• Review: Pathogenesis and Prevention of Gastric Cancer

Review: Pathogenesis and Prevention of Gastric Cancer

New diagnostic protocols, effective medical treatments, and recently developed conservative ablative procedures could make gastric cancer a preventable malignancy, says a review article in the December issue of Clinical Gastroenterology and Hepatology.

Progressive disarrangement of gland architecture during epithelial dedifferentiation. Unrestricted proliferation occurs in the basal portion of the glands through the superficial epithelial layer. These events lead to interruption of the basal membrane, which allows the neoplastic epithelia to spread into the lamina propria (in red the muscularis mucosae).

Gastric cancer is 1 of the 5 most common causes of cancer death, and only 30% of patients survive 5 years after diagnosis. However, more than 90% of gastric adenocarcinomas are believed to result from long-term mucosal inflammation. Helicobacter pylori infection is the leading cause of non–self-limiting gastritis, which leads to atrophy of the gastric mucosa and impairments in acid secretion. This results in molecular and phenotypic changes to gastric cells and carcinogenesis.

Massimo Rugge et al review strategies to interfere with this carcinogenic pathway. For example, eradication of H pylori and endoscopy can prevent or limit progression to gastric cancer.

Rugge et al explain that the changes that occur during progression to cancer with gastric atrophy (loss of glandular structures or their replacement by metaplastic-transformed glands, pseudopyloric and/or intestinal). The metaplastic epithelia dedifferentiate further to acquire properties of neoplastic cells without invasive activity (dysplasia, also called intraepithelial neoplasia). Cells then become invasive and progresses into malignant gastric tumors (see figure).

Other risk factors for gastric cancer beyond H pylori infection include Epstein-Barr virus infection, autoimmune gastritis, Ménétrier’s disease, alkaline reflux disease, pernicious anemia, as well as environmental/lifestye factorsand family history.

The authors review approaches for assessing patients with gastritis and precancerous gastric lesions (endoscopy), as well as histologic evaluation of dysplasia, imaging techniques to detect early-stage lesions, and surveillance of advanced precancerous lesions.

Rugge et al walk readers through the pathways by which different risk factors lead to molecular changes in gastric cells, transformation, and tumorigenesis. They also explain how different strains of H pylori promote mutagenesis and genes that are mutated or aberrantly expressed during progression to gastric cancer.

They outline strategies for prevention in addition to H pylori eradication, which include vaccination to prevent H pylori infection and endoscopy and serologic screening.

The authors state that strategies for gastric cancer prevention should be modified based on country-specific gastric cancer incidence and socioeconomic and cultural factors, and require a team comprising gastroenterologists, oncologists, and pathologists.

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