表观遗传学
组蛋白
癌症表观遗传学
癌症研究
DNA甲基化
小RNA
染色质
生物
BAP1型
染色质重塑
基因
遗传学
癌症
CpG站点
医学
组蛋白甲基转移酶
基因表达
作者
Mark R. Morris,Farida Latif
标识
DOI:10.1038/nrneph.2016.168
摘要
New data suggests that, in addition to mutations in tumour-suppressor genes, renal cancer is associated with epigenetic aberrations. Here, the authors discuss the mechanisms by which epigenetically silenced genes and mutations in genes that are involved in histone modification or chromatin remodelling dysregulate crucial cellular pathways in renal cancer. The majority of kidney cancers are associated with mutations in the von Hippel-Lindau gene and a small proportion are associated with infrequent mutations in other well characterized tumour-suppressor genes. In the past 15 years, efforts to uncover other key genes involved in renal cancer have identified many genes that are dysregulated or silenced via epigenetic mechanisms, mainly through methylation of promoter CpG islands or dysregulation of specific microRNAs. In addition, the advent of next-generation sequencing has led to the identification of several novel genes that are mutated in renal cancer, such as PBRM1, BAP1 and SETD2, which are all involved in histone modification and nucleosome and chromatin remodelling. In this Review, we discuss how altered DNA methylation, microRNA dysregulation and mutations in histone-modifying enzymes disrupt cellular pathways in renal cancers.
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