43 Citations (Scopus)

Abstract

Reactive oxygen species (ROS) are highly reactive molecules that arise from a number of cellular sources, including oxidative metabolism in mitochondria. At low levels they can be advantageous to cells, activating signaling pathways that promote proliferation or survival. At higher levels, ROS can damage or kill cells by oxidizing proteins, lipids, and nucleic acids. It was hypothesized that antioxidants might benefit high-risk patients by reducing the rate of ROS-induced mutations and delaying cancer initiation. However, dietary supplementation with antioxidants has generally proven ineffective or detrimental in clinical trials. High ROS levels limit cancer cell survival during certain windows of cancer initiation and progression. During these periods, dietary supplementation with antioxidants may promote cancer cell survival and cancer progression. This raises the possibility that rather than treating cancer patients with antioxidants, they should be treated with pro-oxidants that exacerbate oxidative stress or block metabolic adaptations that confer oxidative stress resistance.

Original languageEnglish (US)
Pages (from-to)163-175
Number of pages13
JournalCold Spring Harbor Symposia on Quantitative Biology
Volume81
Issue number1
DOIs
StatePublished - 2016

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Oxidative stress
Reactive Oxygen Species
Oxidative Stress
Neoplasm Metastasis
Antioxidants
Neoplasms
Dietary Supplements
Cells
Cell Survival
Mitochondria
Metabolism
Nucleic Acids
Lipids
Molecules
Clinical Trials
Mutation
Survival
Proteins

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Genetics

Cite this

Cancer, oxidative stress, and metastasis. / Gill, Jennifer G.; Piskounova, Elena; Morrison, Sean J.

In: Cold Spring Harbor Symposia on Quantitative Biology, Vol. 81, No. 1, 2016, p. 163-175.

Research output: Contribution to journalArticle

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