[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.

Conclusion: 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.