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Published on: July 29, 2010
Colonic chicken-skin mucosa in children with polyps is not a preneoplastic lesion
Michael J Nowicki1, Phyllis R Bishop, Charu Subramony
1Division of Pediatric Gastroenterology, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Insights
Chicken-skin mucosa (CSM) is not a preneoplastic lesion. Studies show CSM lacks markers for cell replication and malignant transformation, unlike adenomas and adenocarcinomas.
Area of Science:
- Gastroenterology
- Oncology
- Pathology
Background:
- Colonic polyps are common, with varying malignant potential.
- Chicken-skin mucosa (CSM) was initially linked to preneoplastic lesions but later observed with benign juvenile polyps.
- This raised questions about CSM's role in dysplasia.
Purpose of the Study:
- To investigate whether chicken-skin mucosa (CSM) is a preneoplastic lesion.
- To compare cell replication and malignant transformation markers in CSM versus other colonic tissues.
Main Methods:
- Examined colonic mucosal biopsies using immunostaining for Ki-67 (cell replication) and p53 (malignant transformation).
- Compared staining in CSM, normal colonic tissue, tubular adenomas, and adenocarcinomas.
Main Results:
- Ki-67 staining was similar in CSM and normal tissue, but significantly higher in tubular adenomas and adenocarcinomas.
- p53 staining was absent in CSM and normal tissue, but present in tubular adenomas and adenocarcinomas.
Conclusions:
- CSM lacks histologic markers of increased cell replication and malignant transformation.
- The findings suggest CSM is not preneoplastic and likely results from local mucosal damage near polyps of any type.
Abstract:
Colonic polyps are common both in adults and children; however, the malignant potential varies according to the type of polyp. Most childhood polyps are solitary juvenile polyps, which have negligible malignant potential. Chicken-skin mucosa (CSM) is an endoscopic finding initially described associated with adenomatous polyps and adenocarcinoma, suggesting a preneoplastic lesion. Subsequently, CSM was described in association with juvenile polyps, suggesting that this mucosal finding is not a precursor to dysplasia. To determine whether CSM represents a preneoplastic lesion, we studied endoscopic colonic mucosal biopsies for markers of cell replication (Ki-67) and malignant transformation (p53) in mucosal biopsies of CSM, normal colonic tissue, tubular adenomas, and adenocarcinomas. Samples were subjected to immunostaining for the presence of Ki-67 and p53. The degree of Ki-67-positive staining cells was similar for CSM and normal colonic tissue, whereas there was significantly increased staining for both tubular adenomas and adenocarcinomas. There was no evidence of p53 staining in CSM and normal colonic mucosa, whereas there was varying degrees of staining in tubular adenomas and adenocarcinomas. The association of CSM with benign juvenile polyps and the absence of histologic markers for increased replication and malignant transformation support the notion that this endoscopic finding is not preneoplastic. Rather, CSM arises in proximity to polyps of all histologic types because of local mucosal damage.
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