Chu Hyung Jun, Heo Jeong, Seo Soo Boon, Kim Gwang Ha, Kang Dae Hwan, Song Geun Am, Cho Mong, Yang Ung Suk
Department of Internal Medicine, Pusan National University College of Medicine, 1-10 Ami-dong, Seo-gu, Busan 602-739, Korea.
J Korean Med Sci. 2004 Feb;19(1):83-6. doi: 10.3346/jkms.2004.19.1.83.
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.
肝细胞癌（HCC）存在基因组改变，包括与乙肝病毒（HBV）DNA整合相关的DNA重排、杂合性缺失和染色体扩增。最常涉及的基因是那些编码肿瘤抑制因子的基因。p16INK4A肿瘤抑制基因在HCC组织中经常出现基因改变。本研究旨在检测肝硬化（LC）和HCC患者血清中p16INK4A甲基化的发生率，并评估其作为HCC肿瘤标志物的作用。本研究检测了23例LC患者和46例HCC患者的血清。通过对血清样本进行甲基化特异性PCR来评估p16INK4A的甲基化状态。在17.4%（4/23）的LC患者和47.8%（22/46）的HCC患者中检测到甲基化的p16INK4A。未发现p16INK4A甲基化与血清甲胎蛋白（AFP）水平之间存在关联。由于p16INK4A甲基化状态与血清AFP水平无关，它可能具有作为HCC肿瘤标志物的作用。
