title: Multifaceted link between cancer and inflammation.
abstract: Increasing evidence from epidemiological, preclinical and clinical studies suggests that dysregulated inflammatory response plays a pivotal role in a multitude of chronic ailments including cancer. The molecular mechanism(s) by which chronic inflammation drives cancer initiation and promotion include increased production of pro-inflammatory mediators, such as cytokines, chemokines, reactive oxygen intermediates, increased expression of oncogenes, COX-2 (cyclo-oxygenase-2), 5-LOX (5-lipoxygenase) and MMPs (matrix metalloproteinases), and pro-inflammatory transcription factors such as NF-κB (nuclear factor κB), STAT3 (signal transducer and activator of transcription 3), AP-1 (activator protein 1) and HIF-1α (hypoxia-inducible factor 1α) that mediate tumour cell proliferation, transformation, metastasis, survival, invasion, angiogenesis, chemoresistance and radioresistance. These inflammation-associated molecules are activated by a number of environmental and lifestyle-related factors including infectious agents, tobacco, stress, diet, obesity and alcohol, which together are thought to drive as much as 90% of all cancers. The present review will focus primarily on the role of various inflammatory intermediates responsible for tumour initiation and progression, and discuss in detail the critical link between inflammation and cancer.
authors: Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597, Singapore. gautam_sethi@nuhs.edu.sg
authors: Gautam
authors: G
authors: Sethi
authors: Muthu K
authors: MK
authors: Shanmugam
authors: Lalitha
authors: L
authors: Ramachandran
authors: Alan Prem
authors: AP
authors: Kumar
authors: Vinay
authors: V
authors: Tergaonkar
mesh_terms: D001094:Arachidonate 5-Lipoxygenase / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism; D002908:Chronic Disease; D051546:Cyclooxygenase 2 / Q000235:genetics / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D007249:Inflammation / Q000378:metabolism*; D018836:Inflammation Mediators; D008019:Life Style; D020782:Matrix Metalloproteinases / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D009369:Neoplasms / Q000209:etiology / Q000235:genetics / Q000378:metabolism*; D009857:Oncogenes; D050796:STAT3 Transcription Factor / Q000378:metabolism; D018808:Transcription Factor AP-1 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D018925:Chemokines; D016207:Cytokines; C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D018836:Inflammation Mediators; D016328:NF-kappa B; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D018808:Transcription Factor AP-1; D014409:Tumor Necrosis Factor-alpha; D001094:Arachidonate 5-Lipoxygenase; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D020782:Matrix Metalloproteinases