BACKGROUND: The present study was performed to estimate the frequency of methylated p16INK4A in the sera of patients with hepatitis C virus (HCV)-related chronic active hepatitis (CAH), liver cirrhosis (LC), and hepatocellular carcinoma (HCC) and to evaluate the role of p16INK4A as a tumor marker of HCC. MATERIAL/ METHODS: The sera of 17 CAH, 20 LC, and 25 HCC patients were examined in this study. The methylation status of p16INK4A was evaluated by methylation-specific PCR of the serum samples. RESULTS: Methylated p16INK4A was detected in 47.1% (8/17) of the CAH patients, 5% (4/20) of the LC patients, and in 92% (23/25) of the HCC patients. HBV markers were detected in (4/25) of HCC patients; all had methylated p16INK4A. No association was demonstrated between p16INK4A methylation and serum AFP level in the HCC group. CONCLUSIONS: The results of this study indicate that aberrant DNA methylation contributes to hepatocarcinogenesis and it may be an early event during hepatocarcinogenesis. As the status of p16INK4A methylation was not associated with serum AFP level, it may have a complementary role with AFP as a tumor marker of HCC.
BACKGROUND: The present study was performed to estimate the frequency of methylated p16INK4A in the sera of patients with hepatitis C virus (HCV)-related chronic active hepatitis (CAH), liver cirrhosis (LC), and hepatocellular carcinoma (HCC) and to evaluate the role of p16INK4A as a tumor marker of HCC. MATERIAL/ METHODS: The sera of 17 CAH, 20 LC, and 25 HCC patients were examined in this study. The methylation status of p16INK4A was evaluated by methylation-specific PCR of the serum samples. RESULTS: Methylated p16INK4A was detected in 47.1% (8/17) of the CAH patients, 5% (4/20) of the LC patients, and in 92% (23/25) of the HCC patients. HBV markers were detected in (4/25) of HCC patients; all had methylated p16INK4A. No association was demonstrated between p16INK4A methylation and serum AFP level in the HCC group. CONCLUSIONS: The results of this study indicate that aberrant DNA methylation contributes to hepatocarcinogenesis and it may be an early event during hepatocarcinogenesis. As the status of p16INK4A methylation was not associated with serum AFP level, it may have a complementary role with AFP as a tumor marker of HCC.
Authors: Jing Shen; Shuang Wang; Yu-Jing Zhang; Hui-Chen Wu; Muhammad G Kibriya; Farzana Jasmine; Habibul Ahsan; David P H Wu; Abby B Siegel; Helen Remotti; Regina M Santella Journal: Epigenetics Date: 2012-12-03 Impact factor: 4.528