Gastric Cancer Clinical Presentation

Updated: Apr 25, 2023
  • Author: Elwyn C Cabebe, MD; Chief Editor: N Joseph Espat, MD, MS, FACS  more...
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In the United States, about 25% of stomach cancer patients present with localized disease, 31% present with regional disease, and 32% present with distant metastatic disease; the remainder of cases surveyed were listed as unstaged. [3]

Early disease has no associated symptoms; however, some patients with incidental complaints are diagnosed with early gastric cancer. Most symptoms of gastric cancer reflect advanced disease. Patients may complain of one or more of the following:

  • Indigestion
  • Nausea or vomiting
  • Postprandial fullness
  • Loss of appetite
  • Melena
  • Hematemesis
  • Weight loss

Late complications include the following:

  • Pathologic peritoneal and pleural effusions
  • Obstruction of the gastric outlet, gastroesophageal junction, or small bowel
  • Bleeding in the stomach from esophageal varices or at the anastomosis after surgery
  • Intrahepatic jaundice caused by hepatomegaly
  • Extrahepatic jaundice
  • Inanition resulting from starvation or cachexia of tumor origin


All physical signs are late events. By the time they develop, the disease is almost invariably too far advanced for curative procedures.

Signs may include a palpable enlarged stomach with succussion splash; hepatomegaly; periumbilical metastasis (Sister Mary Joseph nodule); and enlarged lymph nodes such as Virchow nodes (ie, left supraclavicular) and Irish node (anterior axillary). Blumer shelf (ie, shelflike tumor of the anterior rectal wall) may also be present. Some patients experience weight loss, and others may present with melena or pallor from anemia.

Paraneoplastic syndromes such as dermatomyositis, acanthosis nigricans, and circinate erythemas are poor prognostic features.

Other associated abnormalities include peripheral thrombophlebitis and microangiopathic hemolytic anemia.



Gastric cancer may often be multifactorial, involving both inherited predisposition and environmental factors. [10] Environmental factors implicated in the development of gastric cancer include the following:

  • Diet
  • Helicobacter pylori infection
  • Previous gastric surgery
  • Pernicious anemia
  • Adenomatous polyps
  • Chronic atrophic gastritis
  • Radiation exposure


A diet rich in pickled vegetables, salted fish, salt, and smoked meats correlates with an increased incidence of gastric cancer. [10]

A diet that includes fruits and vegetables rich in vitamin C may have a protective effect. [11]


Smoking is associated with an increased incidence of stomach cancer in a dose-dependent manner, both for number of cigarettes and for duration of smoking. Smoking increases the risk of cardiac and noncardiac forms of stomach cancer. [12] Cessation of smoking reduces the risk. A meta-analysis of 40 studies estimated that the risk was increased by approximately 1.5- to 1.6-fold and was higher in men. [13]

Helicobacter pylori infection

Chronic bacterial infection with H pylori is the strongest risk factor for stomach cancer.

H pylori may infect 50% of the world's population, but many fewer than 5% of infected individuals develop cancer. It may be that only a particular strain of H pylori is strongly associated with malignancy, probably because it is capable of producing the greatest amount of inflammation. In addition, full malignant transformation of affected parts of the stomach may require that the human host have a particular genotype of interleukin (IL) to cause the increased inflammation and an increased suppression of gastric acid secretion. For example, IL-17A and IL-17F are inflammatory cytokines that play a critical role in inflammation. Wu et al found that carriage of IL-17F 7488GA and GG genotypes were associated with an increased risk of gastric cancer. [14]

H pylori infection is associated with chronic atrophic gastritis, and patients with a history of prolonged gastritis have a sixfold increased risk of developing gastric cancer. Interestingly, this association is particularly strong for tumors located in the antrum, body, and fundus of the stomach but does not seem to hold for tumors originating in the cardia. [16]

A large-scale, long-term study from Korea—which along with China and Japan is a high-risk country for gastric cancer—concluded that in patients with a family history of gastric cancer, treatment of H pylori infection more than halves their risk of developing gastric cancer. In the study, which included 1676 patients ages 40 to 65 years with confirmed H pylori infection and at least one first-degree relative with gastric cancer, patients were randomized to triple antibiotic therapy or placebo and followed with surveillance endoscopy every 2 years. [17, 18]

Over a median follow-up of 9.2 years, gastric cancer developed in 1.2% of patients in the treatment group, versus 2.7% of those in the placebo group. Among patients with persistent infection (n = 979), gastric cancer developed in 2.9%, compared with 0.8% of those in whom the infection had been eradicated (hazard ratio, 0.27). [17, 18]

A study by Cheung et al found that risk of gastric cancer was increased in patients who used proton pump inhibitors (PPIs) long-term after successful treatment for H pylori infection. [19] In the study, which included 63,397 patients from a territory-wide Hong Kong health database with a median follow-up of 7.6 years, PPIs use was associated with more than a doubled risk of gastric cancer (hazard ratio [HR] 2.44; 95% confidence index [CI], 1.42 to 4.20). The risk increased with duration of PPIs use, as follows:

  • ≥1 year - HR 5.04 (95% CI 1.23–20.61)
  • ≥2 years - HR 6.65 (95% CI 1.62–27.26)
  • ≥3 years - HR 8.34 (95% CI 2.02–34.41) 

The relevance of this study to clinical practice remains uncertain, however, as the results could be due to residual confounding or detection bias. [20]

Previous gastric surgery

Previous surgery is implicated as a risk factor. The rationale is that surgery alters the normal pH of the stomach, which may in turn lead to metaplastic and dysplastic changes in luminal cells. [21]

Retrospective studies demonstrate that a small percentage of patients who undergo gastric polyp removal have evidence of invasive carcinoma within the polyp. This discovery has led some researchers to conclude that polyps might represent premalignant conditions.

Genetic factors

Some 10% of stomach cancer cases are familial in origin. Genetic factors involved in gastric cancer remain poorly understood, though specific mutations have been identified in a subset of gastric cancer patients. For example, germline truncating mutations of the E-cadherin gene (CDH1) are detected in 50% of diffuse-type gastric cancers, and families that harbor these mutations have an autosomal dominant pattern of inheritance with a very high penetrance. [22]

Other hereditary syndromes with a predisposition for stomach cancer include the following:

Other factors

See the list below:

  • Infection with the Epstein-Barr virus may be associated with a rare (< 1%) form of stomach cancer, lymphoepithelioma-like carcinoma.
  • Pernicious anemia associated with advanced atrophic gastritis and intrinsic factor deficiency is a risk factor for gastric carcinoma.
  • Gastric cancer may develop in the remaining portion of the stomach following a partial gastrectomy for gastric ulcer.  Benign gastric ulcers may themselves develop into malignancy.
  • Obesity increases the risk of gastric cardia cancer.
  • Radiation exposure: Survivors of atomic bomb blasts have had an increased rate of stomach cancer. Other populations exposed to radiation may also have an increased rate of stomach cancer.


A large cohort study examined whether use of oral bisphosphonates was associated with an increased risk of esophageal or gastric cancers. No significant difference was observed for increased risk of esophageal or gastric cancers between the bisphosphonate cohort and the control group. [23]



Direct mortality rate within 30 days after a surgical procedure for gastric cancer has been reduced substantially over the last 40 years. Most major centers report a direct mortality rate of 1-2%.

Early postoperative complications include anastomotic failure, bleeding, ileus, transit failure at the anastomosis, cholecystitis (often occult sepsis without localizing signs), pancreatitis, pulmonary infections, and thromboembolism. Further surgery may be required for anastomotic leaks.

Late mechanicophysiologic complications include dumping syndrome, vitamin B-12 deficiency, reflux esophagitis, and bone disorders, especially osteoporosis.

Postgastrectomy patients often are immunologically deficient, as measured by blastogenic and delayed cutaneous hypersensitivity responses.