人类甲状旁腺肿瘤的表观遗传学

IF 1.2
V. Chiara, Corbetta Sabrina
{"title":"人类甲状旁腺肿瘤的表观遗传学","authors":"V. Chiara, Corbetta Sabrina","doi":"10.2217/IJE-2017-0002","DOIUrl":null,"url":null,"abstract":"Parathyroid tumors are common endocrine neoplasia associated with primary hyperparathyroidism, a metabolic disorder sustained by parathormone hypersecretion. The epigenetic scenario in parathyroid tumors is beginning to be decoded. Here, main findings are reviewed: hypermethylation of specific DNA CpG islands has been described, despite global DNA promoter hypomethylation was not detectable; embryonic-related miRNAs, belonging to the C19MC and miR‐371-373 clusters, and miR‐296, are deregulated; expression of histone H1.2 and H2B is increased; expression of histone methyltransferase EZH2, BMI1 and RIZ1 is impaired; the tumor suppressor HIC1, MEN1 and CDC73 gene products, key molecules in parathyroid tumorigenesis, may be involved in epigenetic aberrant changes. Epigenetic changes are more frequent and more consistent in parathyroid malignancies, and positively correlated with severity of primary hyperparathyroidism.","PeriodicalId":42691,"journal":{"name":"International Journal of Endocrine Oncology","volume":null,"pages":null},"PeriodicalIF":1.2000,"publicationDate":"2017-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/IJE-2017-0002","citationCount":"3","resultStr":"{\"title\":\"Epigenetics of human parathyroid tumors\",\"authors\":\"V. Chiara, Corbetta Sabrina\",\"doi\":\"10.2217/IJE-2017-0002\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Parathyroid tumors are common endocrine neoplasia associated with primary hyperparathyroidism, a metabolic disorder sustained by parathormone hypersecretion. The epigenetic scenario in parathyroid tumors is beginning to be decoded. Here, main findings are reviewed: hypermethylation of specific DNA CpG islands has been described, despite global DNA promoter hypomethylation was not detectable; embryonic-related miRNAs, belonging to the C19MC and miR‐371-373 clusters, and miR‐296, are deregulated; expression of histone H1.2 and H2B is increased; expression of histone methyltransferase EZH2, BMI1 and RIZ1 is impaired; the tumor suppressor HIC1, MEN1 and CDC73 gene products, key molecules in parathyroid tumorigenesis, may be involved in epigenetic aberrant changes. Epigenetic changes are more frequent and more consistent in parathyroid malignancies, and positively correlated with severity of primary hyperparathyroidism.\",\"PeriodicalId\":42691,\"journal\":{\"name\":\"International Journal of Endocrine Oncology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.2000,\"publicationDate\":\"2017-05-08\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.2217/IJE-2017-0002\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International Journal of Endocrine Oncology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2217/IJE-2017-0002\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Endocrine Oncology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2217/IJE-2017-0002","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 3

摘要

甲状旁腺瘤是一种常见的内分泌肿瘤,与原发性甲状旁腺功能亢进有关,甲状旁腺功能亢进是一种由甲状旁腺激素分泌过多引起的代谢紊乱。甲状旁腺肿瘤的表观遗传机制开始被破译。在这里,主要研究结果进行了回顾:尽管没有检测到全局DNA启动子低甲基化,但已经描述了特定DNA CpG岛的超甲基化;属于C19MC和miR‐371-373簇以及miR‐296的胚胎相关mirna被解除调控;组蛋白H1.2、H2B表达升高;组蛋白甲基转移酶EZH2、BMI1、RIZ1表达受损;肿瘤抑制因子HIC1、MEN1和CDC73基因产物是甲状旁腺肿瘤发生的关键分子,可能参与了表观遗传异常改变。表观遗传改变在甲状旁腺恶性肿瘤中更为频繁和一致,并与原发性甲状旁腺功能亢进的严重程度呈正相关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Epigenetics of human parathyroid tumors
Parathyroid tumors are common endocrine neoplasia associated with primary hyperparathyroidism, a metabolic disorder sustained by parathormone hypersecretion. The epigenetic scenario in parathyroid tumors is beginning to be decoded. Here, main findings are reviewed: hypermethylation of specific DNA CpG islands has been described, despite global DNA promoter hypomethylation was not detectable; embryonic-related miRNAs, belonging to the C19MC and miR‐371-373 clusters, and miR‐296, are deregulated; expression of histone H1.2 and H2B is increased; expression of histone methyltransferase EZH2, BMI1 and RIZ1 is impaired; the tumor suppressor HIC1, MEN1 and CDC73 gene products, key molecules in parathyroid tumorigenesis, may be involved in epigenetic aberrant changes. Epigenetic changes are more frequent and more consistent in parathyroid malignancies, and positively correlated with severity of primary hyperparathyroidism.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
审稿时长
13 weeks
期刊介绍: International Journal of Endocrine Oncology is a quarterly, peer-reviewed journal that helps the clinician to keep up to date with best practice in this fast-moving field. The journal highlights significant advances in basic and translational research, and places them in context for future therapy. The journal presents the latest research findings in diagnosis and management of endocrine cancer, together with authoritative reviews, cutting-edge editorials and perspectives that highlight hot topics and controversy in the field. Independent drug evaluations assess newly approved medications and their role in clinical practice. The journal welcomes the unsolicited submission of article proposals and original research manuscripts.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信