Gastric tumors

A) Benign Neoplasms — Gastric Polyps

• Polyp: any nodule/mass that projects above the level of surrounding mucosa
• Gastric polyps are uncommon (colonic polyps are more common)

3 types:

1. Hyperplastic polyps (80–85%): non-neoplastic; hyperplastic mucosal epithelium + inflamed edematous stroma; seen in chronic gastritis
2. Fundic gland polyps (10%): non-neoplastic; seen in chronic gastritis
3. Adenomatous polyps (5%): true neoplasm → strong potential for malignant change (dysplasia); solitary, >1 cm, mainly in the antrum

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B) Malignant Neoplasms

• Gastric carcinoma (90–95%) → adenocarcinoma
• Gastric lymphomas (4%) → MALT lymphoma
• Stromal tumors (2%) → GIST

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C) Adenocarcinoma

• 2nd leading cause of cancer-related deaths in the world
• Highest incidence in Japan and South Korea
• Favored location: lesser curvature of the antropyloric region

Macroscopic patterns:

• Mucosal flattening + thickening with erosions
• Linitis plastica (diffuse thickening of gastric wall)
• Large ulcers or polypoid fungating masses
• Desmoplasia: non-neoplastic host response; CT (fibroblasts, lymphocytes, ECM) grows around the tumor

Classification — 3 parameters:

1. Depth of invasion:

• Early gastric carcinoma: confined to mucosa + submucosa (regardless of LN mets); precursor = gastric mucosal dysplasia; very good prognosis
• Advanced gastric carcinoma: extends below submucosa into muscular wall; bad prognosis

2. Macroscopic growth pattern:

1. Expansive: protrusion into lumen
2. Infiltrative: slightly elevated/depressed
3. Excavated: deep ulcerated lesions

3. Histological appearance:

Intestinal type:

• Gastric mucous cells that have undergone intestinal metaplasia
• Major risk: H. pylori-associated chronic gastritis → gastritis → metaplasia → dysplasia → cancer
• Other risk factors: smoked foods diet, low fruits/vegetables, alcohol, smoking
• Better prognosis than diffuse type

Diffuse type:

• Diffuse infiltration by scattered individual tumor cells → mucus secretion → “signet-ring” cell conformation
• Not associated with chronic gastritis
• E-cadherin gene mutation
• Highly malignant → poor prognosis

Metastatic spread:

• Directly to serosa; invasion of duodenum, pancreas, retroperitoneum
• Then to: regional LN (Virchow node = supraclavicular LN), liver, peritoneum (carcinosis), ovaries → Krukenberg tumor (bilateral ovarian signet-ring cell metastasis)

Clinical:

• Usually asymptomatic early; found by endoscopy in high-risk patients
• Advanced: abdominal discomfort, dysphagia, weight loss
• Cure possible with early diagnosis + surgical removal

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D) GIST (Gastrointestinal Stromal Tumor)

• Occurs in stomach (60%) and small intestine (~30%); can be anywhere in GI tract
• Low-grade smooth muscle spindle cell neoplasm; can be benign or malignant

Pathogenesis:

• c-KIT oncogene mutation → c-KIT encodes KIT CD117 receptor tyrosine kinase (cell survival, proliferation, differentiation)
• Mutation → constant receptor activation (ligand-independent) → uncontrolled growth

Clinical:

• Usually asymptomatic; when symptomatic: abdominal pain, nausea/vomiting, blood in stool/vomit, obstruction, abdominal mass
• Malignancy assessed by: (1) mitotic number + (2) tumor size
  • High mitotic count + large size → high aggressiveness
  • Low mitotic count + small size → low aggressiveness

Treatment:

• Imatinib (Gleevec): tyrosine kinase inhibitor; blocks KIT activity
• Resistance from new kinase domain mutations → Dasatinib (Sprycel): overcomes most imatinib-resistance mutations

💡 High-yield: Gastric adenocarcinoma = 2nd cancer death worldwide; Japan/Korea. Intestinal type = H. pylori → metaplasia → dysplasia; better prognosis. Diffuse type = signet-ring cells; E-cadherin mutation; poor prognosis. Virchow node = supraclavicular LN; Krukenberg = bilateral ovary mets. GIST = c-KIT mutation; imatinib treatment. Adenomatous polyp = only type with malignant potential.