Racial disparity in uterine leiomyoma: new insights of genetic and environmental burden in myometrial cells.

IF 3.6 2区 医学 Q2 DEVELOPMENTAL BIOLOGY Molecular human reproduction Pub Date : 2024-02-29 DOI:10.1093/molehr/gaae004
Nazeer H Khan, Ross McNally, J Julie Kim, Jian-Jun Wei
{"title":"Racial disparity in uterine leiomyoma: new insights of genetic and environmental burden in myometrial cells.","authors":"Nazeer H Khan, Ross McNally, J Julie Kim, Jian-Jun Wei","doi":"10.1093/molehr/gaae004","DOIUrl":null,"url":null,"abstract":"<p><p>Uterine leiomyoma (LM), also known as uterine fibroids, are common gynecological tumors and can reach a prevalence of 70% among women by the age of 50 years. Notably, the LM burden is much higher in Black women with earlier onset, a greater tumor number, size, and severity compared to White women. Published knowledge shows that there are genetic, environmental, and lifestyle-based risk factors associated with racial disparity for LM. Significant strides have been made on genomic, epigenomic, and transcriptomic data levels in Black and White women to elucidate the underlying pathomolecular reasons of racial disparity in LM development. However, racial disparity of LM remains a major area of concern in gynecological research. This review highlights risk factors of LM and their role in different races. Furthermore, we discuss the genetics and uterine myometrial microenvironment in LM development. Comparative findings revealed that a major racial difference in the disease is linked to myometrial oxidative burden and altered ROS pathways which is relevant to the oxidized guanine in genomic DNA and MED12 mutations that drive the LM genesis. Considering the burden and morbidity of LM, we anticipate that this review on genetic risk and myometrial microenvironment will strengthen understanding and propel the growth of research to address the racial disparity of LM burden.</p>","PeriodicalId":18759,"journal":{"name":"Molecular human reproduction","volume":null,"pages":null},"PeriodicalIF":3.6000,"publicationDate":"2024-02-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10904341/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular human reproduction","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/molehr/gaae004","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"DEVELOPMENTAL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Uterine leiomyoma (LM), also known as uterine fibroids, are common gynecological tumors and can reach a prevalence of 70% among women by the age of 50 years. Notably, the LM burden is much higher in Black women with earlier onset, a greater tumor number, size, and severity compared to White women. Published knowledge shows that there are genetic, environmental, and lifestyle-based risk factors associated with racial disparity for LM. Significant strides have been made on genomic, epigenomic, and transcriptomic data levels in Black and White women to elucidate the underlying pathomolecular reasons of racial disparity in LM development. However, racial disparity of LM remains a major area of concern in gynecological research. This review highlights risk factors of LM and their role in different races. Furthermore, we discuss the genetics and uterine myometrial microenvironment in LM development. Comparative findings revealed that a major racial difference in the disease is linked to myometrial oxidative burden and altered ROS pathways which is relevant to the oxidized guanine in genomic DNA and MED12 mutations that drive the LM genesis. Considering the burden and morbidity of LM, we anticipate that this review on genetic risk and myometrial microenvironment will strengthen understanding and propel the growth of research to address the racial disparity of LM burden.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
子宫肌瘤的种族差异:子宫肌瘤细胞遗传和环境负担的新见解。
子宫良性肌瘤(LM)又称子宫肌瘤,是一种常见的妇科肿瘤,50 岁妇女的患病率可达 70%。值得注意的是,与白人妇女相比,黑人妇女的子宫肌瘤发病率更高,肿瘤的数量、大小和严重程度也更大。已公布的知识表明,遗传、环境和生活方式等风险因素与 LM 的种族差异有关。在黑人和白人妇女的基因组、表观基因组和转录组数据水平上取得了重大进展,以阐明 LM 发病的种族差异的病理分子原因。然而,LM 的种族差异仍然是妇科研究的一个主要关注领域。这篇综述强调了 LM 的风险因素及其在不同种族中的作用。此外,我们还讨论了 LM 发生过程中的遗传学和子宫肌层微环境。比较研究结果表明,该疾病的主要种族差异与子宫肌层氧化负担和 ROS 途径的改变有关,这与基因组 DNA 中的氧化鸟嘌呤和 MED12 基因突变有关,而 MED12 基因突变是 LM 发生的驱动力。考虑到 LM 的负担和发病率,我们希望这篇关于遗传风险和子宫肌层微环境的综述能加强人们对 LM 负担的种族差异的理解,并推动相关研究的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Molecular human reproduction
Molecular human reproduction 生物-发育生物学
CiteScore
8.30
自引率
0.00%
发文量
37
审稿时长
6-12 weeks
期刊介绍: MHR publishes original research reports, commentaries and reviews on topics in the basic science of reproduction, including: reproductive tract physiology and pathology; gonad function and gametogenesis; fertilization; embryo development; implantation; and pregnancy and parturition. Irrespective of the study subject, research papers should have a mechanistic aspect.
期刊最新文献
Sperm-carried IGF2: Towards the discovery of a spark contributing to embryo growth and development. Maturational competence of equine oocytes is associated with alterations in their “cumulome” Variants in NLRP2 and ZFP36L2, non-core components of the human subcortical maternal complex, cause female infertility with embryonic development arrest. Adjusting methylation levels with nucleus proportions highlights functional significance of differentially methylated cytosines associated with preeclampsia Oocyte-specific EXOC5 expression is required for mouse oogenesis and folliculogenesis.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1