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Detection of aberrant p16INK4A methylation in sera of patients with liver cirrhosis and hepatocellular carcinoma.

Chu HJ, Heo J, Seo SB, Kim GH, Kang DH, Song GA, Cho M, Yang US - J. Korean Med. Sci. (2004)

Bottom Line: Hepatocellular carcinomas (HCCs) show genomic alterations, including DNA rearrangements associated with HBV DNA integration, loss of heterozygosity, and chromosomal amplification.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Pusan National University College of Medicine, 1-10 Ami-dong, Seo-gu, Busan 602-739, Korea. mcho@pusan.ac.kr

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.

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Related in: MedlinePlus

Detection of aberrant p16INK4A methylation (sample numbers 14, 38, 39 and 40, as indicated with arrows) in the sera of patients with liver cirrhosis (LC) and hepatocellular carcinoma (HCC). U, unmethylated; M, methylated; bp, base pairs.
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Figure 1: Detection of aberrant p16INK4A methylation (sample numbers 14, 38, 39 and 40, as indicated with arrows) in the sera of patients with liver cirrhosis (LC) and hepatocellular carcinoma (HCC). U, unmethylated; M, methylated; bp, base pairs.

Mentions: Methylated p16INK4A was detected in 47.8% (22/46) of HCC patients, a significantly higher rate than the 17.4% (4/23) seen in LC patients (p=0.014) (Fig. 1).


Detection of aberrant p16INK4A methylation in sera of patients with liver cirrhosis and hepatocellular carcinoma.

Chu HJ, Heo J, Seo SB, Kim GH, Kang DH, Song GA, Cho M, Yang US - J. Korean Med. Sci. (2004)

Detection of aberrant p16INK4A methylation (sample numbers 14, 38, 39 and 40, as indicated with arrows) in the sera of patients with liver cirrhosis (LC) and hepatocellular carcinoma (HCC). U, unmethylated; M, methylated; bp, base pairs.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2822270&req=5

Figure 1: Detection of aberrant p16INK4A methylation (sample numbers 14, 38, 39 and 40, as indicated with arrows) in the sera of patients with liver cirrhosis (LC) and hepatocellular carcinoma (HCC). U, unmethylated; M, methylated; bp, base pairs.
Mentions: Methylated p16INK4A was detected in 47.8% (22/46) of HCC patients, a significantly higher rate than the 17.4% (4/23) seen in LC patients (p=0.014) (Fig. 1).

Bottom Line: Hepatocellular carcinomas (HCCs) show genomic alterations, including DNA rearrangements associated with HBV DNA integration, loss of heterozygosity, and chromosomal amplification.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine, Pusan National University College of Medicine, 1-10 Ami-dong, Seo-gu, Busan 602-739, Korea. mcho@pusan.ac.kr

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.

Show MeSH
Related in: MedlinePlus