Chronic inflammation and oxidative stress in human carcinogenesis
Abstract
A wide array of chronic inflammatory conditions predispose susceptible cells to neoplastic transformation. In general, the longer the inflammation persists, the higher the risk of cancer. A mutated cell is a sine qua non for carcinogenesis. Inflammatory processes may induce DNA mutations in cells via oxidative/nitrosative stress. This condition occurs when the generation of free radicals and active intermediates in a system exceeds the system's ability to neutralize and eliminate them. Inflammatory cells and cancer cells themselves produce free radicals and soluble mediators such as metabolites of arachidonic acid, cytokines and chemokines, which act by further producing reactive species. These, in turn, strongly recruit inflammatory cells in a vicious circle. Reactive intermediates of oxygen and nitrogen may directly oxidize DNA, or may interfere with mechanisms of DNA repair. These reactive substances may also rapidly react with proteins, carbohydrates and lipids, and the derivative products may induce a high perturbation in the intracellular and intercellular homeostasis, until DNA mutation. The main substances that link inflammation to cancer via oxidative/nitrosative stress are prostaglandins and cytokines. The effectors are represented by an imbalance between pro‐oxidant and antioxidant enzyme activities (lipoxygenase, cyclooxygenase and phospholipid hydroperoxide glutathione‐peroxidase), hydroperoxides and lipoperoxides, aldehydes and peroxinitrite. This review focalizes some of these intricate events by discussing the relationships occurring among oxidative/nitrosative/metabolic stress, inflammation and cancer. © 2007 Wiley‐Liss, Inc.
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These transcription factors are responsible for gene transcription of proinflammatory cytokines such as TNF-α and interleukins IL-8 and IL-6, which sequestrate leukocytes such as neutrophils and macrophages, forming part of an inflammatory pathway.
“These transcription factors are responsible for the gene transcription of proinflammatory cytokines, such as tumor necrosis factor (TNF-α) and interleukins IL-8 and IL-6 which in turn sequestrate leukocytes such as neutrophils and macrophages forming thus a part of an inflammatory pathway (Drost et al. 2005; Federico et al. 2007).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Federico et al. 2007
Exogenous sources including tobacco smoke, asbestos, radon, and others increase ROS formation, which activates transcription factors NF-κB and AP-1.
“Exogenous sources, involving tobacco smoke, asbestos, radon, and others increase ROS formation which consequently activates transcription factors NF-κB and activator protein AP-1.”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Federico et al. 2007
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- Authors
- Federico, A., Morgillo, F., Tuccillo, C., Ciardiello, F., & Loguercio, C.
- Affiliations
- University of Campania "Luigi Vanvitelli" (IT)
- Corresponding author
- Federico, Alessandro
- ORCID
- Venue
- International Journal of Cancer
- Publisher
- Wiley
- Published
- 2007-09-24
- Volume
- 121
- Issue
- 11
- Pages
- 2381-2386
- ISSN
- 0020-7136 (ISSN-L)
- 1097-0215
- OpenAlex
- W2149979963
- Cited by
- 1,001
- References
- 104
- Citations by year
- 2026: 30 · 2025: 45 · 2024: 55 · 2023: 50 · 2022: 65 · 2021: 61 · 2020: 64 · 2019: 45 · 2018: 54 · 2017: 46 · 2016: 62 · 2015: 56 · 2014: 59 · 2013: 60 · 2012: 76
- FWCI
- 4.24
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- International Journal of Cancer (publishedVersion)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca - Università degli Studi della Campania "Luigi Vanvitelli" (submittedVersion)
- Topics
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer and biochemical research
- Keywords
- chronic inflammation, oxidative stress, nitrosative stress, carcinogenesis, DNA damage, free radicals, reactive oxygen species, reactive nitrogen species, DNA repair, arachidonic acid metabolites, prostaglandins, cytokines, chemokines, lipoxygenase, cyclooxygenase, phospholipid hydroperoxide glutathione peroxidase, lipid peroxidation, peroxynitrite, aldehydes, oncogenic transformation
- MeSH terms
- Cell Transformation, Neoplastic, Chronic Disease, DNA Damage, Free Radicals, Humans, Inflammation, Mutation, Neoplasms, Oxidation-Reduction, Prostaglandins, Cytokines, Reactive Oxygen Species, Oxidative Stress, Reactive Nitrogen Species
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