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Cancers of the Stomach
Cancer involving the stomach is the second most common cancer in the world. Although it is decreasing in North America, stomach cancer continues to increase throughout the rest of the world. The incidence of adenocarcinoma has increased only in lesions at the cardioesophageal junction ( Fig. 39.1 ).
Cancers of the Stomach.
The etiology of stomach cancer remains complex, and multiple factors are involved. Tobacco, alcohol, dietary nitrates, nitrites, and nitrosamines have all been implicated. High intake of salt has also been implicated in certain parts of the world, whereas increased refrigeration has been associated with a decrease in cancer. Epidemiologic studies show that Helicobacter pylori plays a role in gastric carcinogenesis. Chronic inflammation associated with H. pylori gastritis is the presumed mechanism. Atrophy of the gastric mucosa (as in pernicious anemia) and intestinal metaplasia are predisposing factors (see Chapter 33 ).
Most stomach cancers conform to one or two types: the intestinal form, which contains glandlike tubular structures, and the diffuse form, which contains poorly differentiated cells. The intestinal form is thought to involve steplike development, with the predisposing atrophic gastritis and intestinal metaplasia progressing to dysplasia and finally to cancer.
Genetic changes include loss of heterogenicity and loss of the effectiveness of P53G suppression and, in some patients, mutation of the APC/β-catenin pathway; expression of P16 and P27 is also decreased. Decreased expression of the epithelial cadherin gene in patients with diffuse gastric cancer may account for the morphologic differences between intestinal and diffuse gastric lesions. Families with hereditary diffuse gastric cancer have mutations in epithelial cadherin. Geneticists are beginning to understand the effect of environmental factors on the development of stomach cancer.
Clinical Picture
The clinical picture of stomach cancer varies greatly depending on the site of the cancer. Lesions at the cardioesophageal junction, which are increasing in incidence in North America, tend to manifest early; they cause dysphagia or early dyspepsia and are diagnosed at endoscopy in the work-up. Larger lesions in the fundus and body or ulcerating lesions may cause dyspeptic symptoms, anemia, or frank bleeding. Many are associated with anorexia and weight loss and manifest at a later stage. Of particular interest is linitis plastica, which diffusely involves the stomach, with a fibrotic-type histology that results in anorexia and weight loss.
Diagnosis
As endoscopy becomes more effective, the diagnosis of stomach cancer is frequently made on visualization and biopsy of the lesion. Radiographic studies, still used in many parts of the world, show the classic lesions, from a bottleneck linitis plastica to an ulceration that requires endoscopic evaluation and biopsy. It is still difficult to differentiate between a benign and a malignant ulcer. Differentiating gastric ulcer requires biopsy, as well as healing. Reevaluation is done in 3 to 6 weeks to ensure the ulcer has healed; if not, vigorous repeat biopsy evaluation is necessary.
Once the lesion has been identified on histologic evaluation, endoscopic ultrasound (EUS) can be helpful in determining the extent of the lesion through the stomach wall and whether lymph nodes are involved. Small nodes can still contain malignant cells and therefore can be diagnosed only during surgical exploration. Computed tomography (CT) can assist in identifying nodes missed on EUS and should be used for full evaluation. Endoscopy, EUS, and CT enable classification and staging of the disease.
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