Cited by 1,974Inflammatory mediators and NSAID effectsImmune cells in cancerInflammatory Bowel Disease

Inflammation and Colon Cancer

Terzić, Janoš, Grivennikov, Sergei, Karin, Eliad, Karin, Michael·2010·Gastroenterology

Abstract

The connection between inflammation and tumorigenesis is well-established and in the last decade has received a great deal of supporting evidence from genetic, pharmacological, and epidemiological data. Inflammatory bowel disease is an important risk factor for the development of colon cancer. Inflammation is also likely to be involved with other forms of sporadic as well as heritable colon cancer. The molecular mechanisms by which inflammation promotes cancer development are still being uncovered and could differ between colitis-associated and other forms of colorectal cancer. Recent work has elucidated the role of distinct immune cells, cytokines, and other immune mediators in virtually all steps of colon tumorigenesis, including initiation, promotion, progression, and metastasis. These mechanisms, as well as new approaches to prevention and therapy, are discussed in this review.

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Crossref · 10.1053/j.gastro.2010.01.058

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243 of 243 references verified0 citation errors · 0 not checkable

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  • Chronic intestinal inflammation has been associated with the development of CRC and it can result from an aberrant ratio of protective (tolerogenic) to aggressive (proinflammatory, pro-tumorigenic) microbiota.

    “Chronic intestinal inflammation has been associated with the development of CRC and it can result from an aberrant ratio of protective (tolerogenic) to aggressive (proinflammatory, pro-tumorigenic) microbiota [45] .”
  • Many bacterial species were found to be enriched in colorectal tumour samples and adjacent tissue: Bacteroides fragilis, Bacteroides vulgatus, Bifidobacterium longum, Clostridium butyricum, Mitsuokella multiacida, Escherichia coli, Enterococcus faecalis, and Streptococcus bovis.

    “Many bacterial species were found to be enriched in colorectal tumour samples and adjacent tissue: B. fragilis, Bacteroides vulgatus, Bifidobacterium longum, Clostridium butyricum, Mitsuokella multiacida, E. coli, Enterococcus faecalis, and S. bovis [45] .”

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Authors
Terzić, J., Grivennikov, S., Karin, E., & Karin, M.
Affiliations
  • University of California San Diego (US)
  • Tel Aviv Sourasky Medical Center (IL)
Corresponding author
Karin, Michael
Venue
Gastroenterology
Publisher
Elsevier BV
Published
2010-05
Volume
138
Issue
6
Pages
2101-2114.e5
ISSN
0016-5085 (ISSN-L)
OpenAlex
W2085852125
Cited by
1,974
References
247
Citations by year
2026: 41 · 2025: 80 · 2024: 106 · 2023: 140 · 2022: 147 · 2021: 192 · 2020: 159 · 2019: 139 · 2018: 144 · 2017: 145 · 2016: 136 · 2015: 127 · 2014: 112 · 2013: 119 · 2012: 86
FWCI
10.78
Type
journal article
Language
en
Open access
closed
Locations
  • Gastroenterology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • Crohn's and Colitis Foundation of America (1762)
  • American Association for Cancer Research
  • American Cancer Society
Topics
  • Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
  • Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
Keywords
inflammation, colon cancer, colorectal cancer, inflammatory bowel disease, colitis-associated colorectal cancer, carcinogenesis, immune cells, cytokines, cancer prevention, cancer therapy, metastasis
MeSH terms
Animals, Anti-Inflammatory Agents, Cell Transformation, Neoplastic, Colon, Colonic Neoplasms, Humans, Neoplasm Invasiveness, Risk Factors, Colorectal Neoplasms, Inflammatory Bowel Diseases, Signal Transduction, Gene Expression Regulation, Neoplastic, Cytokines, Anticarcinogenic Agents, Risk Assessment, Inflammation Mediators, Genetic Predisposition to Disease

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