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The mechanisms causing resistance to chemotherapeutic drugs in cancer patients are poorly understood. Recent evidence suggests that different forms of chemotherapy may exert their cytotoxic effects by inducing apoptosis¹. The tumor suppressor gene P53 has a pivotal role inducing apoptosis in response to cellular damage. In vitro investigations have shown intact p53 to play a critical role executing cell death in response to treatment with cytotoxic drugs like 5–fluorouracil, etoposide and doxorubicin². Recently, mutations in the P53 gene were found to confer resistance to anthracyclines in a mouse sarcoma tumor model³, and overexpression of the p53 protein (which, in most cases, is due to a mutated gene) was found to be associated with lack of response to cisplatin–based chemotherapy in non–small cell lung cancer⁴. Previous studies have shown mutations in the P53 gene or overexpression of the p53 …