Defining the pathologic diagnosis of metaplasia, atrophy, dysplasia, and gastric adenocarcinoma.
Epidemiologic and pathologic studies have confirmed that the development of gastric cancer spans over several decades starting with Helicobacter pylori chronic active gastritis followed, over time and only in a subset of patients, with the development of intestinal metaplasia and atrophy, dysplasia, and finally gastric adenocarcinoma. It has also been established that the pathogenesis of gastric cancer is a multifactorial process in which both environmental and host-related factors play significant role. Improvement in upper endoscopic techniques make possible the detection of not only early gastric cancers but also the mucosal alterations that predate malignant degeneration. A better understanding of the gastric carcinogenic sequence will allow us to better identify the patients at risk and to implement preventive strategies. We review the histopathologic steps that predate the development of gastric cancer and evaluate the risks of transformation that they confer.
Lauwers
Gregory Y
GY
Department of Pathology, Massachusetts General Hospital (WRN 2), 55 Fruit Street, Boston, MA 02114, USA. glauwers@partners.org
D000230:Adenocarcinoma / Q000209:etiology* / Q000382:microbiology / Q000473:pathology; D002908:Chronic Disease; D018450:Disease Progression; D005757:Gastritis, Atrophic / Q000150:complications* / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications* / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D007410:Intestinal Diseases / Q000150:complications / Q000473:pathology*; D008679:Metaplasia; D011230:Precancerous Conditions / Q000473:pathology; D013274:Stomach Neoplasms / Q000209:etiology* / Q000382:microbiology / Q000473:pathology