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PH-GI14

Gastric tumours

How the gastric lining gives rise to intestinal-type and diffuse-type adenocarcinoma, why loss of E-cadherin makes linitis plastica, how gastric cancer spreads to nodes, peritoneum and liver, and MALT lymphoma, GIST and neuroendocrine tumours.

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  • 5 steps · 10 questions
  • 3D normal anatomy

By the end, you can

  • Relate the layers of the stomach wall and its lymphatic drainage to how gastric tumours grow and spread.
  • Compare intestinal-type and diffuse-type adenocarcinoma: precursors, causes, appearance and the role of E-cadherin (CDH1).
  • Describe gastric MALT lymphoma, GIST and neuroendocrine tumours by their cell of origin and main driver.
  • Explain the Virchow node, Krukenberg tumours and peritoneal spread in terms of the routes of spread.
  • Explain what the stage and grade of a gastric cancer measure and relate the main symptoms to growth and spread.
  • Recognise the classic appearances (signet-ring cells, linitis plastica, lymphoepithelial lesions, KIT- and DOG1-positive spindle cells), staging and tests of gastric tumours, and explain how endoscopic resection, gastrectomy, chemotherapy, targeted antibodies, H. pylori eradication and imatinib act on them.

What it is

Gastric tumours are neoplasms of the stomach wall. About nine in ten malignant ones are adenocarcinomas of the glandular lining, divided by Laurén into intestinal and diffuse types. The rest are mainly MALT lymphoma, gastrointestinal stromal tumour (GIST) and neuroendocrine tumours; benign epithelial polyps are covered with the precancerous changes.

5 types to tell apart
Intestinal-type adenocarcinoma
Gland-forming and cohesive; arises through chronic gastritis, intestinal metaplasia and dysplasia, mostly in the antrum.
Diffuse-type adenocarcinoma
Poorly cohesive cells, often signet-ring cells, infiltrating singly after loss of E-cadherin; can make the whole wall rigid (linitis plastica).
MALT lymphoma
A marginal zone B-cell lymphoma arising in lymphoid tissue induced by Helicobacter pylori.
Gastrointestinal stromal tumour (GIST)
A mesenchymal tumour of the interstitial cells of Cajal, driven by activating KIT or PDGFRA mutations; the stomach is its commonest site.
Neuroendocrine tumour (NET)
From the ECL cells of the mucosa; “carcinoid” is the older name, NET the current WHO term. Most arise in autoimmune gastritis.

US spelling: tumours → tumors, tumour → tumor, coeliac → celiac.

Normal function

Layers, lymphatics and a serosa facing the peritoneum

The stomach wall has a glandular mucosa of over the and , a loose , three layers of muscle (, and ) and a , the visceral peritoneum. Each layer has cells that can give rise to a tumour: glandular epithelium (adenocarcinoma), neuroendocrine cells in the glands, lymphocytes (lymphoma) and, between the muscle layers, the interstitial cells of Cajal, the pacemakers of gastric movement (GIST).

Lymphatics begin in the lamina propria just above the muscularis mucosae and form a rich network in the submucosa. Lymph drains to nodes along the lesser and greater curvatures, then to nodes along the arteries of the coeliac trunk and the coeliac nodes, and from there through the thoracic duct, which empties into the veins at the root of the left side of the neck. Venous blood drains into the portal vein and reaches the liver first.

The serosa faces the peritoneal cavity, so a tumour that grows through it can shed cells into the peritoneal fluid.

Point to it on the model