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<article article-type="research-article" dtd-version="1.2" xml:lang="ru" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"><front><journal-meta><journal-id journal-id-type="issn">2658-6533</journal-id><journal-title-group><journal-title>Научные результаты биомедицинских исследований</journal-title></journal-title-group><issn pub-type="epub">2658-6533</issn></journal-meta><article-meta><article-id pub-id-type="doi">10.18413/2658-6533-2021-7-2-0-6</article-id><article-id pub-id-type="publisher-id">2390</article-id><article-categories><subj-group subj-group-type="heading"><subject>Клиническая медицина</subject></subj-group></article-categories><title-group><article-title>&lt;strong&gt;Estrogens and uterine fibroids: an integrated view&lt;/strong&gt;&lt;br /&gt;
&amp;nbsp;</article-title><trans-title-group xml:lang="en"><trans-title>&lt;strong&gt;Estrogens and uterine fibroids: an integrated view&lt;/strong&gt;&lt;br /&gt;
&amp;nbsp;</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="ru"><surname>Alsudairi</surname><given-names>Hadeel N.</given-names></name><name xml:lang="en"><surname>Alsudairi</surname><given-names>Hadeel N.</given-names></name></name-alternatives><email>halsudairi@alfaisal.edu</email></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="ru"><surname>Alrasheed</surname><given-names>Alanoud T.</given-names></name><name xml:lang="en"><surname>Alrasheed</surname><given-names>Alanoud T.</given-names></name></name-alternatives><email>atalrasheed@alfaisal.edu</email></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="ru"><surname>Dvornyk</surname><given-names>Volodymyr</given-names></name><name xml:lang="en"><surname>Dvornyk</surname><given-names>Volodymyr</given-names></name></name-alternatives><email>vdvornyk@alfaisal.edu</email></contrib></contrib-group><pub-date pub-type="epub"><year>2021</year></pub-date><volume>7</volume><issue>2</issue><fpage>0</fpage><lpage>0</lpage><self-uri content-type="pdf" xlink:href="/media/medicine/2021/2/Биомед_июнь-51-58_WLC8M3m.pdf" /><abstract xml:lang="ru"><p>Background: Uterine fibroids or uterine leiomyomata (UL) are common benign tumors of the uterine myometrium affecting a significant proportion of women at reproductive age. UL is a disease with complex etiology determined by many genetic and environmental factors. Estrogen is widely acknowledged as one of the main factors contributing to the risk and pathogenesis of UL. The aim of the study: To summarize available literature data about the estrogen-related environmental factors, genes and metabolic pathways, which may play a role in the disease. Materials and methods: The PubMed, Scopus, and Web of Science literature databases were searched for relevant articles using such keywords as &amp;ldquo;uterine fibroids&amp;rdquo;, &amp;ldquo;uterine leiomyoma&amp;rdquo;, &amp;ldquo;estrogen&amp;rdquo;, &amp;ldquo;gene&amp;rdquo;, &amp;ldquo;association&amp;rdquo;, &amp;ldquo;expression&amp;rdquo;, &amp;ldquo;epigenetic&amp;rdquo; in various combinations. Results: Estrogen contributes to the risk and pathophysiology of UL in multiple ways. Apart from the well-known effect of estrogen on expression of many genes mediated by estrogen receptors, it increases sensitivity of myometrium to progesterone and thus influences expression of the progesterone-controlled genes. On the other hand, the data about association of various estrogen-related genes with UL are largely inconsistent and inconclusive. Conclusion: The observed heterogeneity of UL apparently results from the diversity of mechanisms contributing to the disease. This makes identification of the causative genetic variants challenging and prompts for further studies of this problem.</p></abstract><trans-abstract xml:lang="en"><p>Background: Uterine fibroids or uterine leiomyomata (UL) are common benign tumors of the uterine myometrium affecting a significant proportion of women at reproductive age. UL is a disease with complex etiology determined by many genetic and environmental factors. Estrogen is widely acknowledged as one of the main factors contributing to the risk and pathogenesis of UL. The aim of the study: To summarize available literature data about the estrogen-related environmental factors, genes and metabolic pathways, which may play a role in the disease. Materials and methods: The PubMed, Scopus, and Web of Science literature databases were searched for relevant articles using such keywords as &amp;ldquo;uterine fibroids&amp;rdquo;, &amp;ldquo;uterine leiomyoma&amp;rdquo;, &amp;ldquo;estrogen&amp;rdquo;, &amp;ldquo;gene&amp;rdquo;, &amp;ldquo;association&amp;rdquo;, &amp;ldquo;expression&amp;rdquo;, &amp;ldquo;epigenetic&amp;rdquo; in various combinations. Results: Estrogen contributes to the risk and pathophysiology of UL in multiple ways. Apart from the well-known effect of estrogen on expression of many genes mediated by estrogen receptors, it increases sensitivity of myometrium to progesterone and thus influences expression of the progesterone-controlled genes. On the other hand, the data about association of various estrogen-related genes with UL are largely inconsistent and inconclusive. Conclusion: The observed heterogeneity of UL apparently results from the diversity of mechanisms contributing to the disease. This makes identification of the causative genetic variants challenging and prompts for further studies of this problem.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>uterine fibroids</kwd><kwd>estrogen</kwd><kwd>pathogenesis</kwd><kwd>genetics</kwd><kwd>epigenetics</kwd><kwd>transcriptomics</kwd></kwd-group><kwd-group xml:lang="en"><kwd>uterine fibroids</kwd><kwd>estrogen</kwd><kwd>pathogenesis</kwd><kwd>genetics</kwd><kwd>epigenetics</kwd><kwd>transcriptomics</kwd></kwd-group></article-meta></front><back><ref-list><title>Список литературы</title><ref id="B1"><mixed-citation>1.&amp;nbsp;&amp;nbsp;&amp;nbsp; Stewart EA, Cookson CL, Gandolfo RA, et al. Epidemiology of uterine fibroids: a systematic review. British Journal of Obstetrics and Gynaecology. 2017;124(10):1501-12. DOI: https://doi.org/10.1111/1471-0528.14640</mixed-citation></ref><ref id="B2"><mixed-citation>2.&amp;nbsp;&amp;nbsp;&amp;nbsp; Cook H, Ezzati M, Segars JH, et al. The impact of uterine leiomyomas on reproductive outcomes. Minerva Ginecol. 2010;62(3):225-36.</mixed-citation></ref><ref id="B3"><mixed-citation>3.&amp;nbsp;&amp;nbsp;&amp;nbsp; Cardozo ER, Clark AD, Banks NK, et al. The estimated annual cost of uterine leiomyomata in the United States. American Journal of Obstetrics and Gynecology. 2012;206(3):211.e1-9. DOI: https://doi.org/10.1016/j.ajog.2011.12.002</mixed-citation></ref><ref id="B4"><mixed-citation>4.&amp;nbsp;&amp;nbsp;&amp;nbsp; Reis FM, Bloise E, Ortiga-Carvalho TM. Hormones and pathogenesis of uterine fibroids. Best Practice and Research in Clinical Obstetrics and Gynaecology. 2016;34:13-24. DOI: https://doi.org/10.1016/j.bpobgyn.2015.11.015</mixed-citation></ref><ref id="B5"><mixed-citation>5.&amp;nbsp;&amp;nbsp;&amp;nbsp; Andersen J, DyReyes VM, Barbieri RL, et al. Leiomyoma primary cultures have elevated transcriptional response to estrogen compared with autologous myometrial cultures. Journal of the Society for Gynecologic Investigation. 1995;2(3):542-51. DOI: https://doi.org/10.1016/1071-5576(94)00053-4</mixed-citation></ref><ref id="B6"><mixed-citation>6.&amp;nbsp;&amp;nbsp;&amp;nbsp; Maruo T, Ohara N, Wang J, et al. Sex steroidal regulation of uterine leiomyoma growth and apoptosis. Human Reproduction Update. 2004;10(3):207-20. DOI: https://doi.org/10.1093/humupd/dmh019</mixed-citation></ref><ref id="B7"><mixed-citation>7.&amp;nbsp;&amp;nbsp;&amp;nbsp; Bulun SE, Simpson ER, Word RA. Expression of the CYP19 gene and its product aromatase cytochrome P450 in human uterine leiomyoma tissues and cells in culture. Journal of Clinical Endocrinology and Metabolism. 1994;78(3):736-43. DOI: https://doi.org/10.1210/jcem.78.3.8126151</mixed-citation></ref><ref id="B8"><mixed-citation>8.&amp;nbsp;&amp;nbsp;&amp;nbsp; Sumitani H, Shozu M, Segawa T, et al. In situ estrogen synthesized by aromatase P450 in uterine leiomyoma cells promotes cell growth probably via an autocrine/intracrine mechanism. Endocrinology. 2000;141(10):3852-61. DOI: https://doi.org/10.1210/endo.141.10.7719</mixed-citation></ref><ref id="B9"><mixed-citation>9.&amp;nbsp;&amp;nbsp;&amp;nbsp; Bulus AD, Asci A, Erkekoglu P, et al. The evaluation of possible role of endocrine disruptors in central and peripheral precocious puberty. Toxicology Mechanisms and Methods. 2016;26(7):493-500. DOI: https://doi.org/10.3109/15376516.2016.1158894</mixed-citation></ref><ref id="B10"><mixed-citation>10.&amp;nbsp; D&amp;#39;Aloisio AA, Baird DD, DeRoo LA, et al. Early-life exposures and early-onset uterine leiomyomata in black women in the Sister Study. Environmental Health Perspectives. 2012;120(3):406-12. DOI: https://doi.org/10.1289/ehp.1103620</mixed-citation></ref><ref id="B11"><mixed-citation>11.&amp;nbsp; Roy JR, Chakraborty S, Chakraborty TR. Estrogen-like endocrine disrupting chemicals affecting puberty in humans--a review. Medical Science Monitor. 2009;15(6):RA137-45.</mixed-citation></ref><ref id="B12"><mixed-citation>12.&amp;nbsp; Patel SA, Sunde J. Primary non-clear-cell adenocarcinoma of the vagina in a diethylstilbestrol exposed woman. Military Medicine. 2014;179(4):e461-2. DOI: https://doi.org/10.7205/MILMED-D-13-00316</mixed-citation></ref><ref id="B13"><mixed-citation>13.&amp;nbsp; Mahalingaiah S, Hart JE, Wise LA, et al. Prenatal diethylstilbestrol exposure and risk of uterine leiomyomata in the Nurses&amp;#39; Health Study II. American Journal of Epidemiology. 2014;179(2):186-91. DOI: https://doi.org/10.1093/aje/kwt250</mixed-citation></ref><ref id="B14"><mixed-citation>14.&amp;nbsp; Ishikawa H, Ishi K, Serna VA, et al. Progesterone is essential for maintenance and growth of uterine leiomyoma. Endocrinology. 2010;151(6):2433-42. DOI: https://doi.org/10.1210/en.2009-1225</mixed-citation></ref><ref id="B15"><mixed-citation>15.&amp;nbsp; Shimomura Y, Matsuo H, Samoto T, et al. Up-regulation by progesterone of proliferating cell nuclear antigen and epidermal growth factor expression in human uterine leiomyoma. Journal of Clinical Endocrinology and Metabolism. 1998;83(6):2192-8. DOI: https://doi.org/10.1210/jcem.83.6.4879</mixed-citation></ref><ref id="B16"><mixed-citation>16.&amp;nbsp; Hyder SM, Huang JC, Nawaz Z, et al. Regulation of vascular endothelial growth factor expression by estrogens and progestins. Environmental Health Perspectives. 2000;108 Suppl 5:785-90. DOI: https://doi.org/10.1289/ehp.00108s5785</mixed-citation></ref><ref id="B17"><mixed-citation>17.&amp;nbsp; Swartz CD, Afshari CA, Yu L, et al. Estrogen-induced changes in IGF-I, Myb family and MAP kinase pathway genes in human uterine leiomyoma and normal uterine smooth muscle cell lines. Molecular Human Reproduction. 2005;11(6):441-50. DOI: https://doi.org/10.1093/molehr/gah174</mixed-citation></ref><ref id="B18"><mixed-citation>18.&amp;nbsp; Yu L, Moore AB, Castro L, et al. Estrogen regulates MAPK-related genes through genomic and nongenomic interactions between IGF-I receptor tyrosine kinase and estrogen receptor-alpha signaling pathways in human uterine leiomyoma cells. Journal of Signal Transduction. 2012;2012:204236. DOI: https://doi.org/10.1155/2012/204236</mixed-citation></ref><ref id="B19"><mixed-citation>19.&amp;nbsp; Ciarmela P, Islam MS, Reis FM, et al. Growth factors and myometrium: biological effects in uterine fibroid and possible clinical implications. Human Reproduction Update. 2011;17(6):772-90. DOI: https://doi.org/10.1093/humupd/dmr031</mixed-citation></ref><ref id="B20"><mixed-citation>20.&amp;nbsp; Barbarisi A, Petillo O, Di Lieto A, et al. 17-beta estradiol elicits an autocrine leiomyoma cell proliferation: evidence for a stimulation of protein kinase-dependent pathway. Journal of Cellular Physiology. 2001;186(3):414-24. DOI: https://doi.org/10.1002/1097-4652(2000)9999:999&amp;lt;000::AID-JCP1040&amp;gt;3.0.CO;2-E</mixed-citation></ref><ref id="B21"><mixed-citation>21.&amp;nbsp; Ciarmela P, Bloise E, Gray PC, et al. Activin-A and myostatin response and steroid regulation in human myometrium: disruption of their signalling in uterine fibroid. Journal of Clinical Endocrinology and Metabolism. 2011;96(3):755-65. DOI: https://doi.org/10.1210/jc.2010-0501</mixed-citation></ref><ref id="B22"><mixed-citation>22.&amp;nbsp; Wang H, Wu X, Englund K, et al. Different expression of estrogen receptors alpha and beta in human myometrium and leiomyoma during the proliferative phase of the menstrual cycle and after GnRHa treatment. Gynecological Endocrinology. 2001;15(6):443-52.</mixed-citation></ref><ref id="B23"><mixed-citation>23.&amp;nbsp; Al-Hendy A, Diamond MP, El-Sohemy A, et al. 1,25-dihydroxyvitamin D3 regulates expression of sex steroid receptors in human uterine fibroid cells. Journal of Clinical Endocrinology and Metabolism. 2015;100(4):E572-82. DOI: https://doi.org/10.1210/jc.2014-4011</mixed-citation></ref><ref id="B24"><mixed-citation>24.&amp;nbsp; Bakas P, Liapis A, Vlahopoulos S, et al. Estrogen receptor alpha and beta in uterine fibroids: a basis for altered estrogen responsiveness. Fertility and Sterility. 2008;90(5):1878-85. DOI: https://doi.org/10.1016/j.fertnstert.2007.09.019</mixed-citation></ref><ref id="B25"><mixed-citation>25.&amp;nbsp; Wei T, Geiser AG, Qian HR, et al. DNA microarray data integration by ortholog gene analysis reveals potential molecular mechanisms of estrogen-dependent growth of human uterine fibroids. BMC Women&amp;#39;s Health. 2007;7:5. DOI: https://doi.org/10.1186/1472-6874-7-5</mixed-citation></ref><ref id="B26"><mixed-citation>26.&amp;nbsp; Luo N, Guan Q, Zheng L, et al. Estrogen-mediated activation of fibroblasts and its effects on the fibroid cell proliferation. Translational Research. 2014;163(3):232-41. DOI: https://doi.org/10.1016/j.trsl.2013.11.008</mixed-citation></ref><ref id="B27"><mixed-citation>27.&amp;nbsp; Govindan S, Shaik NA, Vedicherla B, et al. Estrogen receptor-alpha gene (T/C) Pvu II polymorphism in endometriosis and uterine fibroids. Disease Markers. 2009;26(4):149-54. DOI: https://doi.org/10.3233/dma-2009-0625</mixed-citation></ref><ref id="B28"><mixed-citation>28.&amp;nbsp; Bharathi C, Anupama D, Pratibha N, et al. Impact of genetic variants in estrogen receptor-beta gene in the etiology of uterine leiomyomas. Journal of Reproduction and Infertility. 2019;20(3):151-60.</mixed-citation></ref><ref id="B29"><mixed-citation>29.&amp;nbsp; El-Shennawy GA, Elbialy AA, Isamil AE, et al. Is genetic polymorphism of ER-alpha, CYP1A1, and CYP1B1 a risk factor for uterine leiomyoma? Archives of Gynecology and Obstetrics. 2011;283(6):1313-8. DOI: https://doi.org/10.1007/s00404-010-1550-x</mixed-citation></ref><ref id="B30"><mixed-citation>30.&amp;nbsp; Feng Y, Zhao X, Zhou C, et al. The associations between the Val158Met in the catechol-O-methyltransferase (COMT) gene and the risk of uterine leiomyoma (ULM). Gene. 2013;529(2):296-9. DOI: https://doi.org/10.1016/j.gene.2013.07.019</mixed-citation></ref><ref id="B31"><mixed-citation>31.&amp;nbsp; Shen Y, Xu Q, Ren M, et al. Role of single nucleotide polymorphisms in estrogen-metabolizing enzymes and susceptibility to uterine leiomyoma in Han Chinese: a case-control study. Journal of Obstetrics and Gynaecology Research. 2014;40(4):1077-84. DOI: https://doi.org/10.1111/jog.12275</mixed-citation></ref><ref id="B32"><mixed-citation>32.&amp;nbsp; Rafnar T, Gunnarsson B, Stefansson OA, et al. Variants associating with uterine leiomyoma highlight genetic background shared by various cancers and hormone-related traits. Nature Communications. 2018;9(1):3636. DOI: https://doi.org/10.1038/s41467-018-05428-6</mixed-citation></ref><ref id="B33"><mixed-citation>33.&amp;nbsp; Gallagher CS, Makinen N, Harris HR, et al. Genome-wide association and epidemiological analyses reveal common genetic origins between uterine leiomyomata and endometriosis. Nature Communications. 2019;10(1):4857. DOI: https://doi.org/10.1038/s41467-019-12536-4</mixed-citation></ref><ref id="B34"><mixed-citation>34.&amp;nbsp; Edwards TL, Giri A, Hellwege JN, et al. A trans-ethnic genome-wide association study of uterine fibroids. Frontiers in Genetics. 2019;10:511. DOI: https://doi.org/10.3389/fgene.2019.00511</mixed-citation></ref><ref id="B35"><mixed-citation>35.&amp;nbsp; Sakai K, Tanikawa C, Hirasawa A, et al. Identification of a novel uterine leiomyoma GWAS locus in a Japanese population. Scientific Reports. 2020;10(1):1197. DOI: https://doi.org/10.1038/s41598-020-58066-8</mixed-citation></ref><ref id="B36"><mixed-citation>36.&amp;nbsp; Sun K, Xie Y, Zhao N, et al. A case-control study of the relationship between visceral fat and development of uterine fibroids. Experimental and Therapeutic Medicine. 2019;18(1):404-10. DOI: https://doi.org/10.3892/etm.2019.7575</mixed-citation></ref><ref id="B37"><mixed-citation>37.&amp;nbsp; Ciavattini A, Di Giuseppe J, Stortoni P, et al. Uterine fibroids: pathogenesis and interactions with endometrium and endomyometrial junction. Obstetrics and Gynecology International. 2013;2013:173184. DOI: https://doi.org/10.1155/2013/173184</mixed-citation></ref><ref id="B38"><mixed-citation>38.&amp;nbsp; Qin H, Lin Z, Vasquez E, et al. Association between obesity and the risk of uterine fibroids: a systematic review and meta-analysis. Journal of Epidemiology and Community Health. 2021;75:197-204. DOI: https://doi.org/10.1136/jech-2019-213364</mixed-citation></ref><ref id="B39"><mixed-citation>39.&amp;nbsp; Wise LA, Laughlin-Tommaso SK. Epidemiology of uterine fibroids: from menarche to menopause. Clinical Obstetrics and Gynecology. 2016;59(1):2-24. DOI: https://doi.org/10.1097/GRF.0000000000000164</mixed-citation></ref><ref id="B40"><mixed-citation>40.&amp;nbsp; Wong JY, Gold EB, Johnson WO, et al. Circulating sex hormones and risk of uterine fibroids: Study of Women&amp;#39;s Health Across the Nation (SWAN). Journal of Clinical Endocrinology and Metabolism. 2016;101(1):123-30. DOI: https://doi.org/10.1210/jc.2015-2935</mixed-citation></ref><ref id="B41"><mixed-citation>41.&amp;nbsp; Yang Q, Mas A, Diamond MP, et al. The mechanism and function of epigenetics in uterine leiomyoma development. Reproductive Sciences. 2016;23(2):163-75. DOI: https://doi.org/10.1177/1933719115584449</mixed-citation></ref><ref id="B42"><mixed-citation>42.&amp;nbsp; Maekawa R, Sato S, Yamagata Y, et al. Genome-wide DNA methylation analysis reveals a potential mechanism for the pathogenesis and development of uterine leiomyomas. PLoS One. 2013;8(6):e66632. DOI: https://doi.org/10.1371/journal.pone.0066632</mixed-citation></ref><ref id="B43"><mixed-citation>43.&amp;nbsp; Alleyne AT, Bideau VS. Haplotypes of CYP1B1 and CCDC57 genes in an Afro-Caribbean female population with uterine leiomyoma. Molecular Biology Reports. 2019;46(3):3299-306. DOI: https://doi.org/10.1007/s11033-019-04790-y</mixed-citation></ref><ref id="B44"><mixed-citation>44.&amp;nbsp; Bideau VS, Alleyne AT. Leu/Val SNP polymorphism of CYP1B1 and risk of uterine leiomyoma in a Black population. Tumour Biology. 2016;37(3):4035-40. DOI: https://doi.org/10.1007/s13277-015-4239-8</mixed-citation></ref><ref id="B45"><mixed-citation>45.&amp;nbsp; Huang PC, Li WF, Liao PC, et al. Risk for estrogen-dependent diseases in relation to phthalate exposure and polymorphisms of CYP17A1 and estrogen receptor genes. Environmental Science and Pollution Research. 2014;21(24):13964-73. DOI: https://doi.org/10.1007/s11356-014-3260-6</mixed-citation></ref><ref id="B46"><mixed-citation>46.&amp;nbsp; Toprak M, Ates O, Ozsoy AZ, et al. Analysis of estrogen and progesterone receptor gene polymorphisms in leiomyoma. Journal of Clinical Laboratory Analysis. 2019;33(3):e22704. DOI: https://doi.org/10.1002/jcla.22704</mixed-citation></ref><ref id="B47"><mixed-citation>47.&amp;nbsp; Hsieh YY, Wang YK, Chang CC, et al. Estrogen receptor alpha-351 XbaI*G and -397 PvuII*C-related genotypes and alleles are associated with higher susceptibilities of endometriosis and leiomyoma. Molecular Human Reproduction. 2007;13(2):117-22. DOI: https://doi.org/10.1093/molehr/gal099</mixed-citation></ref><ref id="B48"><mixed-citation>48.&amp;nbsp; Denschlag D, Bentz EK, Hefler L, et al. Genotype distribution of estrogen receptor-alpha, catechol-O-methyltransferase, and cytochrome P450 17 gene polymorphisms in Caucasian women with uterine leiomyomas. Fertility and Sterility. 2006;85(2):462-7. DOI: https://doi.org/10.1016/j.fertnstert.2005.07.1308</mixed-citation></ref><ref id="B49"><mixed-citation>49.&amp;nbsp; Al-Hendy A, Salama SA. Ethnic distribution of estrogen receptor-a polymorphism is associated with a higher prevalence of uterine leiomyomas in black Americans. Fertility and Sterility. 2006;86(3):686-93. DOI: https://doi.org/10.1016/j.fertnstert.2006.01.052</mixed-citation></ref><ref id="B50"><mixed-citation>50.&amp;nbsp; Villanova FE, Andrade PM, Otsuka AY, et al. Estrogen receptor alpha polymorphism and susceptibility to uterine leiomyoma. Steroids. 2006;71(11-12):960-5. DOI: https://doi.org/10.1016/j.steroids.2006.07.005</mixed-citation></ref><ref id="B51"><mixed-citation>51.&amp;nbsp; Veronica M, Ali A, Venkateshwari A, et al. Association of estrogen and progesterone receptor gene polymorphisms and their respective hormones in uterine leiomyomas. Tumor Biology. 2016;37(6):8067-74. DOI: https://doi.org/10.1007/s13277-015-4711-5</mixed-citation></ref><ref id="B52"><mixed-citation>52.&amp;nbsp; Zhai XD, Ye Y, Yang Y, et al. No association between estrogen receptor beta polymorphisms and uterine leiomyoma. DNA and Cell Biology. 2009;28(12):633-6. DOI: https://doi.org/10.1089/dna.2009.0917</mixed-citation></ref><ref id="B53"><mixed-citation>53.&amp;nbsp; Fischer C, Juhasz-Boess I, Lattrich C, et al. Estrogen receptor beta gene polymorphisms and susceptibility to uterine fibroids. Gynecological Endocrinology. 2010;26(1):4-9. DOI: https://doi.org/10.3109/09513590903159573</mixed-citation></ref><ref id="B54"><mixed-citation>54.&amp;nbsp; Kasap B, Turhan NO, Edgunlu T, et al. G-protein-coupled estrogen receptor-30 gene polymorphisms are associated with uterine leiomyoma risk. Bosnian Journal of Basic Medical Sciences. 2016;16(1):39-45. DOI: https://doi.org/10.17305/bjbms.2016.683</mixed-citation></ref><ref id="B55"><mixed-citation>55.&amp;nbsp; da Silva F, Pabalan N, Ekaratcharoenchai N, et al. PROGINS polymorphism of the progesterone receptor gene and the susceptibility to uterine leiomyomas: a systematic review and meta-analysis. Genetic Testing and Molecular Biomarkers. 2018;22(5):295-301. DOI: https://doi.org/10.1089/gtmb.2017.0233</mixed-citation></ref></ref-list></back></article>