Abstract
Over the last 2 decades, the role of apoptosis in anticancer agent cytotoxicity has become clear. Defects in the regulation of apoptosis (programmed cell death) make important contributions to the pathogenesis and progression of most cancers and leukemias. Apoptosis defects also have a key role in cell resistance to chemotherapy. Mitochondria play a central part in cell death in response to anticancer agents. Most of these agents target mitochondria via caspases or other regulator elements of the apoptotic machinery. Nevertheless, some anticancer agents, already in clinical use (paclitaxel, vinblastine, lonidamine, etoposide, arsenic trioxide) or in pre-clinical development (betulinic acid, MT21), directly target and permeabilize mitochondria. The acknowledgement of mitochondria as a new target for anticancer agents provides a new way to bypass cancer cell chemoresistance.
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