Genetic determinants of oxidative stress-mediated sensitization of drug-resistant cancer cells

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 oxyg...

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Bibliographic Details
Published in:International journal of cancer 2012-01, Vol.130 (1), p.1-9
Main Author: Maiti, Amit K.
Format: Article
Language:English
Subjects:
Animals
Antineoplastic Agents - therapeutic use
Biological and medical sciences
Cancer
Drug resistance
Drug Resistance, Neoplasm
Humans
Medical research
Medical sciences
Neoplasms - drug therapy
Neoplasms - genetics
Oxidative Stress
ROS
ROS maintaining genes
Tumors
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Summary: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.
ISSN:0020-7136
1097-0215
DOI:10.1002/ijc.26306