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散发型及与雄激素性-双亲嵌合相关的肝间叶性错构瘤中19号染色体臂微小RNA簇的甲基化状态

Methylation status of the chromosome arm 19q MicroRNA cluster in sporadic and androgenetic-Biparental mosaicism-associated hepatic mesenchymal hamartoma.

作者信息

Keller Rachel B, Demellawy Dina El, Quaglia Alberto, Finegold Milton, Kapur Raj P

出版信息

Pediatr Dev Pathol. 2015 May-Jun;18(3):218-27. doi: 10.2350/15-01-1600-OA.1. Epub 2015 Mar 9.

Abstract

The C19MC gene on chromosome band 19q13.4 encodes a cluster of 46 microRNAs; those microRNAs are normally only expressed from the paternal allele and in the placenta. Placental expression correlates with selective demethylation of the paternal C19MC promoter, in contrast to methylation of both maternal and paternal alleles in nonplacental tissues. Prior investigations demonstrated "ectopic" activation of this gene in most hepatic mesenchymal hamartomas, including sporadic tumors and others with androgenetic-biparental mosaicism (subset of cells are diploid, but contain only paternally derived chromosomes). In the present investigation of C19MC promoter methylation status in a series of 14 mesenchymal hamartomas, a demethylated allele was identified in 6 tumors, including all 4 with androgenetic-biparental mosaicism. Conversely, only methylated alleles were cloned from sporadic hamartomas, including 3 tumors with chromosomal rearrangements thought likely to activate C19MC expression independent of the native promoter. In conjunction with published data, the findings suggest multiple molecular mechanisms for C19MC activation in hepatic mesenchymal hamartoma, including the existence of a normal placental imprinting pattern in mesenchymal cells in a subset of cases. Some or all of the latter hamartomas may result from placental "grafting," a hypothesis supported by endothelial expression of the placental vascular marker, glucose transporter-1, in 1 of the 6 cases with a demethylated allele.

摘要

位于19号染色体19q13.4带的C19MC基因编码一组46个微小RNA;这些微小RNA通常仅从父本等位基因表达,且仅在胎盘中表达。胎盘表达与父本C19MC启动子的选择性去甲基化相关,与之形成对比的是,在非胎盘组织中,母本和父本等位基因均发生甲基化。先前的研究表明,在大多数肝间叶性错构瘤中,包括散发性肿瘤和其他具有雄激素-双亲嵌合体的肿瘤(部分细胞为二倍体,但仅含有父本来源的染色体),该基因会发生“异位”激活。在本次对一系列14例间叶性错构瘤的C19MC启动子甲基化状态的研究中,在6例肿瘤中鉴定出了一个去甲基化等位基因,其中包括所有4例具有雄激素-双亲嵌合体的肿瘤。相反,仅从散发性错构瘤中克隆出了甲基化等位基因,包括3例被认为可能通过独立于天然启动子的机制激活C19MC表达的具有染色体重排的肿瘤。结合已发表的数据,这些发现提示了肝间叶性错构瘤中C19MC激活的多种分子机制,包括在部分病例中间叶细胞中存在正常胎盘印记模式。部分或所有后一种错构瘤可能是胎盘“植入”的结果,这一假说是由6例具有去甲基化等位基因的病例中的1例中胎盘血管标志物葡萄糖转运蛋白-1的内皮表达所支持的。

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