Volume 10, No 4, Dec 2000

ISSN: 1001-0602 
EISSN: 1748-7838 2018 
impact factor 17.848* 
(Clarivate Analytics, 2019)

Volume 10 Issue 4, December 2000: 311-323

ORIGINAL ARTICLES

Genetic aberration in primary hepatocellular carcinoma: correlation between p53 gene mutation and loss-of-hetero- zygosity on chromosome 16q21-q23 and 9p21-p23

WANG Gang^1,2, Chang Hui HUANG², Yan ZHAO², Ling CAI², Ying WANG², Shi Jin XIU², Zheng Wen JIANG², Shuang YANG², Xin Tai ZHAO¹, Wei HUANG², Jian Ren GU^1,*

¹National Laboratory for Oncogene and Related Genes, Shanghai Cancer Institute, 25/2200, Xie-tu Rd, Shanghai 200032, China
²Chinese Human Genome Center at Shanghai, 351 Guo Shou Jin Road, Zhangjiang High Tech Park, Shanghai 201203, China Correspondence:

To elucidate the molecular pathology underlying the development of hepatocellular carcinoma (HCC), we used 41 highly polymorphic microsatellite markers to examine 55 HCC and corresponding non-tumor liver tissues on chromosome 9, 16 and 17. Loss-of-heterozygosity (LOH) is observed with high frequency on chromosomal region 17p13 (36/55, 65 %), 9p21-p23 (28/55, 51 %), 16q21-q23 (27/55, 49 %) in tumors. Meanwhile, microsatellite instability is rarely found in these microsatellite loci. Direct sequencing was performed to detect the tentative mutation of tumor suppressor genes in these regions: p53, MTS1/p16, and CDH1/E-cadherin. Within exon 5-9 of p53 gene, 14 out of 55 HCC specimens (24 %) have somatic mutations, and nucleotide deletion of this gene is reported in HCC for the first time. Mutation in MTS1/p16 is found only in one tumor case. We do not find mutations in CDH1/E-cadherin. Furthermore, a statistically significant correlation is present between p53 gene mutation and loss of chromosome region 16q21-q23 and 9p21-p23, which indicates that synergism between p53 inactivation and deletion of 16q21-q23 and 9p21-p23 may play a role in the pathogenesis of HCC.

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