title: [Testicular dysgenesis syndrome: an update].
abstract: Researches on the testicular dysgenesis syndrome (TDS) have flourished in the recent decade, and a widely accepted view on its pathogenesis is that environmental endocrine disrupting chemicals (EDCs) act on Leydig cells and/or testicular Sertoli cells, resulting in abnormal development of the testis and leading to the symptoms of TDS. Molecular biological studies suggest a correlation of TDS etiology with insulin-like factor 3 (INSL-3), androgen receptor (AR), P27kip, WT-1 and Müllerian inhibiting substance (MIS). This review focuses on the progress in current researches on the etiology and mechanism of TDS.
authors.affiliation: Department of Urology, Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310003, China. alfh19@yahoo.com.cn
authors.forename: Zhe-Ming
authors.initials: ZM
authors.lastname: Xu
authors.forename: Da-Xing
authors.initials: DX
authors.lastname: Tang
mesh_terms: D003456:Cryptorchidism; D006059:Gonadal Dysgenesis / Q000209:etiology / Q000235:genetics; D006801:Humans; D008297:Male; D013733:Testicular Diseases / Q000209:etiology / Q000235:genetics; D013736:Testicular Neoplasms