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©2010 Baishideng Publishing Group Co.
World J Gastroenterol. Oct 7, 2010; 16(37): 4646-4651
Published online Oct 7, 2010. doi: 10.3748/wjg.v16.i37.4646
Published online Oct 7, 2010. doi: 10.3748/wjg.v16.i37.4646
Table 1 Risk factors for cancer in colitis
| Epithelial cell dysplasia (high-grade > low-grade) |
| Extent of mucosal involvement (pancolitis > distal colitis > proctitis)[3,4] |
| Extended duration of ongoing disease (> 8-10 yr)[1,2,5] |
| Severity of histologic inflammation (?linked to compliant 5-ASA use)[6,7] |
| Onset in childhood (?linked to underlying duration of disease)[3,4,8] |
| Primary sclerosing cholangitis[9,10] |
| Liver transplantation, usually for primary sclerosing cholangitis[11-13] |
| Underlying familial colon cancer risk[14,15] |
| Other (?immunosuppression, ?biologic agents) |
Table 2 Changes positive for dysplasia1
| Nuclear changes | Nuclear enlargement |
| Pleomorphism | |
| Hyperchromatism | |
| Chromatin fragmentation | |
| Increased mitotic numbers | |
| Nuclear stratification | |
| Cellular changes | High nuclear to cytoplasm ratios |
| Enlarged nuclei | |
| Reduced or absent mucus production | |
| Architectural changes | Gland-like arrangement of epithelial cells |
- Citation: Freeman HJ. Surveillance for colitis-associated colon neoplasia. World J Gastroenterol 2010; 16(37): 4646-4651
- URL: https://www.wjgnet.com/1007-9327/full/v16/i37/4646.htm
- DOI: https://dx.doi.org/10.3748/wjg.v16.i37.4646
