Reprint

Paradox Role of Oxidative Stress in Cancer

State of the Art

Edited by
June 2022
214 pages
  • ISBN978-3-0365-4421-2 (Hardback)
  • ISBN978-3-0365-4422-9 (PDF)

This is a Reprint of the Special Issue Paradox Role of Oxidative Stress in Cancer: State of the Art that was published in

Biology & Life Sciences
Summary

Reactive oxygen species (ROS) are produced by healthy cells and are maintained at physiological levels by antioxidant systems. However, when ROS increase in number, a condition of oxidative stress occurs, leading to many human diseases, including cancer. The relationship between oxidative stress and cancer is complex since ROS play a double-edged role in cancer development and under therapy response.

This paradox represents a great challenge for researchers and needs to be investigated. The articles collected in this Special Issue can help to clarify the role of ROS modulation in cancer prevention and treatment, and to dissect the molecular mechanisms underlying its paradoxical role in order to counteract carcinogenesis or enhance sensitivity to anticancer therapy.

Format
  • Hardback
License and Copyright
© 2022 by the authors; CC BY-NC-ND license
Keywords
sonodynamic therapy; carbon doped titanium dioxide; sonosensitizers; ultrasound; cancer treatment; breast cancer treatment; radiotherapy; hematological malignancies; oxidative stress; lymphoma; leukemia; multiple myeloma; apoptosis; mitochondria; ultraviolet-C (UVC); withanolide; combined treatment; oral cancer; DNA damage; cancer therapy; oxidative stress; immune system; Hypericum perforatum; hyperforin; reactive oxygen species; pH regulation; tumor prevention; tumor therapy; apoptosis; cancerogenesis; inflammatory signaling; natural compounds; pancreatic cancer; antitumor agents; coordination polymers; bioinorganic chemistry; reactive oxygen species; cold atmospheric plasma; reactive oxygen and nitrogen species; oxidative stress; nitrite; cancer treatment; cancer stem cells; chemoresistance; glutathione; lipid peroxidation; ZEB-1; GPX4; ferroptosis; HO-1; Nrf2; cancer progression; patients; therapy; prognosis; biomarker; ferroptosis; Eprenetapopt; Erastin; GPX4; glutathione (GSH); SLC7A11; iron; oxidative stress; NRF2; n/a

Related Books