Cancer-prone oxyradical overload disease.
Oxyradical overload disease develops in conditions involving chronic inflammation and may be of inherited etiology, e.g. haemochromatosis and Wilson disease, be acquired, e.g. infection with hepatitis B or C virus or Helicobactor pylori, or be chemically induced, e.g. acid reflux in Barrett oesophagus. Susceptibility to cancer is frequently a pathological consequence of extensive oxyradical damage that leads to a cycle of cell death and regeneration and causes mutations in cancer-related genes. In this brief review, we focus on the possible interactive effects of nitric oxide and the p53 tumour suppressor gene in human carcinogenesis.
Ambs
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Megabios Corporation, Burlingame, CA 94010, USA.
Hussain
S P
SP
Marrogi
A J
AJ
Harris
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CC
D017209:Apoptosis; D003110:Colonic Neoplasms / Q000209:etiology* / Q000235:genetics; D004249:DNA Damage; D018450:Disease Progression; D015971:Gene Expression Regulation, Enzymologic; D015972:Gene Expression Regulation, Neoplastic; D016158:Genes, p53 / Q000235:genetics; D006801:Humans; D008954:Models, Biological; D009154:Mutation; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism
D009569:Nitric Oxide; D019001:Nitric Oxide Synthase