Epidemiology

Although the incidence of gastric carcinoma is decreasing in Western countries, it remains the fourth most frequent cancer diagnosed and the second most lethal cancer worldwide, behind only lung cancer. The number of new cases of gastric carcinoma worldwide was recently estimated as over 600,000 in males and 330,000 in females.³ It is the third most common cancer in males and the fifth most common cancer in females worldwide.⁴ Sixty percent of cases occur in developing countries.⁵ The areas with the highest incidence rates are Eastern Asia, South America, and Eastern Europe. Regions in which gastric carcinoma is least frequent are North America, Western Europe, and parts of Africa. There is approximately a 20-fold difference in the incidence rates between Japan and some white populations in the United States.⁵ In the United States, approximately 21,520 new cases of gastric carcinoma were expected to be diagnosed during 2011, with 10,340 estimated deaths from the disease during the same period.⁶

Of the several classification systems that have been proposed to describe gastric carcinoma, the Lauren classification is the most widely used. The Lauren classification describes tumors based on the microscopic configuration and growth pattern into intestinal and diffuse types.^7,8 Diffuse cancers are noncohesive and diffusely infiltrate the stomach. These often exhibit deep infiltration of the gastric wall and show little or no gland formation. These tumors are often associated with marked desmoplasia and inflammation with relative sparing of the overlying mucosa. The intestinal type, conversely, shows recognizable gland formation similar in microscopic appearance to the colonic mucosa. The glandular formation ranges from well- to poorly differentiated tumors and grows in expanding rather than infiltrative patterns.⁵ Intestinal cancers are believed to be related to environmental factors and are thought to arise secondary to chronic atrophic gastritis. The diffuse cancers, conversely, are less related to environmental factors and occur more often in young patients.⁵ The relative incidence of diffuse cancers is believed to have increased mainly owing to the decrease in the incidence of intestinal cancers.⁹

There are regional differences in the pathology and anatomic location of gastric carcinoma. A predominance of the Lauren intestinal type of adenocarcinoma occurs in high-risk areas, whereas the Lauren diffuse type is relatively more common in low-risk areas. Proximal gastric carcinomas and cancers of the gastroesophageal junction are more common in the West, and distal gastric carcinoma is more common in high-risk regions. At the M. D. Anderson Cancer Center, 41% of all UGI cancers involve the gastroesophageal junction.¹⁰ A steady decline in the incidence and mortality rates of gastric carcinoma has been observed worldwide over the past several decades. This is mainly due to a decrease in the intestinal variety of gastric carcinoma, the incidence of diffuse cancer being relatively stable.⁵

Etiology and Risk Factors

Because gastric carcinoma is more common in Asian than in Western countries, ethnic origin was thought to be an important contributory factor for the observed difference.¹¹ Although first-generation Asian immigrants to Western countries carry the same high susceptibility for gastric carcinoma as their counterparts in their native country, subsequent generations acquire risk levels approaching that of the population of their adopted countries. This epidemiologic pattern underlines the importance of environmental factors in the pathogenesis of gastric carcinoma.¹² Diets poor in fruits and vegetables and rich in smoked or poorly preserved food, salt, nitrates, and nitrites; infection with Helicobacter pylori; and smoking have all been currently implicated as significant risk factors in the development of gastric carcinoma in several studies.^13–15 Chronic atrophic gastritis, previous gastric surgery, gastric polyps, and obesity, as well as low socioeconomic status, are also associated with an increased risk of gastric carcinoma.^16,17

Gastric carcinoma is also seen as a part of the hereditary nonpolyposis colon cancer syndrome and other gastrointestinal (GI) polyposis syndromes such as Peutz-Jeghers syndrome and familial adenomatous polyposis.¹⁷ Mutations in the E-cadherin gene are a well-recognized cause of hereditary diffuse gastric cancer.¹⁸

Anatomy

Being a derivative of the foregut, the stomach is almost entirely supplied by the branches of the celiac trunk (Figure 15-1). The left gastric artery, arising from the celiac axis, and the right gastric artery, a branch of the hepatic artery, supply the lesser curvature in the gastrohepatic ligament and form an anastomotic arcade along the lesser curvature. The left and right gastroepiploic arteries, branches of the splenic artery and the gastroduodenal artery, supply the greater curvature of the stomach and traverse the gastrosplenic ligament and the gastrocolic ligament, respectively. The gastrocolic ligament is the supracolic part of the greater omentum. Numerous short gastric arteries, branches of the splenic artery, also supply the greater curvature. A rich lymphatic network accompanies these vessels, creating a conduit for lymphatic drainage, and traverses these complex ligamentous structures. The various ligamentous attachments can be identified by noting vascular landmarks on cross-sectional imaging (Table 15-1).²⁰ These ligamentous structures are important to understand because they represent the critical conduits for local extension of primary gastric carcinoma.

Figure 15-1 The blood supply of the stomach. The stomach is predominantly supplied by the branches of the celiac artery, being a derivative of the foregut. The greater curvature is supplied by the left and right gastroepiploic arteries, which are branches of the splenic and pancreaticoduodenal arteries. The lesser curvature is supplied by the left and right gastric arteries, which are branches of the celiac and common hepatic artery. In addition, several short gastric arteries (not shown) from the splenic artery supply the posterior wall of the stomach and the fundus. SMA, superior mesenteric artery; SMV, superior mesenteric vein.

Table 15-1 The Various Ligamentous Attachments of the Stomach Can Be Identified by Identifying Vascular Landmarks on Cross-Sectional Imaging

The stomach is divided for descriptive purposes into the fundus, body, pyloric antrum, and pylorus by imaginary lines drawn on its external surface (Figure 15-2). The fundus is dome-shaped, immediately under the left dome of the diaphragm, and is superior to the cardiac orifice. It lies above an imaginary line drawn horizontally at the level of the cardia (incisura cardia) to the greater curvature. At the lower end of the lesser curvature is a constant external notch (incisura angularis). The body extends from the cardia to the incisura angularis. A slight groove, the sulcus intermedius on the greater curvature of the stomach, separates the body from the pyloric antrum. The antrum extends from an imaginary line drawn from the incisura angularis to the sulcus intermedius. The pylorus is the narrowest part of the stomach, measuring only about 1 to 2 cm in length, and terminates into the duodenum (see Figure 15-2).²¹

Figure 15-2 The different parts of the stomach. The incisura cardia, sulcus intermedius, and incisura angularis are the landmarks used to divide the stomach into the fundus, body, and pyloric antrum.

Tumor Detection and Staging

EGD has replaced UGI double-contrast barium study as the modality of choice to detect and diagnose gastric carcinoma owing to its specificity and the advantage of obtaining a tissue biopsy and also the ability to perform EUS, which offers a reliable way to T-stage the tumor.³³ However, some reports indicate that endoscopy and UGI barium studies are equally sensitive in detection of primary gastric carcinoma.^34,35 Gastric carcinoma has various appearances on GI barium studies. These include plaquelike lesions, sessile or pedunculated polypoid lesions, ulcerated lesions, and nondistention of the stomach as in the scirrhous type of carcinoma or linitis plastica with diffuse loss of mucosal detail (Figure 15-4).

Figure 15-4 A, Double-contrast barium meal study in a 54-year-old patient shows a mucosal mass (arrows) due to adenocarcinoma at the greater curvature. B, Linitis plastica seen on double-contrast barium study. The body of the stomach fails to distend (arrows). Irregularity of the mucosa is also seen due to the diffuse infiltrative process.

EUS is superior to all other modalities in visualizing the different layers of the gastric wall and, thus, is most accurate in preoperative local (T) staging of gastric tumors with a accuracy rate of 78% to 94%.^36,37 Despite this, it is not uncommon (particularly for T2 tumors) that there is discordance with the actual pathologic specimen. The gastric wall layers appear as a five-layered structure on EUS with alternating hyperechoic and hypoechoic bands: serosa, muscularis propria, submucosa, deep mucosa, and superficial mucosa.³⁸ Tumors generally are hypoechoic or hyperechoic and are seen disrupting this regular pattern. EUS is also valuable in assessing smaller perigastric lymph nodes (Figure 15-5). EUS is of little to no benefit after preoperative therapy.

Figure 15-5 Endoscopic ultrasound shows the loss of the normal alternating hyper- and hypoechoic bands caused by the gastric carcinoma. Here, the tumor is seen infiltrating through the serosa (arrows). Enlarged perigastric lymph nodes (arrowheads) are also visualized.

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