[Loss of heterozygosity on chromosomes 17 and 16 in primary hepatocellular carcinomas].
OBJECTIVE
38 cases of hepatocellular (HCC) carcinomas were studied to detect loss of heterozygosity(LOH) at specific areas on chromosome 17 and 16, the possible relations were discussed between LOH and HBV/HCV infection and clinic-pathology of HCC.


METHODS
We detected LOH on chromosome 17 and 16 by using PCR based microsatel lite polymorphism analysis.


RESULTS
31 of 38(82%) tumors were deleted for at least one locus of 6 loci on chromosome 17. Loci D17S520 (17p12-p13.3) and TP53(17p13.1) occurred more frequent LOH(> 50%). But only one locus of the four loci on 17q occurred frequent LOH (40%), the other three loci occurred lower frequent LOH (< 30%). 26 (72%) of detected 36 HCC were positive for at least one locus of five loci on chromosome 16, and all 5 loci occurred higher frequent LOH (> 50%). The most frequent LOH(71%) occurred at D16S413(16q24). Relations were observed between LOH of p53 gene and HCV infection and tumor size, but no relations between LOH at other locus on chromosome 17 and 16 and HBV/HCV infection and clinical-pathology of HCC.


CONCLUSIONS
LOH on chromosome 17, especially LOH of p53 gene may play a role in the development of HCC. These results indicated that there may be more than one tumor suppressor gene related to the development and progression of HCC on chromosome 17 and 16.
Shao
J
J
Department of Pathology, Cancer Center, Sun Yat-Sen University of Medical Sciences, Guangzhou 510060.
Li
X
X
Liu
Z
Z
D000328:Adult; D000368:Aged; D006528:Carcinoma, Hepatocellular / Q000235:genetics*; D002885:Chromosomes, Human, Pair 16; D002886:Chromosomes, Human, Pair 17; D005260:Female; D016153:Genes, Suppressor; D016158:Genes, p53; D006801:Humans; D008113:Liver Neoplasms / Q000235:genetics*; D019656:Loss of Heterozygosity; D008297:Male; D008875:Middle Aged