Gastric cáncer: Overview

Abstract

Gastric cancer ranks fourth in incidence and second in mortality among all cancers worldwide. Despite the decrease in incidence in some regions of the world, gastric cancer continues to present a major clinical challenge due to most cases being diagnosed in advanced stages with poor prognosis and limited treatment options. The development of gastric cancer is a complex and multifactorial process involving a number of etiological factors and multiple genetic and epigenetic alterations. Among the predisposing factors are: Helicobacter pylori infection, high salt intake, smoking, and in a small percentage of patients, a familial genetic component. More than 95% of stomach cancer cases are adenocarcinomas, which are classified into two major histologic types: intestinal and diffuse. Intestinal type adenocarcinoma is preceded by a sequence of gastric lesions known as Correa´s cascade and is the histologic type associated with the global decrease in gastric cancer rates. Diffuse type adenocarcinomas have a more aggressive behavior and worse prognosis than those of the intestinal type. According to the anatomical location, adenocarcinomas are classified as proximal (originating in the cardia) and distal (originating in the body and antrum). This classification seems to recognize two different clinical entities. Surgical resection of the tumor at an early stage is the only effective treatment method. Therefore, the identification and surveillance of patients at risk may play a significant role in survival rates. Anti-Helicobacter pylori therapy has been shown to be an effective measure in the prevention of gastric cancer.

Keywords: Gastric cancer; Helicobacter pylori; dysplasia; epidemiology; gastric adenocarcinoma; intestinal metaplasia; multifocal atrophic gastritis.

Figure 1. Age-standardized gastric cancer incidence rates, both sexes. GLOBOCAN 2008.3

Figure 2. Correa's precancerous cascade. A, Normal gastric mucosa. B, Non atrophic chronic gastritis. Abundant inflammatory infiltrate in lamina propria with well-preserved glands observed in the deeper half of the mucosa. C, Multifocal atrophic gastritis without intestinal metaplasia. Marked loss of glands, with prominent inflammatory infiltrate and proliferation of fibrous tissue in the lamina propria. D,Intestinal metaplasia, complete type. Goblet cells alternating with absorptive enterocytes that present well-developed brush border. E, Intestinal metaplasia, incomplete type. Goblet cells alternating with columnar cells that contain mucin droplets of variable sizes. F, Dysplasia. Epithelium with high-grade dysplasia (lower half of the photograph) occurring in a background of incomplete metaplasia (observed in the foveolar superficial epithelium). (H&E; original magnification: A-C x100; D-F x200).Images A-Care reproduced with permission reference 60.

Figure 3. Gastric adenocarcinoma. A-C, Intestinal type. Three different tumors are shown with formation of irregular glands, tubules and papillae. D, Mucinous adenocarcinoma, with small groups of tumor cells floating in pools of mucin. E y F, Diffuse type. Two different tumors are shown composed of non cohesive individual cells infiltrating the stroma. Signet ring cell carcinoma (F) is formed by cells with abundant intracytoplasmic mucin and nuclei displaced to the periphery. This morphology is characteristic of this tumor type.