Oxidative stress refers to the state of imbalance between oxidation and antioxidation in the body. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are mainly involved in oxidation process, including O2. -,. OH, H2O2.NO., NO2,. ONOO- , etc. The antioxidant systems include enzymatic antioxidant systems and non-enzymatic antioxidant system, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH PX), vitamin C, vitamin E, glutathione, melatonin α-lipoic acid, carotenoids, trace elements copper, zinc and so on.

Cancer is a multistage process that involves mutational changes and uncontrolled cell proliferation. Research has firmly established the causal and contributory role of oxidative stress and oxidative damage in cancer initiation and progression. A fast-growing number of studies have been conducted into programmed cell death in cancer therapeutics, such as ferroptosis, cuproptosis, and pyroptosis. Ferroptosis is characterized by iron-dependent oxidative destruction of cellular membranes following the antioxidant system's failure. The sensitivity of ferroptosis is tightly regulated by a series of biological processes in cancer. Cuproptosis is copper-dependent and regulates cell death, which is distinct from known cell death mechanisms and depends on mitochondrial respiration. Cuproptosis is a novel form of copper-induced cell death by targeting lipoylated tricarboxylic acid cycle protein, which is expected to be developed as a key target for cancer treatment. Pyroptosis is a form of programmed cell death associated with antimicrobial responses during inflammation, in which immune cells release cytokines to attract other immune cells to fight the infection. Oxidative stress is extensively involved in the process of programmed cell death.

The aim of this Special Issue is to investigate the possible targets and molecular mechanisms underlying the crosstalk between oxidative stress and programmed cell death in cancer remain unclear. This topic will help to further understand the pathophysiology of cancer and open new perspectives for cancer treatment. Original research and review articles are welcomed.

Potential topics include but are not limited to the following:

• Crosstalk between oxidative stress and programmed cell death in cancer
• The new therapeutic targets based on the crosstalk between oxidative stress and programmed cell death in cancers
• The new molecular mechanisms underlying the crosstalk between oxidative stress and programmed cell death in cancers
• The epigenetic regulators and metabolic changes in the process of crosstalk between oxidative stress and programmed cell death in cancers
• New diagnostic biomarkers and prognostic models established for programmed cell death in cancers
• The key signaling pathways between oxidative stress and programmed cell death in cancers
• Multiomics analysis of oxidative stress-mediated programmed cell deaths in cancer
• Innovation by 3P medicine in the area of programmed cell death: predictive diagnostics, targeted prevention and personalisation of treatment algorithms