title: Pathology of gastric cancer and its precursor lesions.
abstract: Gastric cancers are a histologically heterogenous group of neoplasms arising from unique epidemiologic and molecular backgrounds. There is accumulating evidence that the intestinal type of gastric adenocarcinoma develops through a multistep process beginning with chronic gastritis triggered primarily by Helicobacter pylori and progressing through atrophy, intestinal metaplasia, and dysplasia (intraepithelial neoplasia) to carcinoma. Loss of E-cadherin expression resulting from CDH1 gene alterations is the primary carcinogenetic event in hereditary diffuse gastric cancer. Proximal gastric adenocarcinomas likely result from either gastroesophageal reflux or H pylori gastritis. This article provides an update of the histologic, immunohistochemical, and molecular pathways of gastric cancer and its precursors.
authors: Department of Pathology, Rhode Island Hospital, Providence, RI 02903, USA.
authors: Evgeny
authors: E
authors: Yakirevich
authors: Murray B
authors: MB
authors: Resnick
mesh_terms: D000230:Adenocarcinoma / Q000145:classification / Q000235:genetics / Q000473:pathology*; D000236:Adenoma / Q000473:pathology*; D001327:Autoimmune Diseases / Q000150:complications; D063646:Carcinogenesis / Q000235:genetics / Q000473:pathology*; D002299:Cardia / Q000473:pathology; D002908:Chronic Disease; D005756:Gastritis / Q000276:immunology / Q000382:microbiology / Q000473:pathology*; D005757:Gastritis, Atrophic / Q000473:pathology; D016147:Genes, Tumor Suppressor; D042822:Genomic Instability; D016481:Helicobacter Infections / Q000150:complications* / Q000382:microbiology; D016480:Helicobacter pylori; D006801:Humans; D008679:Metaplasia / Q000473:pathology; D009857:Oncogenes; D013270:Stomach / Q000473:pathology*; D013274:Stomach Neoplasms / Q000145:classification / Q000235:genetics / Q000473:pathology*