Tumors of the stomachAss. Professor Haider Abd Ul Ridha
M.B.ch.B. F.I.C.M.S. path.
Study and understanding the gastric neoplasms
pathological features of gastric tumors.
Gastrointestinal stromal tumor.
Classifications of gastric neoplasms
Benign Epithelial Tumors:
Hyperplastic and inflammatory polyps
Malignant Epithelial Tumors:
Malignant Non - Epithelial Tumors:
Potentially Malignant Tumors:
Endocrine tumors (carcinoid)
Gastric adenocarcinoma (95 % of all gastric malignancy)Risk factors
Socioeconomic level and diet.
Environmental factors: High incidence in Japan, Asia and Russia, decreasing in the Western world.
Diet: Smoked, salted foods, low fresh vegetable diet, Nitrosamines.
Chronic gastritis with atrophy and metaplasia.
H. pylori infection.
Blood group A.
Relatives with stomach cancer.
Pathogenesis of gastric adenocarcinoma
Mutation: Germ line mutations in CDH1, which encodes E-cadherin, a protein that contributes to epithelial intercellular adhesion, are associated with familial gastric cancers, usually of the diffuse type.
H. pylori. Chronic gastritis, increased production of proinflammatory proteins, such as interleukin-1β (IL-1β) and tumor necrosis factor (TNF). Most commonly due to H. pylori infection.
Epstein-Barr virus (EBV). 10 % of gastric carcinoma.
it is notable that EBV episomes in these tumors frequently are clonal, suggesting that infection preceded neoplastic transformation.
TP53 mutations are uncommon in EBV-positive gastric tumors, suggesting that the molecular pathogenesis of these cancers is distinct from that of other gastric adenocarcinomas.
Morphologically, EBV-positive tumors tend to occur in the proximal stomach and most commonly have a diffuse morphology with a marked lymphocytic infiltrate.
Enlarged, hyperchromatic, irregularly outlined, crowded nuclei.
Irregular glands, mitoses.
Adenoma: (10 % of all gastric polyps).
Their incidence increases with age and varies among different populations in parallel with that of gastric adenocarcinoma.
Adenomas almost always occur on a background of chronic gastritis with atrophy and intestinal metaplasia.
All gastrointestinal adenomas exhibit epithelial dysplasia.
Adenocarcinoma particuarly develpoed in lesions greater than 2 cm in diameter.
Sites: classically prepyloric, antral and lesser curvature.
Macroscopic types (Borrmann I-IV):
polypoid, ulcerative, ulcerating and infiltrating, infiltrating.
Microscopic types (Laurens):
Gland forming, distal, better differentiated, usually old age.
Proximal, intracellular mucus, signet ring cells, less differentiated, usually young patient.
Prognosis of gastric carcinoma
The most powerful prognostic indicators for gastric cancer is the depth of invasion and the extent of nodal and distant metastasis at the time of diagnosis.
Local invasion into the duodenum, pancreas, and retroperitoneum .
After surgical resection, the 5-year survival rate for early gastric cancer can exceed 90%, even if lymph node metastases are present.
By contrast, the 5-year survival rate for advanced gastric cancer remains below 20%, in large part because current chemotherapy regimens are have limited impact.
Nearly 5% of all gastric malignancies are primary lymphomas, the most common of which are indolent extranodal marginal zone B-cell lymphomas.
In the gut, these tumors often are referred to as lymphomas of MALT, or MALTomas.
Neuroendocrine (Carcinoid) Tumor
These tumors were called “carcinoid” because they are slower growing than carcinomas. The most current WHO classification describes these as low- or intermediate-grade neuroendocrine tumors. High-grade neuroendocrine tumors, termed neuroendocrine carcinoma.
Neuroendocrine tumors are intramural or submucosal masses that create small polypoid lesions.
Gross features: The tumors are yellow or tan in appearance and elicit an intense desmoplastic reaction that may cause kinking of the bowel and obstruction.
Neuroendocrine tumors are composed of islands, trabeculae, strands, glands, or sheets of uniform cells with scant, pink granular cytoplasm and a round-to-oval stippled nucleus
Gastrointestinal Stromal Tumor
Gastrointestinal stromal tumor (GIST), the most common mesenchymal tumor of the abdomen, more than half of these tumors occur in the stomach.
The most common genetic change underlying the pathogenesis of GISTs is gain-of-function mutations of the gene encoding the tyrosine kinase KIT, the receptor for stem cell factor.
These are present in 75% to 85% of all GISTs.
An additional 8% of GISTs have mutations that activate a related tyrosine kinase, platelet-derived growth factor receptor A (PDGFRA).
Gross Features: Primary gastric GISTs usually form a solitary, well-circumscribed, fleshy, submucosal mass.
Metastases may form multiple small serosal nodules or fewer large nodules in the liver; spread outside of the abdomen is uncommon.
Microscopical features: GISTs can be composed of thin, elongated spindle cells or plumper epithelioid cells. The most useful diagnostic marker is KIT, which is immunohistochemically detectable in 95% of these tumors.