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Elevated Reactive Oxygen Species (ROS) generated by the conventional cancer
therapies and the endogenous production of ROS have been observed in various types of cancers.
In contrast to the harmful effects of oxidative stress in different pathologies other than
cancer, ROS can speed anti-tumorigenic signaling and cause apoptosis of tumor cells via oxidative
stress as demonstrated in several studies. The primary actions of antioxidants in cells
are to provide a redox balance between reduction-oxidation reactions. Antioxidants in tumor
cells can scavenge excess ROS, causing resistance to ROS induced apoptosis. Various chemotherapeutic
drugs, in their clinical use, have evoked drug resistance and serious side effects.
Consequently, drugs having single-targets are not able to provide an effective cancer
therapy. Recently, developed hybrid anticancer drugs promise great therapeutic advantages
due to their capacity to overcome the limitations encountered with conventional chemotherapeutic
agents. Hybrid compounds have advantages in comparison to the single cancer drugs
which have usually low solubility, adverse side effects, and drug resistance. This review addresses
two important treatments strategies in cancer therapy: oxidative stress induced apoptosis
and hybrid anticancer drugs.
Bioinformatic Analysis of the Nicotinamide Binding Site in Poly(ADP-Ribose) Polymerase Family Proteins
