{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T10:07:38Z","timestamp":1789207658412,"version":"build-2803163510"},"reference-count":176,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T00:00:00Z","timestamp":1789171200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T00:00:00Z","timestamp":1789171200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Andrology"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Non\u2010mosaic Klinefelter syndrome (47,XXY) arises from sex\u2010specific meiotic mechanisms leading to nondisjunction during gametogenesis. In maternal cases, errors occur predominantly during meiosis I, frequently involving X chromosomes that lack crossovers or exhibit crossovers outside optimal chromosomal locations; this nondisjunction is further exacerbated by advancing maternal age and the subsequent deterioration of cohesins. Conversely, paternal 47,XXY stems primarily from the failure of obligate recombination within the pseudoautosomal region, which is critical for accurate XY segregation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Drawing on the latest literature, this review transitions from a descriptive account of non\u2010mosaic Klinefelter syndrome (nKS) toward a comprehensive analysis of mechanistic and genomic evidence, establishing a unified framework of sex\u2010specific meiotic vulnerability.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We synthesized recent findings from forward genetic approaches in mouse models with data from human observational and reverse\u2010genetic studies, delineating an updated view of the established and putative mechanisms that modulate sex chromosome segregation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>We frame XX and XY nondisjunction as a genetically modulated process rather than a purely stochastic event. The integrated evidence supports a unified framework in which maternal and paternal mechanisms converge primarily on meiotic recombination failure but differ in timing, chromosomal context, and genetic modulation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>From a clinical standpoint, identifying the molecular drivers of sex chromosome aneuploidy will enhance genetic counseling and risk stratification. Such insights are poised to facilitate informed reproductive decision\u2010making and timely therapeutic support, ultimately reducing the burden of nKS comorbidities and improving patients' quality of life.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/andr.70384","type":"journal-article","created":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T09:29:13Z","timestamp":1789205353000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Meiotic Origins of Non\u2010Mosaic Klinefelter Syndrome (47, XXY): Mechanisms, Dimorphism, and Emerging Genetic Susceptibility"],"prefix":"10.1111","author":[{"ORCID":"https:\/\/orcid.org\/0009-0005-7035-0713","authenticated-orcid":false,"given":"Matteo","family":"Lampitto","sequence":"first","affiliation":[{"name":"Department of Biomedicine and Prevention University of Rome Tor Vergata  Rome Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1104-6234","authenticated-orcid":false,"given":"Marco","family":"Barchi","sequence":"additional","affiliation":[{"name":"Department of Biomedicine and Prevention University of Rome Tor Vergata  Rome Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,9,12]]},"reference":[{"key":"e_1_2_12_2_1","doi-asserted-by":"publisher","DOI":"10.1007\/s40618\u2010016\u20100541\u20106"},{"key":"e_1_2_12_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/s40618\u2010017\u20100619\u20109"},{"key":"e_1_2_12_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/s40618\u2010019\u201001037\u20102"},{"key":"e_1_2_12_5_1","doi-asserted-by":"publisher","DOI":"10.1007\/s40618\u2010022\u201001816\u20104"},{"key":"e_1_2_12_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140\u20106736(04)16678\u20106"},{"key":"e_1_2_12_7_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469\u20101809.1988.tb01084.x"},{"issue":"3","key":"e_1_2_12_8_1","doi-asserted-by":"crossref","first-page":"167","DOI":"10.1002\/(SICI)1098-2280(1996)28:3<167::AID-EM2>3.0.CO;2-B","article-title":"Human Aneuploidy: Incidence, Origin, and 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