Redox signaling in cancer biology

David Gius, Douglas R. Spitz*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

146 Scopus citations

Abstract

Over the last three decades, it is has become increasing clear that intracellular signaling pathways are activated via changes in intracellular metabolic oxidation/reduction (redox) reactions involving reactive oxygen species (ROS; i.e., superoxide and hydrogen peroxide). The initial proposals hypothesized that signaling through metabolic oxidation/reduction (redox) reactions involving ROS could contribute to carcinogenesis and progression to malignancy. Strong evidence for this hypothesis was obtained from studies showing that environmental insults (i.e., ionizing radiation) as well as xenobiotics (i.e., polycyclic aromatic hydrocarbons and phorbol esters) capable of inducing steady-state increases in free radical production and ROS could act as both initiators and promoters of carcinogenesis. This Fonini is directed at understanding possible redox signaling mechanisms governing cellular radiation response, tumor growth, and response to therapy, as well as the role of nitric oxide in cancer biology.

Original languageEnglish (US)
Pages (from-to)1249-1252
Number of pages4
JournalAntioxidants and Redox Signaling
Volume8
Issue number7-8
DOIs
StatePublished - Jul 2006

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

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