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Authors: C.E. Rubin and D.R. Saunders
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J. Gastric Carcinoma

Incidence: About 20,000 new cases of gastric adenocarcinoma are reported in the U.S. yearly. Although the incidence is decreasing, the distribution of this cancer is changing: unexplained is a dramatic increase in adenocarcinomas of the proximal stomach and distal esophagus.

1. Etiology

Unknown etiology This is unknown. Epidemiological data suggest that there is a small genetic element in pathogenesis.

a. Dietary Carcinogens?

b. Precancerous lesions?



H. pylori is a risk factor
  1. Chronic Gastritis:

    This may be the soil in which gastric cancer is more likely to develop. Chronic infection with H. pylori is an etiological factor. Perhaps chronic inflammation induces increased epithelial replication in which mitotic errors are made. Dietary mutagens and inflammatory mediators adversely affect genomic stability so that a cancer develops.


  2. Pernicious Anemia:

    These subjects have three times the incidence of gastric cancer compared with the general population; they all have intestinal metaplasia of the fundal gland area.


  3. Adenomatous Polyps:

    Most gastric carcinomas do not begin as polyps, yet adenomatous polyps more than 2 cm in diameter frequently contain adenocarcinoma.


  4. Postoperative Stomach:

    Gastric cancer can occur near the anastomotic site of a Billroth II operation.
2. Pathology

Growth pattern Some gastric cancers are polypoid and demarcated from the surrounding uninvolved mucosa; these are more amenable to surgical treatment. The growth of the penetrating, infiltrating carcinoma is primarily away from the gastric lumen; there is often a shallow ulcer crater with a necrotic base and nodular raised margins. Sometimes these penetrating carcinomas spread deeply into the gastric wall so that a large portion of the stomach may become thickened, contracted, and rigid (linitis plastica).

Many gastric carcinomas produce mucus; others are more undifferentiated and produce none.

Spread:
locally
lymphatics
blood → liver,
lung,
bone 		Gastric carcinomas spread by direct growth to contiguous organs, by lymphatics, and by the bloodstream (liver, lung, and bone metastases). Sometimes the entire peritoneal cavity may be seeded by tumor tissue. On other occasions pelvic metastases may be apparent as a rectal shelf, or as an enlarged ovary (Krukenberg tumor). Enlarged supraclavicular nodes is known as Virchow's sign.

3. Clinical Aspects

5 year survival < 20%

If cancer confined to mucosa, survival is same as general pop. 		Patients with benign gastric ulcer or gastric cancer may have identical symptoms. In addition to ulcer symptoms, these patients may have nonspecific complaints such as abdominal fullness, anorexia, vague discomfort, and weight loss. Usually these symptoms precede the diagnosis by 6 to 24 months.

The diagnosis of gastric carcinoma is usually suggested by a radiographic study such as a CT scan. Gastroscopic appearance may strongly support the diagnosis of cancer. Definitive diagnosis is achieved by biopsy at gastroscopy.

Less than 20% of total patients, and less than 30% of those in whom a "curative" resection can be performed survive five years. The most important determinant of survival is the extent of invasion of the tumor. The five-year survival of those patients whose tumor is confined to the gastric mucosa is the same as the survival of the general population.


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