Inflammation and cancer: advances and new agents
Abstract
Tumour-promoting inflammation is considered one of the enabling characteristics of cancer development. Chronic inflammatory disease increases the risk of some cancers, and strong epidemiological evidence exists that NSAIDs, particularly aspirin, are powerful chemopreventive agents. Tumour microenvironments contain many different inflammatory cells and mediators; targeting these factors in genetic, transplantable and inducible murine models of cancer substantially reduces the development, growth and spread of disease. Thus, this complex network of inflammation offers targets for prevention and treatment of malignant disease. Much potential exists in this area for novel cancer prevention and treatment strategies, although clinical research to support targeting of cancer-related inflammation and innate immunity in patients with advanced-stage cancer remains in its infancy. Following the initial successes of immunotherapies that modulate the adaptive immune system, we assert that inflammation and innate immunity are important targets in patients with cancer on the basis of extensive preclinical and epidemiological data. The adaptive immune response is heavily dependent on innate immunity, therefore, inhibiting some of the tumour-promoting immunosuppressive actions of the innate immune system might enhance the potential of immunotherapies that activate a nascent antitumour response.
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Inflammatory components of the immune system are often chronically elevated in older people and are linked to higher incidence of cancer, cardiovascular disease, neurodegenerative disorders and other conditions.
“inflammatory components of the immune system are often chronically elevated in aged individuals and associated with an increased incidence of cancer, cardiovascular disease, neurodegenerative disorders and others1–3”
From An inflammatory aging clock (iAge) based on deep learning tracks multimorbidity, immunosenescence, frailty and cardiovascular aging (2021) · cites this paper as [3]
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- Authors
- Crusz, S. M., & Balkwill, F. R.
- Affiliations
- Queen Mary University of London (GB)
- Corresponding author
- Balkwill, Frances R.
- Venue
- Nature Reviews Clinical Oncology
- Published
- 2015-06-30
- Volume
- 12
- Issue
- 10
- Pages
- 584-596
- ISSN
- 1759-4774 (ISSN-L)
- 1759-4782
- OpenAlex
- W2202349529
- Cited by
- 1,184
- References
- 172
- Citations by year
- 2026: 43 · 2025: 90 · 2024: 146 · 2023: 139 · 2022: 144 · 2021: 145 · 2020: 130 · 2019: 103 · 2018: 81 · 2017: 79 · 2016: 68 · 2015: 14
- FWCI
- 7.62
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Clinical Oncology (publishedVersion)
- PubMed (publishedVersion)
- Queen Mary Research Online (Queen Mary University of London) (submittedVersion)
- Funders
- Cancer Research UK (C587/A16354, 16354)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
- Keywords
- tumor inflammation, tumor microenvironment, carcinogenesis, nonsteroidal anti-inflammatory drugs, aspirin, chemoprevention, innate immunity, adaptive immune response, immunotherapy, immunosuppression, inflammatory mediators
- MeSH terms
- Anti-Inflammatory Agents, Non-Steroidal, Humans, Immunotherapy, Inflammation, Neoplasms, Randomized Controlled Trials as Topic, Disease Progression, Chemoprevention
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