Prevention of human cancer by modulation of chronic inflammatory processes
Abstract
Chronic inflammation induced by biological, chemical and physical factors has been associated with increased risk of human cancer at various sites. Inflammation facilitates the initiation of normal cells and their growth and progression to malignancy through production of pro-inflammatory cytokines and diverse reactive oxygen and nitrogen species. These also activate signaling molecules involved in inflammation and carcinogenesis such as nuclear transcription factor (NF-κB), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Several chemopreventive agents act through inhibition of signaling pathways (e.g. NF-κB), inhibition of oxidant-generating enzymes (e.g. iNOS) and mediators of inflammation (e.g. COX-2), scavenging reactive oxygen and nitrogen species, and modulation of xenobiotic-metabolizing enzymes (especially phase II enzyme induction). Some anti-inflammatory drugs have been tested in clinical trials to prevent human cancer at several sites. Better understanding of the molecular mechanisms by which chronic inflammation increases cancer risk will lead to further development of new strategies for cancer prevention at many sites.
- Publication:
-
Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
- Pub Date:
- January 2005
- DOI:
- 10.1016/j.mrfmmm.2005.03.030
- Bibcode:
- 2005MRFMM.591..110O
- Keywords:
-
- Apc;
- adenomatous polyposis coli;
- COX;
- cyclooxygenase;
- EPO;
- eosinophil peroxidase;
- hGPX1;
- human cellular glutathione peroxidase 1;
- IL;
- interleukins;
- iNOS;
- inducible nitric oxide synthase;
- Mdr2;
- multidrug resistance-2;
- Mn-SOD;
- manganese superoxide dismutase;
- MPO;
- myeloperoxidase;
- NF-κB;
- nuclear transcription factor;
- PMA;
- phorbol 12-myristate 13-acetate;
- RNS;
- reactive nitrogen species;
- ROS;
- reactive oxygen species;
- TNF;
- tumor necrosis factor;
- Cancer;
- Inflammation;
- Reactive oxygen species;
- Reactive nitrogen species;
- iNOS;
- COX-2;
- NF-κB