Mutation of p53 tumor suppressor gene in flat neoplastic lesions of the colorectal mucosa.
OBJECTIVE
In a recent comparative histologic survey of flat colorectal neoplasias, we found more lesions with high-grade dysplasia (HGD) and carcinoma in Japanese than in Swedish patients. The purpose of this work was to assess the p53 protein overexpression in flat colorectal neoplasias in Swedish patients and to compare results with those reported in Japan.


METHODS
A total of 57 neoplastic lesions of the colorectal mucosa were investigated: 29 had been regarded both at endoscopy and at histology as flat and the remaining 28 as exophytic. Deparaffinized, rehydrated sections were treated immunohistochemically to detect the p53 protein. Lesions having a moderate (++) or high ( ) staining were considered as overexpressing the p53 protein.


RESULTS
Results indicated that 16.7 percent (1/6) of the exophytic adenomas with low-grade dysplasia (LGD) had distinct p53 overexpression as well as 57.1 percent (8/14) of those with HGD and 87.5 percent (7/8) with invasive growth. In flat neoplastic lesions, 7.7 percent (1/13) of the tubular adenomas with LGD, 25 percent (3/12) of tubular adenomas with HGD, and 75 percent (3/4) of adenocarcinomas arising in flat adenomas had p53 overexpression.


CONCLUSIONS
In Swedish patients, the proportion of flat and exophytic colorectal neoplasias showing p53 immunoreactivity increased with increasing degree of dysplasia, the highest percent being recorded in lesions with invasive growth. Because a similar stepwise increase was reported for exophytic and flat colorectal neoplasias in Japan, it seems that the comparison of results in both countries is justifiable. One possible conclusion from this comparison is that the higher proportion of flat neoplastic colorectal lesions with HGD and carcinoma in the Japanese (compared with the Swedish) takes place for reasons extraneous to the overexpression of the p53 protein.
Rubio
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Gastroenterology and Hepatology Research Laboratory, Karolinska Institute, Stockholm, Sweden.
Rodensjö
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D000230:Adenocarcinoma / Q000235:genetics* / Q000473:pathology; D000236:Adenoma / Q000235:genetics* / Q000473:pathology; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000473:pathology; D015972:Gene Expression Regulation, Neoplastic; D016158:Genes, p53 / Q000235:genetics*; D006801:Humans; D007124:Immunoenzyme Techniques; D007413:Intestinal Mucosa / Q000473:pathology; D007564:Japan; D009154:Mutation; D009361:Neoplasm Invasiveness; D013548:Sweden; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis*; D015854:Up-Regulation
D016159:Tumor Suppressor Protein p53