Immunity, Inflammation, and Cancer

Grivennikov, Sergei I.; Greten, Florian R.; Karin, Michael

doi:10.1016/j.cell.2010.01.025

Cited by 10,755Immune cells in cancerCancer Immunotherapy and BiomarkersCancer, Stress, Anesthesia, and Immune Response

Immunity, Inflammation, and Cancer

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Grivennikov, Sergei I., Greten, Florian R., Karin, Michael·2010·Cell

DOI 10.1016/j.cell.2010.01.025PMC PMC2866629

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Abstract

Inflammatory responses play decisive roles at different stages of tumor development, including initiation, promotion, malignant conversion, invasion, and metastasis. Inflammation also affects immune surveillance and responses to therapy. Immune cells that infiltrate tumors engage in an extensive and dynamic crosstalk with cancer cells, and some of the molecular events that mediate this dialog have been revealed. This review outlines the principal mechanisms that govern the effects of inflammation and immunity on tumor development and discusses attractive new targets for cancer therapy and prevention.

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Chronic inflammation is a cause or an important contributor to virtually every major age-related disease, both degenerative and hyperplastic.
“Chronic inflammation, of course, is a cause of—or an important contributor to—virtually every major age-related disease, both degenerative and hyperplastic (109–111).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [111]
The Introduction and Conclusions and Prospective sections (page unavailable) describe chronic inflammation as a contributor to cancer risk and tumor development. They do not support the broader claim about virtually every major age-related disease, including degenerative diseases. (LLM, conf=0.87)
Experimental — accuracy not yet measured
After chronic stress breaks the balance through a long-term pro-inflammatory response, pro-tumorigenic immune cells and cytokines act on all stages of tumor development including initiation, promotion, malignant transformation, invasion, and metastasis through mutation, epigenetic modification, and regulation of the tumor microenvironment.
“After chronic stress breaks this balance through a long-term pro-inflammatory response, these cells and cytokines can act on all stages of tumor development, including initiation, promotion, malignant transformation, invasion, and metastasis through mutation, epigenetic modification, and regulation of the tumor microenvironment [(50, 51); Figure 3].”
From Chronic Stress Promotes Cancer Development (2020) · cites this paper as [50]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measured
Environmental factors, such as infection, stress, obesity, aging and smoking, each of which can induce chronic inflammation, could be a major cause of oncogenesis.
“Therefore, rather than the dogma that oncogenesis is intrinsically triggered in pre-neoplastic cells, environmental factors, such as infection, stress, obesity, aging and smoking, each of which can induce chronic inflammation, could be a major cause of oncogenesis (4, 6, 9, 233).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [9]
The Introduction links infection, smoking, obesity, and older age to cancer risk or tumor promotion through inflammatory mechanisms; Conclusions and Prospective says inflammation can affect tumorigenesis from initiation onward. Our copy does not support stress as another such environmental factor, and it also describes intrinsic tumor-triggered inflammation rather than ruling it out. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Interactions between a tumor and its microenvironment through the immune system are critical for tumor development and progression.
“Additionally, interactions between a tumor and its microenvironment through the immune system are critical for tumor development and progression (2, 6, 9, 58–60)”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [9]
Chronic inflammation is often accompanied with autoimmune disease and cancer.
“Chronic inflammation is often accompanied with autoimmune disease and cancer (2, 4, 9).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [9]

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Hallmarks of Cancer: The Next Generation
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IL-6 in inflammation, autoimmunity and cancer
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“Chronic inflammation is often accompanied with auto-immune disease and cancer (2, 4, 9).”
Background
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Immune Checkpoint Inhibitors in Cancer Therapy
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The Cytosolic DNA-Sensing cGAS–STING Pathway in Cancer
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Plasma membrane translocation of trimerized MLKL protein is required for TNF-induced necroptosis
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Promotion of Hepatocellular Carcinoma by the Intestinal Microbiota and TLR4
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Age and Age-Related Diseases: Role of Inflammation Triggers and Cytokines
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Damage-associated molecular patterns in inflammatory diseases
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Mesenchymal stem cells: environmentally responsive therapeutics for regenerative medicine
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Targeting Tumor Microenvironment for Cancer Therapy
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Bile acids and the gut microbiota: metabolic interactions and impacts on disease
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MTOR regulates the pro-tumorigenic senescence-associated secretory phenotype by promoting IL1A translation
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Microglial cell origin and phenotypes in health and disease
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TNF and ROS crosstalk in inflammation
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The Continuum of Aging and Age-Related Diseases: Common Mechanisms but Different Rates
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TGFβ biology in cancer progression and immunotherapy
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Voluntary running suppresses tumor growth through epinephrine- and IL-6-dependent NK cell mobilization and redistribution
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NLRP6 Inflammasome Orchestrates the Colonic Host-Microbial Interface by Regulating Goblet Cell Mucus Secretion
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Cancer-associated fibroblasts neutralize the anti-tumor effect of CSF1 receptor blockade by inducing PMN-MDSC infiltration of tumors
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Oral Mucosal Epithelial Cells
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TGF-β Promotes Heterogeneity and Drug Resistance in Squamous Cell Carcinoma
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Background
Oncogenic Kras activates a hematopoietic-to-epithelial IL-17 signaling axis in preinvasive pancreatic neoplasia
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Authors: Grivennikov, S. I., Greten, F. R., & Karin, M.
Affiliations: University of California San Diego (US)
TUM Klinikum (DE)
Corresponding author: Karin, Michael
ORCID: Grivennikov, Sergei I.
Greten, Florian R.
Karin, Michael
Venue: Cell
Publisher: Elsevier BV
Published: 2010-03
Volume: 140
Issue: 6
Pages: 883-899
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/j.cell.2010.01.025
PMC: PMC2866629
OpenAlex: W2118278569
Cited by: 10,755
References: 159
Citations by year: 2026: 464 · 2025: 621 · 2024: 681 · 2023: 751 · 2022: 901 · 2021: 946 · 2020: 856 · 2019: 796 · 2018: 783 · 2017: 810 · 2016: 717 · 2015: 601 · 2014: 523 · 2013: 515 · 2012: 407
FWCI: 33.06
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 1234 d)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
Funders: American Association for Cancer Research
American Cancer Society
Crohn's and Colitis Foundation
Deutsche Forschungsgemeinschaft
Deutsche Krebshilfe
National Institutes of Health
National Cancer Institute (R01CA118165, R01CA127923, R01CA132586)
National Institute of Allergy and Infectious Diseases (R01AI043477)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
Keywords: inflammation, cancer, antitumor immunity, tumor microenvironment, immune surveillance, tumor-promoting inflammation, tumor invasion and metastasis, cancer therapy targets, cancer prevention
MeSH terms: Animals, Cell Transformation, Neoplastic, Humans, Immune System, Inflammation, Neoplasms

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