Coussens and Werb 2002: inflammation and cancer
The review that made the immune cells inside a tumour part of the disease: long-running inflammation, whether from infection, irritation or the tumour's own signals, supplies growth factors, blood vessels and DNA damage that help cancers start and spread.
Overview
Coussens and Werb drew together epidemiology and mouse genetics to argue that chronic inflammation is a cause of cancer rather than a bystander. They reviewed the infections and inflammatory conditions tied to specific cancers, such as Helicobacter pylori and stomach cancer, hepatitis viruses and liver cancer, and inflammatory bowel disease and bowel cancer, and described how macrophages, neutrophils and mast cells in the tumour microenvironment release cytokines, proteases, reactive oxygen species and angiogenic factors that promote proliferation, invasion and new blood vessels. They cited estimates that about 15% of cancers worldwide are linked to infection and proposed that anti-inflammatory strategies could prevent or treat cancer.
- Chronic inflammation from infection or irritation precedes many cancers; the authors cite estimates that about 15% of cancers worldwide are attributable to infections.
- Innate immune cells recruited to tumours supply cytokines, growth factors, proteases and reactive oxygen species that drive proliferation, angiogenesis, invasion and DNA damage.
- Mouse models in which inflammatory cells or their mediators are removed develop fewer or slower tumours.
This paper is why the tumour microenvironment is studied as intensely as the cancer cell itself. It underpins vaccination against HPV and hepatitis B as cancer prevention, aspirin and anti-inflammatory trials in bowel cancer, and the current work on macrophages and myeloid cells as immunotherapy targets.
- A review, so it synthesises rather than tests; several proposed mechanisms rested on mouse models.
- Inflammation is also part of effective anti-tumour immunity, and the balance between the two is still being worked out.
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