The generation of reactive oxygen species (ROS) and an altered redox status are common biochemical aspects in cancer cells. ROS can react with the polyunsaturated fatty acids of lipid membranes and induce lipid peroxidation. The end products of lipid peroxidation, 4-hydroxynonenal (HNE), have been considered to be a second messenger of oxidative stress. Beyond ROS involvement in carcinogenesis, increased ROS level can inhibit tumor cell growth. Indeed, in tumors in advanced stages, a further increase of oxidative stress, such as that occurs when using several anticancer drugs and radiation therapy, can overcome the antioxidant defenses of cancer cells and drive them to apoptosis. High concentrations of HNE can also induce apoptosis in cancer cells. However, some cells escape the apoptosis induced by chemical or radiation therapy through the adaptation to intrinsic oxidative stress which confers drug resistance. This paper is focused on recent advances in the studies of the relation between oxidative stress, lipid peroxidation products, and cancer progression with particular attention to the pro-oxidant anticancer agents and the drug-resistant mechanisms, which could be modulated to obtain a better response to cancer therapy. 1. Oxidative Stress and Lipid Peroxidation A body of evidence suggests that oxidative stress and resulting lipid peroxidation are involved in various and numerous pathological states including inflammation, atherosclerosis, neurodegenerative diseases, and cancer. The term “oxidative stress” is frequently used to describe the imbalances in redox couples such as those reduced to oxidized glutathione (GSH/GSSG) or NADPH/NADP+ ratios. Such metabolic disturbances not only involve the overproduction of reactive free radicals but also occur via a nonfree radical pathway, for example, by hydrogen peroxide [1]. In such cases, the products of its action are molecules that are enriched in one or more oxygen atoms that are generally considered to be markers of oxidative stress [2]. Reactive oxygen species (ROS) are thought to be the major ones responsible for the alteration of macromolecules which is often termed oxidative stress. ROS are generated as by-products of cellular metabolism, primarily in the mitochondria [3] and include free radicals such as superoxide anion ( ), perhydroxyl radical ( ), hydroxyl radical (？OH), nitric oxide (NO), and other species such as hydrogen peroxide (H2O2), singlet oxygen (1O2), hypochlorous acid (HOCl), and peroxynitrite (ONOO？) [4]. The hydroxyl radical ？OH is the most reactive radical that can arise
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