Dear Colleagues,

Reactive oxygen species (ROS) are molecules normally produced by cells due to the activity of NADPH oxidases and during ATP generation in mitochondria. When the rate of ROS generation is balanced by the activity of antioxidant compounds and enzymes, the redox homeostatic balance is maintained. However, when ROS levels are too high, they accumulate in the cells leading to oxidative stress that has deleterious effects on many cellular components including DNA, proteins, and lipids. The damage to these components has been associated with many diseases including cancer.

Many signaling pathways are modulated by oxidative stress including NRF2/KEAP1, NF-kB, PI3K/AKT, MAPK/ERK1/2, Ras and mTOR signaling pathways. These pathways play a key role in regulating many important cellular processes including apoptosis, autophagy, cell proliferation, invasion and differentiation. Moreover, in cancerous cells, these pathways can modulate chemotherapy and radiotherapy responses inducing resistance to these treatments, resulting in decreased survival.

 Many natural and synthetic compounds have shown antioxidant activity protecting cells from ROS damage. Moreover, many of these compounds can increase the response to chemotherapy and radiotherapy when used alone or in combination with other treatments; resulting in improved cancer survival. Furthermore, many antioxidant enzymes have been shown to be important prognostic biomarkers in cancer which allows for a more precise and efficient treatment for these cancer patients.

In this Special Issue, we invite authors to submit research articles or reviews on the importance and potential modulation of oxidative stress in cancer patients. This Special Issue aims to provide new insight into the possible mechanisms involved in carcinogenesis and oxidative stress in order to both prevent cancer and improve survival for patients already diagnosed with a malignancy.

Dr. Giovanni Tossetta

Guest Editor