Author(s): Maiti AK
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Abstract Drug resistance in cancer is an overwhelming problem, because drug-resistant cancer cells are harder to kill with the same drug. The mechanism of drug resistance differs for various cancers based on the type of drug being used for its treatment. Most current drugs are shown to increase reactive oxygen species (ROS) in respective cancer cells that induces apoptosis, but continuous treatment with the same drug may reduce cellular ROS levels and may convert drug sensitive cancer cells into drug resistant cells. In addition, exogenous elevation of ROS in conjunction with drug resensitizes drug-resistant cancer cells. Thus, constant maintenance of higher ROS level in cancer cells may be a prerequisite for drug efficacy in certain type of cancer cells. Thus, modulation of ROS-mediated genetic pathway genes could be an efficient alternative to maintain higher ROS level in cancer cells for "combinational chemotherapy" with the drug. In this review, I discuss whether ROS reduction in drug-resistant cancer cells could be a general mechanism of drug resistance for most cancers with its specific drug, and whether elevation of ROS levels with the drug could be a valuable strategy for increasing drug efficacy in most cancers. Copyright © 2011 UICC.
This article was published in Int J Cancer
and referenced in Chemotherapy: Open Access