作者: D. Mark Pritchard , John A. Hickman
DOI: 10.1007/978-1-59259-725-3_22
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摘要: Current chemotherapeutic drugs used for the treatment of disseminated cancer impose cytotoxicity to tumor cells but also normal tissues, toxicities that are often dose limiting. All antitumor drugs, regardless their modes action, induce apoptosis or programmed cell death, a process which is under genetic control (reviewed in ref. 1). This suggests these agents an active cellular response perturbation rather than direct consequence particular type damage (a fall nucleotide pools DNA strand breaks, example). The menu gene expression controlling genes can either promote suppress deletion “damaged” cells, different types. determines “threshold” at may engage death. Put simply, some will die more readily others with same load damage. It therefore reasonable hypothesize patterns alter threshold undergo contribute not only efficacy chemotherapy terms (2,3), determining host toxicity. Is this hypothesis proven?