Abstract
Chronic inflammation is involved in the pathogenesis of most common cancers. The aetiology of the inflammation is varied and includes microbial, chemical and physical agents. The chronically inflamed milieu is awash with pro-inflammatory cytokines and is characterized by the activation of signalling pathways that cross-talk between inflammation and carcinogenesis. Many of the factors involved in chronic inflammation play a dual role in the process, promoting neoplastic progression but also facilitating cancer prevention. A comprehensive understanding of the molecular and cellular inflammatory mechanisms involved is vital for developing preventive and therapeutic strategies against cancer. The purpose of the present review is to evaluate the mechanistic pathways that underlie chronic inflammation and cancer with particular emphasis on the role of host genetic factors that increase the risk of carcinogenesis.
| Original language | English |
|---|---|
| Pages (from-to) | 225-235 |
| Number of pages | 11 |
| Journal | Biochemical Journal |
| Volume | 410 |
| DOIs | |
| Publication status | Published - 2008 |
Keywords
- cancer
- chronic infection
- genetic polymorphism
- inflammation
- NF-KAPPA-B
- necrosis-factor-alpha
- signal-transduction pathways
- acid-suppressive therapy
- nitric-oxide synthase
- toll-like receptor-4
- gastric-cancer
- helicobacter-pylori
- colorectal-cancer
- increased risk
