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home - Stomach - Gastric Cancer - Stomach Cancer Aetiology Written by Dr Sebastian Zeki

Stomach Cancer Aetiology

Cytokine polymorphismsIL-1 inhibits gastric acid secretion and gets upregulated by H.pylori.Polymorphisms (IL-1B-31T and IL-1RN*2) are especially associated with low acid secretion and gastric atrophy. More common in Africans.Other proinflammatory genotypes of TNFalpha and IL-10 are also associated.IFNG1R polymorphisms are associ-ated with high H.pylori antibodies and more prevalent in Africans (may explain increased prevalence in Africa of H. pylori but decreased pathogenicity. Free radical production Decreased ascorbate Its usual role is protective.It blocks nitrosation.It scavenges free radicals.It reduces pH. Increased gastrin (compensates for increased pH) Cell proliferation Increased N-nitroso compounds Atrophic Decreased acid secretion Inflammation Increased nitrate-reducing bacteria proliferation Neutrophil attractionIt produces inducible NOS with NO and free radical production) Epithelial cell damage Loss of parietal cell mass + Causes Free radical production Correa Hypothesis (intestinal type gastric ca) Gastric cancer Pathogenesis H. pylori related Causes acute and chronic gastritis Normal Acute gastritis Chronic gastritis Atrophic gastritis Intestinal metaplasia (IM) Types:-Type 1 (small intestine type mucosa).-Type 2.-Type 3 (colonic type mucosa). Dysplasia Types:Low grade (progress to ca in 10%).High grade (progress to ca in 70%). Early gastric cancer (limited to mucosa and submucosa regardlessof lymph node involvement) Late gastric cancer These are not always premalignant Written by Dr Sebastian Zeki

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