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Risk factors for gastric cancer

Annie On On Chan, MD
Benjamin Wong, DSc, MD, PhD
Section Editor
Mark Feldman, MD, MACP, AGAF, FACG
Deputy Editor
Diane MF Savarese, MD


Gastric cancer has significant geographical, ethnic, and socioeconomic differences in distribution. This topic review will discuss risk factors for gastric cancer. Epidemiologic aspects are presented separately. (See "Epidemiology of gastric cancer".)

There are two main histologic variants of gastric adenocarcinoma. The most frequent is the "intestinal type," so called because of its morphologic similarity to adenocarcinomas arising in the intestinal tract. The less common diffuse type gastric cancers are characterized by a lack of intercellular adhesions, which leaves them unable to form glandular structures. In patients with inherited form of diffuse type gastric cancer, the absence of intercellular adhesions is caused by a germline mutation in the cell adhesion protein E-cadherin (CDH1). (See 'Hereditary diffuse gastric cancer' below.)


The sequence of molecular events that underlies intestinal type gastric cancer is incompletely understood. In comparison, much more is known about the molecular pathogenesis of diffuse type gastric cancers, which display a prominent molecular abnormality in the cell adhesion protein E-cadherin (CDH1). (See "Molecular genetics of colorectal cancer" and "Pathology and molecular pathogenesis of gastric cancer".)

One model for the "intestinal type" of gastric cancer describes a progression from chronic gastritis to chronic atrophic gastritis, to intestinal metaplasia, dysplasia, and eventually to adenocarcinoma [1,2].

Longstanding chronic superficial gastritis caused by chronic Helicobacter pylori infection, pernicious anemia, or possibly a high salt diet leads eventually to chronic atrophic gastritis and intestinal metaplasia.

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Literature review current through: Sep 2017. | This topic last updated: Sep 26, 2016.
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