Oxidative Stress in Cancer

John Hayes (Lead / Corresponding author), Albena Dinkova-Kostova, Kenneth D. Tew

Research output: Contribution to journalReview articlepeer-review

885 Citations (Scopus)
267 Downloads (Pure)


Contingent upon concentration, reactive oxygen species (ROS) influence cancer evolution in apparently contradictory ways, either initiating/stimulating tumorigenesis and supporting transformation/proliferation of cancer cells or causing cell death. To accommodate high ROS levels, tumor cells modify sulfur-based metabolism, NADPH generation and the activity of antioxidant transcription factors. During initiation, genetic changes enable cell survival under high ROS levels by activating antioxidant transcription factors or increasing NADPH via the pentose phosphate pathway (PPP). During progression and metastasis, tumor cells adapt to oxidative stress by increasing NADPH in various ways, including activation of AMPK, the PPP, and reductive glutamine and folate metabolism.
Original languageEnglish
Pages (from-to)167-197
Number of pages31
JournalCancer Cell
Issue number2
Early online date9 Jul 2020
Publication statusPublished - 10 Aug 2020


  • oxidative stress
  • reactive oxygen species
  • adaptation
  • glutathione
  • thioredoxin
  • NADPH generation
  • pentose phosphate pathway
  • reductive glutamine metabolism
  • folate metabolism
  • redox signaling
  • antioxidant
  • NRF2
  • BACH1
  • AP-1
  • FOXO
  • PGC-1alpha
  • HIF-1alpha
  • HSF1
  • NF-κB
  • TP53
  • tumorigenesis
  • initiation
  • progression
  • metastasis
  • dormant cancer cell
  • recurrent disease

ASJC Scopus subject areas

  • Oncology
  • Cancer Research
  • Cell Biology


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