Gastric Malignancy

Comprises 95% of all gastric tumors

Fourth most common gastrointestinal (GI) malignancy worldwide

Second cause of cancer mortality worldwide (behind lung cancer)

Approximately 25,000 cases reported in United States in 2015

Seventy percent of patients older than 50 (peak in seventh decade of life)

Male to female ratio: 2:1

Greatest incidence in Japan (80 times greater than in the United States)

Sixty-five percent of gastric cancers in the United States present at an advanced stage (T3/T4).

Environmental factors

• a.

  Diet (rich in salt, smoked or poorly preserved foods, nitrates, nitrosamines)

• b.

  Smoking

• c.

  Low socioeconomic status

• d.

  Occupational hazards (metal, rubber, wood, asbestos)

Genetic factors

• a.

  A total of 10% of gastric cancers have an inherited/familial component (90% sporadic).

• b.

  Hereditary diffuse gastric cancer

  • (1)

    Autosomal dominant, 70% penetrance

  • (2)

    Germline mutation of CDH-1 gene that encodes E-cadherin

• c.

  Additional syndromes associated with gastric adenocarcinoma: BRCA1, BRCA2, hereditary nonpolyposis colon cancer syndrome (HNPCC), familial adenomatous polyposis (FAP), Peutz-Jeghers syndrome, Li-Fraumeni syndrome

• d.

  Blood type A (relative risk, 1.2)

• e.

  Ethnicity—increased incidence in Asians, Native Americans, Latinos, and African Americans versus whites

Infectious factors

• a.

  Helicobacter pylori

  • (1)

    Risk increased 6–8 times

  • (2)

    Common in patients with distal cancer, not proximal cancer

• b.

  Epstein-Barr virus

Other risk factors

• a.

  Chronic atrophic gastritis (conditions associated with decreased acid production)

  • (1)

    Hypertrophic gastropathy (Menetrier disease)—hypertrophic disease of the gastric epithelium

  • (2)

    Pernicious anemia (3 times increased risk for development of gastric cancer)

• b.

  Gastric polyps

  • (1)

    Adenomas are associated with intestinal metaplasia.

  • (2)

    Risk of malignancy is directly increased with increased size and degree of dysplasia.

• c.

  Reflux gastritis after subtotal gastrectomy

  • (1)

    Incidence of 1%–2%

  • (2)

    Average latency of 12–30 years

  • (3)

    Risk with Billroth II >> Billroth I reconstruction

Lauren classification—two subtypes: intestinal and diffuse types

• a.

  Intestinal type

  • (1)

    Most common type worldwide

  • (2)

    More prevalent in high-risk populations (Asian and South American)

  • (3)

    Higher association with: high salt diets, tobacco/alcohol use, chronic gastritis from H. pylori infection

  • (4)

    Follow classic progression: chronic gastritis → intestinal metaplasia → dysplasia → invasive adenocarcinoma

  • (5)

    Spread hematogenously

  • (6)

    Distal stomach

  • (7)

    Older patients

  • (8)

    Based on World Health Organization (WHO) classification, these tumors can be further classified as tubular, papillary, and mucinous.

• b.

  Diffuse type

  • (1)

    Arises from lamina propria, lacks organized gland formation

  • (2)

    Loss of expression of protein epithelial cadherin (E-cadherin)

  • (3)

    Common in younger patients, women, and populations with low incidence of gastric cancer (i.e., United States)

  • (4)

    Aggressive and infiltrative growth pattern; spreads transmurally in the submucosa, classic linitis plastica

  • (5)

    Lymphatic invasion and peritoneal metastasis more common

  • (6)

    Signet ring cells are pathognomonic.

  • (7)

    Proximal stomach

  • (8)

    Not typically associated with H. pylori

It often produces no specific symptoms when it is superficial and potentially curable.

Up to 50% of patients may have nonspecific GI complaints, such as dyspepsia.

Other symptoms include abdominal pain, nausea, vomiting, early satiety with bulky tumors, dysphagia, hematemesis, and melena.

• a.

  Patients with these symptoms are often in the late or advanced stage of disease and are incurable.

• b.

  Proximal tumors → dysphagia and achalasia-like symptoms

• c.

  Distal tumors → gastritis-like symptoms and dyspepsia

• d.

  Additional symptoms are related to local invasion: GI bleed, gastric perforation, colonic invasion/fistula

Physical examination

• a.

  This is unhelpful in early gastric cancer.

• b.

  Palpable abdominal mass, cachexia, bowel obstruction, ascites, hepatomegaly, and lower extremity edema are signs of advanced disease.

• c.

  Classic findings:

  • (1)

    Blumer shelf: palpable mass on rectal examination due to peritoneal seeding of pouch of Douglas

  • (2)

    Sister Mary Joseph nodule: peritoneal disease causing a bulging periumbilical mass

  • (3)

    Krukenberg tumor: palpable ovarian mass on pelvic examination—drop metastasis from stomach

  • (4)

    Virchow node: lymphatic involvement with supraclavicular lymphadenopathy

  • (5)

    Irish node: lymphatic involvement with left axillary lymphadenopathy

It is cost effective only in endemic areas, such as Japan and Taiwan.

In the United States, endoscopic surveillance is recommended in high-risk individuals only (history of gastric polyp, FAP, HNPCC, Peutz-Jeghers syndrome).

Endoscopy is the modality of choice for diagnosis.

• a.

  All gastric ulcers seen on endoscopy should undergo biopsy and be followed to ensure they resolve.

• b.

  Minimum of four biopsies is sufficient. Biopsies should be taken from the mucosa at the edge of the ulcer.

• c.

  Repeat biopsy may be necessary if ulcer remains despite medical therapy.

• d.

  Less than 3% of gastric ulcers are malignant.

Endoscopic ultrasound is the most useful tool for preoperative tumor and nodal staging.

• a.

  Evaluate depth of tumor invasion.

• b.

  Perform fine-needle aspiration (FNA) sampling of suspicious nodes to determine lymph node status.

Computed tomography (CT) scan demonstrates primary tumor extent (invasion into surrounding structures) and metastatic disease.

• a.

  Obtain with intravenous (IV) contrast and low-density oral contrast (water).

• b.

  Specific findings include peritoneal disease, liver and lung lesions, and ascites.

Diagnostic laparoscopy

• a.

  Perform in all patients with T3/4 disease and no nodal or distant disease.

• b.

  Examine peritoneal surface, liver, and omentum.

• c.

  Cytologic analysis of peritoneal washings can aid in staging.

• d.

  A total of 10%–15% of patients are upstaged at time of diagnostic laparoscopy.

T = Primary tumor

• a.

  Tis— carcinoma in situ—no invasion of lamina propria

• b.

  T1a— Tumor invades lamina propria or muscularis mucosa.

• c.

  T1b— Tumor invades submucosa.

• d.

  T2— Tumor invades muscularis propria or subserosa.

• e.

  T3— penetrates serosa

• f.

  T4— Tumor invades adjacent structures.

N = Regional lymph nodes involved

• a.

  N0— No regional lymph nodes involved.

• b.

  N1— metastasis in 1–2 regional lymph nodes

• c.

  N2— metastasis in 3–6 regional lymph nodes

• d.

  N3a— metastasis in 7–15 regional lymph nodes

• e.

  N3b— more than 16 regional nodes involved

M = Distant metastasis

• a.

  M0— no distant metastasis

• b.

  M1— distant metastasis