title: Inducible Nitric Oxide Synthase in the Carcinogenesis of Gastrointestinal Cancers.
abstract: Gastrointestinal (GI) cancer taken together constitutes one of the most common cancers worldwide with a broad range of etiological mechanisms. In this review, we have examined the impact of nitric oxide (NO) on the etiology of colon, colorectal, gastric, esophageal, and liver cancers. Recent Advances: Despite differences in etiology, initiation, and progression, chronic inflammation has been shown to be a common element within these cancers showing interactions of numerous pathways. NO generated at the inflammatory site contributes to the initiation and progression of disease. The amount of NO generated, time, and site vary and are an important determinant of the biological effects initiated. Among the nitric oxide synthase enzymes, the inducible isoform has the most diverse range, participating in numerous carcinogenic processes. There is emerging evidence showing that inducible nitric oxide synthase (NOS2) plays a central role in the process of tumor initiation and/or development.
  
  
  
  Redox inflammation through NOS2 and cyclooxygenase-2 participates in driving the mechanisms of initiation and progression in GI cancers.
  
  
  
  Understanding the underlying mechanism involved in NOS2 activation can provide new insights into important prevention and treatment strategies. Antioxid. Redox Signal. 26, 1059-1077.
authors: 1 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland.
authors: Graciele Almeida
authors: GA
authors: de Oliveira
authors: 1 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland.
authors: Robert Y S
authors: RYS
authors: Cheng
authors: 1 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland.
authors: Lisa A
authors: LA
authors: Ridnour
authors: 1 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland.
authors: Debashree
authors: D
authors: Basudhar
authors: 1 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland.
authors: Veena
authors: V
authors: Somasundaram
authors: 1 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland.
authors: Daniel W
authors: DW
authors: McVicar
authors: 2 Laboratório de Sinalização Celular, Universidade Federal de São Paulo , São Paulo, Brazil .
authors: Hugo Pequeno
authors: HP
authors: Monteiro
authors: 1 Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland.
authors: David A
authors: DA
authors: Wink
mesh_terms: D000818:Animals; D063646:Carcinogenesis / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000378:metabolism*; D018450:Disease Progression; D005770:Gastrointestinal Neoplasms / Q000201:enzymology* / Q000209:etiology; D006801:Humans; D007249:Inflammation / Q000201:enzymology* / Q000209:etiology; D009569:Nitric Oxide / Q000276:immunology; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism*; D010084:Oxidation-Reduction
chemical_list: D009569:Nitric Oxide; C496319:NOS2 protein, human; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human
keywords: gastrointestinal cancer; liver; nitric oxide