{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,27]],"date-time":"2025-11-27T20:56:48Z","timestamp":1764277008120,"version":"3.37.3"},"reference-count":79,"publisher":"The Endocrine Society","issue":"9","license":[{"start":{"date-parts":[[2020,6,28]],"date-time":"2020-06-28T00:00:00Z","timestamp":1593302400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>We have searched the literature for information on the risk of breast cancer (BC) in relation to gender, breast development, and gonadal function in the following 8 populations: 1) females with the Turner syndrome (45, XO); 2) females and males with congenital hypogonadotropic hypogonadism and the Kallmann syndrome; 3) pure gonadal dysgenesis (PGD) in genotypic and phenotypic females and genotypic males (Swyer syndrome); 4) males with the Klinefelter syndrome (47, XXY); 5) male-to-female transgender individuals; 6) female-to-male transgender individuals; 7) genotypic males, but phenotypic females with the complete androgen insensitivity syndrome, and 8) females with Mayer-Rokitansky-K\u00fcster-Hauser (MRKH) syndrome (m\u00fcllerian agenesis).<\/jats:p>\n               <jats:p>Based on this search, we have drawn 3 major conclusions. First, the presence of a Y chromosome protects against the development of BC, even when female-size breasts and female-level estrogens are present. Second, without menstrual cycles, BC hardly occurs with an incidence comparable to males. There is a strong correlation between the lifetime number of menstrual cycles and the risk of BC. In our populations the BC risk in genetic females not exposed to progesterone (P4) is very low and comparable to males. Third, BC has been reported only once in genetic females with MRKH syndrome who have normal breasts and ovulating ovaries with normal levels of estrogens and P4. We hypothesize that the oncogenic glycoprotein WNT family member 4 is the link between the genetic cause of MRKH and the absence of BC women with MRKH syndrome.<\/jats:p>","DOI":"10.1210\/clinem\/dgaa404","type":"journal-article","created":{"date-parts":[[2020,6,28]],"date-time":"2020-06-28T18:13:51Z","timestamp":1593368031000},"page":"e3065-e3074","source":"Crossref","is-referenced-by-count":8,"title":["Breast Cancer and Major Deviations of Genetic and Gender-related Structures and Function"],"prefix":"10.1210","volume":"105","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1550-9400","authenticated-orcid":false,"given":"Herjan J T","family":"Coelingh Bennink","sequence":"first","affiliation":[{"name":"Pantarhei Oncology BV, AL Zeist, the Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5042-5360","authenticated-orcid":false,"given":"Jan F M","family":"Egberts","sequence":"additional","affiliation":[{"name":"Terminal 4 Communications, AR Hilversum, the Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0843-8088","authenticated-orcid":false,"given":"Jan A","family":"Mol","sequence":"additional","affiliation":[{"name":"Faculty of Veterinary Medicine, University of Utrecht, GA Utrecht, the Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6775-1963","authenticated-orcid":false,"given":"Kit C B","family":"Roes","sequence":"additional","affiliation":[{"name":"Department of Health Evidence, Section Biostatistics, Radboud University Medical Centre, GA Nijmegen, the Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0658-2745","authenticated-orcid":false,"given":"Paul J","family":"van Diest","sequence":"additional","affiliation":[{"name":"Department of Pathology, University Medical Center Utrecht, GA Utrecht, the Netherlands"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"80","published-online":{"date-parts":[[2020,6,28]]},"reference":[{"author":"American Cancer Society.","key":"2021122202411816100_CIT0001"},{"author":"American Cancer Society.","key":"2021122202411816100_CIT0002"},{"issue":"24","key":"2021122202411816100_CIT0003","doi-asserted-by":"crossref","first-page":"2311","DOI":"10.1056\/NEJMra1707939","article-title":"Breast cancer in men","volume":"378","author":"Giordano","year":"2018","journal-title":"N Engl J Med."},{"author":"Cancer Research UK.","key":"2021122202411816100_CIT0004"},{"year":"2017","author":"Pharmacy Times.","key":"2021122202411816100_CIT0005"},{"issue":"4","key":"2021122202411816100_CIT0006","doi-asserted-by":"crossref","first-page":"780","DOI":"10.1016\/j.fertnstert.2012.07.1104","article-title":"The patient with Turner syndrome: puberty and medical management concerns","volume":"98","author":"Gonzalez","year":"2012","journal-title":"Fertil Steril."},{"issue":"4","key":"2021122202411816100_CIT0007","doi-asserted-by":"crossref","first-page":"463","DOI":"10.1038\/ng1122","article-title":"Loss-of-function mutations in FGFR1 cause autosomal dominant Kallmann syndrome","volume":"33","author":"Dod\u00e9","year":"2003","journal-title":"Nat Genet."},{"author":"National Organization of Rare Disorders (NORD).","key":"2021122202411816100_CIT0008"},{"issue":"2","key":"2021122202411816100_CIT0009","doi-asserted-by":"crossref","first-page":"622","DOI":"10.1210\/jc.2002-021491","article-title":"Prenatal and postnatal prevalence of Klinefelter syndrome: a national registry study","volume":"88","author":"Bojesen","year":"2003","journal-title":"J Clin Endocrinol Metab."},{"issue":"13","key":"2021122202411816100_CIT0010","doi-asserted-by":"crossref","first-page":"1251","DOI":"10.1056\/NEJMcp1008161","article-title":"Clinical practice. 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