Mechanisms linking pathogens-associated inflammation and cancer
Abstract
It has been estimated that chronic infections with viruses, bacteria and parasites are the causative agents of 8-17% of global cancers burden. Carcinogenesis associated with infections is a complex process, often mediated by chronic inflammatory conditions and accumulating evidence indicate that a smouldering inflammation is a component of the tumor microenvironment and represents the 7th hallmark of cancer. Selected infectious agents promote a cascade of events culminating in chronic inflammatory responses, thus predisposing target tissues to increased cancer susceptibility. A causal link also exists between an inflammatory microenvironment, consisting of inflammatory cells and mediators, and tumor progression. Tumor-Associated Macrophages (TAM) represent the major inflammatory population present in tumors, orchestrating various aspects of cancer, including: diversion and skewing of adaptive responses; cell growth; angiogenesis; matrix deposition and remodelling; construction of a metastatic niche and actual metastasis; response to hormones and chemotherapeutic agents. Recent studies on human and murine tumors indicate that TAM show a remarkable degree of plasticity and functional heterogeneity, during tumour development. In established tumors, TAM acquire an M2 polarized phenotype are engaged in immunosuppression and the promotion of tumor angiogenesis and metastasis. Being a first line of the innate defence mechanisms, macrophages are also equipped with pathogen-recognitio…
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The extrinsic pathway of tumorigenesis is initially characterized by a chronic pro-inflammatory environment from persistent microbial infection, autoimmune disease, or unknown etiology.
“This “extrinsic pathway” is initially characterized by a chronic pro-inflammatory environment resulting from a persistent microbial infection, autoimmune disease, or other etiology of unknown origin [37,38].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [37]
Chronic production of inflammatory mediators can lead to tumor cell proliferation/survival or genetic instability in normal cells, resulting in oncogene expression and immune suppressive cytokines.
“The chronic production of large quantities of inflammatory mediators in these cases can lead, through a number of pathways, to tumor cell proliferation and survival or to the induction of genetic instabilities in normal cells, with resultant expression of oncogenes and production of immune suppressive cytokines [37,38].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [37]
Early tumor development is often characterized by a polarized inflammatory M1-like environment.
“Thus, early tumor development is, in many cases, characterized by a polarized inflammatory, M1-like, environment.”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [37]
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“in normal cells, with resultant expression of oncogenes and production of immune suppressive cytokines [37,38].”
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Self-citation
- Authors
- Porta, C., Riboldi, E., & Sica, A.
- Affiliations
- Università degli Studi del Piemonte Orientale “Amedeo Avogadro” (IT)
- Corresponding author
- Sica, Antonio
- Venue
- Cancer Letters
- Publisher
- Elsevier BV
- Published
- 2011-06
- Volume
- 305
- Issue
- 2
- Pages
- 250-262
- ISSN
- 0304-3835 (ISSN-L)
- OpenAlex
- W2046502194
- Cited by
- 119
- References
- 11
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 5 · 2023: 9 · 2022: 5 · 2021: 9 · 2020: 6 · 2019: 5 · 2018: 3 · 2017: 11 · 2016: 5 · 2015: 10 · 2014: 15 · 2013: 7 · 2012: 15
- FWCI
- 0.69
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cancer Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Associazione Italiana Ricerca sul Cancro (AIRC), Italy
- Fondazione Cariplo, Italy
- Ministero Università Ricerca (MUR), Italy
- Ministero della Salute
- Regione Piemonte
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- chronic inflammation, infection-associated cancer, tumor microenvironment, tumor-associated macrophages, M2 macrophage polarization, pathogen recognition receptors, tumor angiogenesis, metastasis, immunosuppression, cancer prevention, cancer therapy
- MeSH terms
- Animals, Humans, Inflammation, Macrophages, Mice, Transgenic, Neoplasms, Phenotype, Signal Transduction, Cytokines, NF-kappa B, Oxidative Stress, Mice, Cyclooxygenase 2, Hypoxia-Inducible Factor 1
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