Gastric cancers develop from single cells, based on data from clonality analysis in C3H/HeN → BALB/c chimeric mice. We can conclude that IM is important not as a precancerous lesion but as a paracancerous cord from such studies of clonality of gastric cancers and of phenotypic expression of each intestinal metaplastic or stomach cancer cell. Intestinalization progresses from G, through GI, to I types in noncancerous and cancerous tissue independently, accompanied by homeotic transformation of underlying control factors. H. pylori is not an initiator, but rather a strong promoter in gastric carcinogenesis, and its eradication, together with reduction in salt intake, might effectively prevent gastric cancer development.
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