eMedicine Specialties > Radiology > Gastrointestinal

Gastric Carcinoma

Isaac Hassan, MB, ChB, FRCR, DMRD, Former Senior Consultant Radiologist, Department of Radiology, St Bernard's Hospital, Gibraltar
Contributor Information and Disclosures

Updated: Oct 19, 2006

Introduction

Background

Gastric carcinoma is the most common cancer in the world after lung cancer and is a major cause of mortality and morbidity. Though a marked reduction has been observed in the incidence of gastric carcinoma in North America and Western Europe in the last 50 years, 5-year survival rates are less than 20%, as most patients present late and are unsuitable for curative, radical surgery.

Pathophysiology

The accepted pathway involves transitions from gastritis, to gastric atrophy, to metaplasia, to dysplasia, and, finally, to cancer.

Several dietary and environmental factors may influence this pathway.

• Dietary nitrates: Bacteria in the stomach break down nitrites to compounds (eg, N -nitroso compounds) that are carcinogenic in animals.
• Hypochlorhydria: This condition occurs in gastric atrophy and promotes bacterial colonization of the stomach. It leads to increased nitrite formation, which may have a mutagenic effect on the atrophic gastric mucosa.
• Helicobacter pylori: Antral gastritis caused by H pylori has been linked to the development of gastric cancer. Patients with H pylori gastritis are 3-6 times more likely to develop gastric cancer than individuals without the infection.
• Certain foods: Starch, pickled vegetables, salted fish and meat, smoked foods, and salt have all been implicated in the development of gastric carcinoma.
• Cigarette smoking: Those who smoke more than 30 cigarettes per day have a 5-fold increased risk of gastric carcinoma.

Several precancerous conditions are recognized:

• Chronic atrophic gastritis (see Image 1)
• Pernicious anemia
• Previous partial gastrectomy
• Ménétrier disease
• Gastric dysplasia
• Adenomatous polyps (20% of all gastric polyps)
• Hereditary factors

Adenocarcinomas account for approximately 95% of all malignant gastric neoplasms. The remaining 5% of tumors are lymphomas, leiomyosarcomas, carcinoids, or sarcomas.

Gastric adenocarcinomas are divided into 2 types:

• An intestinal type (type 1), with well-formed glandular structures: This type is more likely to involve the distal stomach and occur in patients with atrophic gastritis. It has a strong environmental association.
• A diffuse type (type 2), with poorly cohesive cells that tend to infiltrate the gastric wall: Tumors of this type may involve any part of the stomach, especially the cardia, and have a worse prognosis than the intestinal type. Unlike type 1 gastric cancers, type 2 cancers have similar frequencies in all geographic areas.

With gastric carcinomas, advanced lesions will have already invaded the muscularis propria. They are associated with metastases to regional lymph nodes or to local or distant structures.

Early gastric lesions are confined to the mucosa or submucosa. Patients with these tumors have a 5-year survival rate of 90%. Most reports are from Japan as a result of mass screening in that country.

Before 1950, most gastric tumors detected were located in the antrum. Since then, the location has gradually shifted from the antrum to the body and fundus because of the rapidly increasing incidence of carcinoma in the gastric cardia and lower esophagus. Today, 30% of gastric lesions are found in the antrum, 30% are in the body, and 40% are in the fundus and cardia.

Frequency

United States

The incidence decreased from 33 cases per 100,000 population in 1930 to 3.7 cases per 100,000 population in 1990. In 1996, about 22,800 new cases of gastric adenocarcinoma occurred. In Western countries, the incidence of carcinoma of the cardia has increased rapidly in the last 20 years, in contrast to the decline in gastric cancer as a whole, particularly in tumors of the body and antrum.

International

Worldwide, gastric adenocarcinoma is the second most common cancer (second to lung cancer). The global incidence of gastric cancer varies 10-fold. The highest incidence (>30 cases per 100,000 population) is in Japan, Russia, China, South America, and Eastern Europe. The lowest incidence ( <3.7 cases per 100,000 population) is in North America, Western Europe, Australia, and New Zealand.

Mortality/Morbidity

• In 1996, gastric cancer caused approximately 14,000 deaths in the United States.
• Worldwide, gastric cancer is second only to lung cancer as the most common cause of cancer deaths.
• Most patients present late, and the 5-year survival rate is approximately 20%.

Race

• Overall, gastric carcinoma is 1.5-2.5 times more common in African Americans, Hispanics, and American Indians than in whites.
• Among Japanese who immigrate to the United States, the incidence gradually decreases (to 25% of their original incidence). The rate further decreases in their children, and their grandchildren have a rate comparable to that of the general population in the United States.
• The incidence of adenocarcinoma of the cardia is highest among white men.

Sex

Gastric carcinoma is 2 times more common in men than in women. Moreover, carcinoma of the cardia of the stomach is up to 7 times as common in men as in women.

Age

Gastric carcinoma has a peak incidence in those aged 50-70 years; however, approximately 5% of patients with gastric cancer are younger than 35 years, and 1% are younger than 30 years. Younger patients have more aggressive lesions with a worse prognosis.

Anatomy

The stomach consists of the cardia (adjacent to the gastroesophageal junction), the fundus, the body, the antrum, and the pylorus. The fundus is dome-shaped and extends above and to the left of the cardia, toward the left hemidiaphragm. The body extends from the fundus to the lower end of the lesser curve, known as the incisura angularis. The antrum extends from the incisura to the pyloric canal.

The stomach is lined by peritoneum. The lesser omentum and greater omentum are double layers of peritoneum that extend from the lesser curve and greater curve, respectively.

The right and left gastric, right and left gastroepiploic, and short gastric arteries supply the stomach. These arteries originate from all 3 branches of the celiac trunk. The venous drainage is into the portal vein or one of its branches. The lymphatic drainage is into the celiac lymph nodes surrounding the celiac trunk.

Presentation

Presentation

Most patients present with advanced disease because they are often asymptomatic in the earlier stages. Common presenting features include epigastric pain, bloating, early satiety, nausea, vomiting, dysphagia, anorexia, weight loss, and upper GI bleeding (hematemesis, melena, iron deficiency anemia, positive results with fecal occult blood tests).

Differential diagnosis

Because peptic ulcers and gastritis cause similar findings, diagnosis is often delayed. Jaundice and hepatomegaly may be due to hepatic metastases. Pelvic masses may be the result of ovarian metastases (Krukenberg tumors).

Prognosis and staging

The prognosis is related to the stage of the disease at the time of diagnosis and to the histologic grade of the carcinoma.

Pathologic staging is based on tumor stage, nodal stage, and metastasis stage (TMN).

• T stage - Extent of penetration through the gastric wall
  • Tis - Carcinoma in situ, intraepithelial tumor
  • T1 - Tumor extension to submucosa
  • T2 - Tumor extension to the muscularis propria or subserosa
  • T3 - Tumor penetration of the serosa
  • T4 - Tumor invasion of the adjacent organs
• N stage - Number and site of draining lymph nodes involved (see also N staging in the CT Scan, Findings section, below)
  • N0 - No lymph nodes involved
  • N1 - Metastases in 1-6 regional lymph nodes
  • N2 - Metastases in 7-15 regional lymph nodes
  • N3 - Metastases in >15 regional lymph nodes
• M stage - Presence of metastases
  • M0 - No distant metastases
  • M1 - Distant metastases

Staging and 5-Year Survival Rates

Open table in new window

*Tx indicates any T stage; Nx, any N stage.

Preferred Examination

• Begin the evaluation with history taking and physical examination.
• Perform blood tests, including a full blood count determination and liver function tests.
• Inspect the stool, and test for occult blood.
• Perform either fiberoptic endoscopy or a double-contrast study (barium and gas) of the upper GI tract.
  • Endoscopy has become the diagnostic procedure of choice for patients with suspected gastric carcinoma. Biopsy samples obtained during endoscopy enable histologic diagnosis. However, endoscopy is more invasive and more costly than a double-contrast study.
  • Double-contrast examinations of the upper GI tract remain a useful alternative to endoscopy and have similar sensitivity in the detection of gastric cancer.
• CT, MRI, and endoscopic ultrasonography (EUS) are used in staging but not usually in the primary detection of gastric cancers (see the CAT Scan, MRI, and Ultrasound sections).

Limitations of Techniques

Endoscopy with biopsy has a sensitivity of 95%. Multiple biopsy specimens are needed to avoid sampling errors. Endoscopy is less reliable in the diagnosis of scirrhous tumors (35-70%). False-negative biopsy results may delay diagnosis.

Single-contrast barium studies have an overall sensitivity of 75%, but double-contrast barium examinations have a sensitivity of 90-95% in the detection of gastric cancer, comparable to endoscopy.

Differential Diagnoses

Crohn Disease
Gastric Ulcer
Gastrointestinal Stromal Tumors - Leiomyoma/Leiomyosarcoma

Other Problems to Be Considered

• Gastric lymphoma
• Gastric metastases
• Gastritis
• Gastric varices
• Gastric polyps
• Peptic ulcers

References

• Crohn Disease
• Gastric Ulcer
• Gastrointestinal Stromal Tumors - Leiomyoma/Leiomyosarcoma