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Oxidative stress, inflammation, and cancer: How are they linked?
Open accessAbstract
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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“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].”
From Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022) · cites this paper as [18]
In the citing paper
“In these rats, biweekly phlebotomy was probably not sufficient to attenuate the tumor progression because a low level of oxidative stress might activate cellular proliferation, angiogenesis, and metastasis in tumors.38, 39”
From Phlebotomy as a preventive measure for crocidolite-induced mesothelioma in male rats (2018) · cites this paper as [38]
In the citing paper
“a low level of oxidative stress might activate cellular proliferation, angiogenesis, and metastasis in tumors.38, 39”
From Phlebotomy as a preventive measure for crocidolite-induced mesothelioma in male rats (2018) · cites this paper as [38]
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Metadata
- 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)
- PMC
- PMC2990475
- 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
- green
- www.ncbi.nlm.nih.gov
- Licence
- 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 (medical) › 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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