Cited by 5,441Redox biology and oxidative stressAntioxidant Activity and Oxidative StressCancer and biochemical research

Oxidative stress, inflammation, and cancer: How are they linked?

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Reuter, Simone, Gupta, Subash C., Chaturvedi, Madan M., Aggarwal, Bharat B.·2010·Free Radical Biology and Medicine

Abstract

Extensive research during the past 2 decades has revealed the mechanism by which continued oxidative stress can lead to chronic inflammation, which in turn could mediate most chronic diseases including cancer, diabetes, and cardiovascular, neurological, and pulmonary diseases. Oxidative stress can activate a variety of transcription factors including NF-κB, AP-1, p53, HIF-1α, PPAR-γ, β-catenin/Wnt, and Nrf2. Activation of these transcription factors can lead to the expression of over 500 different genes, including those for growth factors, inflammatory cytokines, chemokines, cell cycle regulatory molecules, and anti-inflammatory molecules. How oxidative stress activates inflammatory pathways leading to transformation of a normal cell to tumor cell, tumor cell survival, proliferation, chemoresistance, radioresistance, invasion, angiogenesis, and stem cell survival is the focus of this review. Overall, observations to date suggest that oxidative stress, chronic inflammation, and cancer are closely linked.

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Crossref · 10.1016/j.freeradbiomed.2010.09.006

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  • Chronic oxidative stress and resultant oxidative damage have been implicated in many human diseases including cardiovascular disease, neurodegenerative diseases, diabetes, cancer, and aging.

    “Chronic oxidative stress and the resultant oxidative damage have been implicated in many human diseases including cardiovascular disease, neurodegenerative diseases, diabetes, cancer, and the aging process [18,19,20,21,22].”

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Authors
Reuter, S., Gupta, S. C., Chaturvedi, M. M., & Aggarwal, B. B.
Affiliations
The University of Texas MD Anderson Cancer Center (US)
Corresponding author
Aggarwal, Bharat B.
Venue
Free Radical Biology and Medicine
Publisher
Elsevier BV
Published
2010-12
Volume
49
Issue
11
Pages
1603-1616
ISSN
0891-5849 (ISSN-L)
OpenAlex
W2094156327
Cited by
5,441
References
316
Citations by year
2026: 362 · 2025: 413 · 2024: 418 · 2023: 429 · 2022: 516 · 2021: 507 · 2020: 421 · 2019: 407 · 2018: 391 · 2017: 371 · 2016: 316 · 2015: 238 · 2014: 240 · 2013: 177 · 2012: 131
FWCI
11.28
Type
journal article
Language
en
Open access
Locations
  • Free Radical Biology and Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Fonds National de la Recherche Luxembourg (PDR-08-017)
  • National Institutes of Health (CA-16672, CA-124787-01A2)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer and biochemical research
Keywords
oxidative stress, chronic inflammation, cancer, transcription factors, NF-κB, AP-1, p53, HIF-1α, PPARγ, Nrf2, inflammatory cytokines, chemokines, chemoresistance, radioresistance (biology), tumor invasion, angiogenesis, cancer stem cells, tumor cell survival
MeSH terms
Animals, Cell Survival, Cell Transformation, Neoplastic, Humans, Inflammation, Models, Biological, Neoplasms, Neovascularization, Pathologic, Signal Transduction, Oxidative Stress, Drug Resistance, Neoplasm, Tumor Escape, Cell Proliferation

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