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PH-GI16

Malignant tumours of the small and large intestine

How colorectal adenocarcinoma grows from a precursor, invades the bowel wall, spreads to nodes, liver and peritoneum and causes bleeding or obstruction; why small-bowel cancer is rare; and neuroendocrine tumours, GIST and lymphoma.

By the end, you can

  • Relate the cells of the intestinal wall to the malignant tumours that arise from them.
  • Explain the chromosomal-instability and microsatellite-instability pathways from precursor to colorectal adenocarcinoma.
  • Describe how a colorectal carcinoma invades the wall and spreads, and what grade and T, N and M stage measure.
  • Explain why right-sided and left-sided colorectal cancers tend to present differently.
  • Describe intestinal neuroendocrine tumours, GIST and lymphoma, and why carcinoid syndrome usually means liver metastases.
  • Recognise the classic appearances (dirty necrosis, annular left-sided and polypoid right-sided growth, mucinous and MSI-high features), staging, screening and tests of colorectal cancer, and explain how polypectomy, colectomy, chemotherapy, anti-EGFR and anti-VEGF antibodies and checkpoint inhibitors act on it.

What it is

Colorectal adenocarcinoma, a malignant tumour of the glandular lining of the colon and rectum, is by far the commonest intestinal malignancy, and most arise over years from a precursor polyp. The small intestine, despite its length, rarely develops cancer; its malignancies are adenocarcinoma, neuroendocrine tumours (NETs, the older name being carcinoid), lymphoma and gastrointestinal stromal tumour (GIST).

5 types to tell apart
Colorectal adenocarcinoma
Malignant glands invading at least the submucosa, usually from an adenoma or a serrated lesion. Mucinous and signet-ring cell carcinoma are recognised variants.
Small-intestinal adenocarcinoma
Rare, and commonest in the duodenum. Familial adenomatous polyposis, Lynch syndrome, coeliac disease and Crohn’s disease raise the risk.
Neuroendocrine tumour (NET)
A tumour of the hormone-making cells scattered in the mucosa, commonest in the ileum, appendix and rectum. “Carcinoid” is the older, still common name; the WHO classification now uses NET (graded 1 to 3 by proliferation) and calls poorly differentiated tumours neuroendocrine carcinoma.
Gastrointestinal stromal tumour (GIST)
A mesenchymal tumour of the interstitial cells of Cajal, the gut’s pacemaker cells, usually driven by an activating KIT or PDGFRA mutation; commonest in the stomach, then the small intestine.
Lymphoma
Arises from the lymphoid tissue of the wall; enteropathy-associated T-cell lymphoma is a rare complication of long-standing coeliac disease.

US spelling: tumours → tumors, tumour → tumor.

Normal function

The intestinal wall and its renewing lining

The colon has no villi: its mucosa is a flat sheet of straight lined by absorptive cells and many . Stem cells at the base of each crypt divide under the control of Wnt signalling; their daughters climb the crypt, mature and are shed within about a week. The protein APC keeps this in check by marking β-catenin, the messenger of Wnt signalling, for destruction once cells leave the crypt base.

Below the lies the thin , then the with its larger blood vessels and lymphatics, the and (the muscularis propria) and the . In the colon, lymphatics are sparse above the muscularis mucosae, a detail that matters for spread.

Other cells give rise to other tumours: hormone-making neuroendocrine cells scattered in the crypts, the interstitial cells of Cajal between the muscle layers that set the rhythm of peristalsis, and lymphoid tissue, plentiful in the ileum as Peyer’s patches.

Point to it on the model