Histogenesis of human colorectal adenomas and hyperplastic polyps: the role of cell proliferation and crypt fission
- 1Histopathology Unit, Imperial Cancer Research Fund, Lincoln's Inn Fields, London WC2A 3PX, UK and University Department of Medicine, Queen Mary Hospital, University of Hong Kong, Pokfulam Road, Hong Kong (SAR), China
- 2Histopathology Unit, Imperial Cancer Research Fund, Lincoln's Inn Field, London WC2A 3PX, UK
- 3Histopathology Unit, Imperial Cancer Research Fund, Lincoln's Inn Fields, London WC2A 3PX, UK and Department of Histopathology, Imperial College of Science, Technology, and Medicine, Hammersmith Campus, Du Cane Road, London W12 0NN, UK
- 4University Department of Medicine, Queen Mary Hospital, University of Hong Kong, Pokfulam Road, Hong Kong (SAR), China
- Correspondence to:
Dr W-M Wong, University Department of Medicine, Queen Mary Hospital, Pokfulam Road, Hong Kong;
- Accepted 1 May 2001
Background: The histogenesis of human colorectal hyperplastic polyps and colorectal adenomas is poorly understood even now.
Method: Human colorectal adenomas, hyperplastic polyps, and normal colorectal mucosae (patients with familial adenomatous polyposis and hereditary non-polyposis colorectal carcinoma were excluded) were obtained during colonoscopy and microdissected into individual crypts. Morphology, cell proliferation characteristics, and fission indices of crypts isolated from these lesions were then studied.
Results: Crypts isolated from colorectal adenomas and colorectal hyperplastic polyps were significantly larger (p<0.001) than crypts from normal colorectal mucosae. Crypt fission was an uncommon event in normal colonic mucosae but common in crypts isolated from adenomas and hyperplastic polyps (p<0.001). Analysis of the distribution of mitoses suggested an upward expansion of the proliferation compartment in adenomas to the surface of the crypt with no reversal of proliferating cell distribution, as has previously been described.
Conclusions: Sporadic human colorectal adenomas and hyperplastic polyps grow by the process of crypt fission. Expansion of the proliferative compartment was demonstrated in crypts from adenomas, consistent with deregulation of cell cycle control.
- APC gene, adenomatous polyposis coli gene
- FAP, familial adenomatous polyposis
- MIN, multiple intestinal neoplasia