LOSS OF EXPRESSION OF THE DCC GENE DURING PROGRESSION OF COLORECTAL CARCINOMAS IN FAMILIAL ADENOMATOUS POLYPOSIS AND NONFAMILIAL ADENOMATOUS POLYPOSIS PATIENTS

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作者
KIKUCHIYANOSHITA, R
KONISHI, M
FUKUNARI, H
TANAKA, K
MIYAKI, M
机构
[1] TOKYO METROPOLITAN INST MED SCI,DEPT BIOCHEM,3-18-22 HONKOMAGOME,BUNKYO KU,TOKYO 113,JAPAN
[2] TOKYO MED & DENT UNIV,DEPT SURG,BUNKYO KU,TOKYO 113,JAPAN
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中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
We have previously observed that the frequency of loss of heterozygosity (LOH) on chromosome 18q was low in adenomas and intramucosal carcinomas, whereas invasive carcinomas exhibited a high frequency in familial adenomatous polyposis patients (M. Miyaki et al., Cancer Res., 50: 7166-7173, 1990). In the present study, LOH at the DCC locus on chromosome 18q and the expression of DCC gene into mRNA were analyzed in colorectal tumors with distinct histopathological types. The carcinomas that showed 18q LOH also lost the DCC locus. The expression of DCC gene into mRNA was examined at the level of 233-base pair fragments of nucleotide 986-1218 in DCC complementary DNA. In a moderate-to-severe adenoma, 5 carcinoma-in-adenomas, and 4 intramucosal carcinomas, the level of expression was as high as in normal colorectal mucosa, whereas it was greatly reduced or not detectable in most (13 of 16) invasive carcinomas. Among these invasive carcinomas, 7 of 11 showed 18q LOH, but 4 showed no LOH. These results suggest that the DCC gene is included in the allelic deletion on chromosome 18q, and that the progression of colorectal carcinoma from early stage to advanced stage accompanies the inactivation of the DCC gene through LOH and other mechanisms.
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页码:3801 / 3803
页数:3
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