Epidemiological studies have revealed that chronic inflammation predisposes to different forms of cancer.

Monday, 26/07/2010  |   Chemokines, Inflammation  |  no comments

chronic inflammation
Epidemiological studies have revealed that chronic inflammation predisposes to different forms of cancer. Selected extrinsic inflammatory conditions increase the risk of cancer and an inflammatory component is also present also in the microenvironment of tumours epidemiologically unrelated to inflammation. An intrinsic (driven by genetic events that cause neoplasia) and an extrinsic (driven by inflammatory conditions which predispose to cancer) pathway link inflammation and cancer. Smouldering inflammation in the tumour microenvironment contributes to proliferation and survival of malignant cells, angiogenesis, metastasis, subversion of adaptive immunity, response to hormones, and chemotherapeutic agents. In the intrinsic pathway, activation of different classes of oncogenes orchestrates the construction of an inflammatory microenvironment. In the extrinsic pathway inflammatory conditions promote cancer development (e.g. colitis-associated cancer of the intestine). Key orchestrators at the intersection of the intrinsic and extrinsic pathway include transcription factors (e.g. nuclear factor kappa-B (NF?B)) (2), cytokines (e.g. TNF), and chemokines. Thus, cancer related inflammation (CRI) is a key component of the tumour microenvironment and may represent the seventh hall-mark of cancer. Emerging evidence also suggests that cancer-related inflammation promotes genetic instability.
Cytokines are a key component and orchestrator of the inflammatory microenvironment of tumours. As such they represent a prime target in therapeutic efforts aimed at taming tumour-promoting CRI. For many years all efforts to treat cancer have concentrated on the destruction/inhibition of tumour cells. Strategies to modulate the host microenvironment offer a complementary perspective. Thus, cancer-related inflammation represents a target for innovative diagnostic and therapeutic strategies.

Mantovani, A., Garlanda, C. & Allavena, P. Molecular pathways and targets in cancer-related inflammation. Annals of Medicine. 2010; 42:Pp. 161–70

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