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- Mucosal immunity
- experimental colitis
- IBD clinical
- inflammatory bowel disease
- IBD basic research
- pancreatic cancer
- Helicobacter pylori
- acid-related diseases
- non-ulcer dyspepsia
- genetic polymorphisms
- inflammation
- IBD
- 5-aminosalicylic acid (5-ASA)
- inflammatory mechanisms
- radiation enteritis
The intrinsic connection between inflammation and cancer promotion is well established and is especially strong in patients with colorectal cancer (CRC), the second most common cause of cancer-related death in Western countries.1 2 The administration of non-steroidal anti-inflammatory drugs in controlled studies reduces the incidence of colon cancer in patients with familial adenoma polyposis, confirming the link between inflammation and colon cancer.3 Several lines of evidence indicate that chronic inflammation predisposes the tissue to cancer by inducing gene mutation, inhibiting apoptosis or stimulating angiogenesis and cell proliferation. Patients with inflammatory bowel disease (IBD) are at increased risk of developing CRC and, in particular, an association between IBD and the development of colitis-associated cancer (CAC) has been reported. Although the severity and extent of disease and the duration of inflammation seem to be major factors associated with the development of CAC in patients with IBD, the molecular determinants of this link have only recently started to be elucidated. Studies have highlighted the presence of leucocyte infiltration and inflammatory mediators in the tumour microenvironment, indicating that immune cells are major players in tumour promotion.2 4
Preclinical models of CAC are helping to clarify the mechanisms underlying cancer-related inflammation. The direct role of the adaptive immune response in promoting CAC is becoming more evident.2 Although T cell responses fuel the inflammatory process and orchestrate the microenvironment surrounding tumours by contributing to the proliferation, migration and survival of cancer cells, activation of the adaptive immune system also …
Footnotes
Linked article 300612.
Competing interests None.
Provenance and peer review Commissioned; externally peer reviewed.