Abstract

The main clinical problem in cancer treatment is the development of multidrug resistance. Tumors can be intrinsically drug-resistant or develop resistance to chemotherapy. Multidrug resistance can develop by diverse mechanisms including decreased rate of drug uptake, increased drug efflux, alterations in drug metabolism, mutation of drug targets, activation of DNA repair mechanisms, and evasion of apoptosis. The use of modern genomic, proteomic, bioinformatic, and systems biology approaches has resulted in a substantial increase in our ability to identify molecular mechanisms that are involved in multidrug resistance in cancer and to find drugs that may block or reverse the development of drug resistance.

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