Loss of parental-specific methylation at the IGF2 locus in human hepatocellular carcinoma
Loss of parental-specific methylation at the IGF2 locus in human hepatocellular carcinoma
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DOI：
10.1002/path.1477
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发表时间：
2003-11-01
影响因子：
7.3
通讯作者：
Terris, B
中科院分区：
文献类型：
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作者：
Poirier, K;Chalas, C;Terris, B
据报道，生长因子IGF2在人肝细胞癌(HCCs)中大量产生。可以推测，与该基因座甲基化变化相关的干扰或影响11p15.5印迹结构域作为一个整体在肝癌中是可能的。在本研究中，分析了71例病毒相关性和非病毒相关性肝癌组织和6例正常肝组织中跨越11p15结构域的印迹基因TSSC5、LIT1和IGF2的差异甲基化状态。TSSC5和LIT1的甲基化改变分别只在6%和8%的肝癌中观察到，而IGF2基因的甲基化改变占89%，这表明这些基因座没有伴随的异常调节。这些观察表明IGF2基因上父母特异性甲基化的缺失可能与肝细胞癌的发生有关，无论是病毒相关的还是非病毒相关的，并且发生在肝硬变或非肝硬变的肝脏中。版权所有(C)2003 John Wiley Sons，Ltd.
Significant production of the growth factor IGF2 has been reported in human hepatocellular carcinomas (HCCs). Disturbances associated with changes in methylation at this locus or affecting the 11p15.5 imprinting domain as a whole can be postulated in HCCs. In the present study, the methylation status of differentially methylated regions of the imprinted genes TSSC5, LIT1, and IGF2, which span the 11p15 domain, was analysed in 71 liver tissues from virus-associated and non-virus-associated HCCs compared with six normal liver tissues. Altered methylation of TSSC5 and LIT1 was observed in only 6% and 8% of HCCs, respectively, compared with 89% at the IGF2 locus, suggesting that these loci were not concomitantly dysregulated. These observations suggest that loss of parental-specific methylation at the IGF2 locus may be specifically associated with HCC, whether virus-associated or non-virus-associated, and arising in cirrhotic or non-cirrhotic livers. Copyright (C) 2003 John Wiley Sons, Ltd.