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Successful drug treatment in human disease requires an adequate therapeutic index reflecting the treatment’s specific effects on target cells and its lack of clinically significant effects on the host. In cancer, the therapeutic goal is to trigger tumor-selective cell death. The mechanisms responsible for such death are of obvious importance in determining the efficacy of specific treatments. With the discovery that distinct death pathways exist in biology, and that certain of these are evolutionarily selected and highly efficient, came an explosion of interest in connecting such pathways to the pathophysiology of cancer. Thus, the biology of neoplasia has expanded to incorporate not only lesions that cause dysregulated growth, but also those that lead to inefficient cell death.
Sellers et al. (Wed,) studied this question.
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