues from the side effects of cancer treatment. Expand
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It is demonstrated that an oncogene, specifically the adenovirus E1A gene, can sensitize fibroblasts to apoptosis induced by ionizing radiation, 5-fluorouracil, etoposide, and adriamycin, and the involvement of p53 in the apoptotic response suggests a mechanism whereby tumor cells can acquire cross-resistance to anticancer agents. Expand
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It is suggested that processes related to control of senescence, response to DNA damage, and transformation involve different functions of the p53 protein and furthermore indicate a regulatory role for the 3'-untranslated region of p53 mRNA. Expand
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Results suggest that cyclin G might participate in a p53‐mediated pathway to prevent tumorigenesis. Expand
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