Detection of Aberrant p16INK4A Methylation in Sera of Patients with Liver Cirrhosis and Hepatocellular Carcinoma.
10.3346/jkms.2004.19.1.83
- Author:
Hyung Jun CHU
1
;
Jeong HEO
;
Soo Boon SEO
;
Gwang Ha KIM
;
Dae Hwan KANG
;
Geun Am SONG
;
Mong CHO
;
Ung Suk YANG
Author Information
1. Department of Internal Medicine, Pusan National University College of Medicine, Busan, Korea. mcho@pusan.ac.kr
- Publication Type:Original Article
- Keywords:
p16INK4A Methylation;
PCR, Methylation-Specific;
Carcinoma, Hepatocellular;
Liver Cirrhosis
- MeSH:
Aged;
Carcinoma, Hepatocellular/*genetics;
DNA/metabolism;
*DNA Methylation;
Female;
Fibrosis;
*Genes, p16;
Human;
Liver/pathology;
Liver Cirrhosis/*genetics;
Liver Neoplasms/*genetics;
Male;
Middle Aged;
Polymerase Chain Reaction;
Predictive Value of Tests;
Protein p16/*blood;
Sensitivity and Specificity;
Time Factors;
Tumor Markers, Biological
- From:Journal of Korean Medical Science
2004;19(1):83-86
- CountryRepublic of Korea
- Language:English
-
Abstract:
Hepatocellular carcinomas (HCCs) show genomic alterations, including DNA rearrangements associated with HBV DNA integration, loss of heterozygosity, and chromosomal amplification. The genes most frequently involved are those encoding tumor suppressors. The p16INK4A tumor suppressor gene frequently displays genetic alteration in HCC tissues. The present study was performed to examine the incidence of methylated p16INK4A in the sera of liver cirrhosis (LC) and HCC patients, and to evaluate its role as a tumor marker of HCC. The sera of 23 LC patients and 46 HCC patients were examined in this study. The methylation status of p16INK4A was evaluated by methylation-specific PCR of serum samples. Methylated p16INK4A was detected in 17.4% (4/23) of LC patients and in 47.8% (22/46) of HCC patients. No association was demonstrated between p16INK4A methylation and serum AFP level. As the status of p16INK4A methylation was not associated with serum AFP level, it may have a role as a tumor marker of HCC.
