摘要: Basic cancer research provides a theoretical foundation for rational approaches to improve diagnosis, prognosis, and therapy. For example, the p53 tumor suppressor can facilitate apoptosis induced by anticancer agents, implying that mutations should contribute radiation drug resistance in human tumors. Indeed, do correlate with some types, reintroduction of into mutant tumors enhances chemosensitivity vitro vivo. However, many settings, relationship between p53, apoptosis, remains ambiguous. Although methodological shortcomings clearly this confusion, situation is further confounded fact p53’s apoptotic activity depends on context. Hence, chemotherapeutic agent, type, genetic background may each impact chemosensitivity. An improved understanding complexity will be necessary guide future efforts exploiting or other genes treatment.