title: Feasible etiology of vanishing testis regarding disturbance of testicular development: histopathological and immunohistochemical evaluation of testicular nubbins.
abstract: OBJECTIVE
  To identify the causes of vanishing testis besides vascular events secondary to testicular torsion.
  
  
  METHODS
  A total of 102 boys with vanishing testis were treated in our hospital from 1984 to 2011. Of these cases, 91 testicular nubbins were excised. Immunohistochemical analysis of testicular nubbins was carried out using anti-Wilms tumor 1 antibody, which is a stable marker of Sertoli cells. Reverse transcription polymerase chain reaction was also carried out using Wilms tumor 1-specific primers.
  
  
  RESULTS
  Most testicular nubbins were associated with inguinal lesion (51 patients, 56.0%). Light microscopy showed that 11 patients (12.5%) had seminiferous tubules (with germ cells in three patients [3.4%]), and 77 patients lacked seminiferous tubules, some of which had calcification (26 patients, 29.5%), and/or deposition of hemosiderin (21 patients, 23.9%). Immunohistochemical analysis showed Wilms tumor 1 expression not only in the Sertoli cells of the seminiferous tubules in the seminiferous tubule-positive patients, but also in the interstitium of testicular nubbins in the seminiferous tubule-negative patients. Reverse transcription polymerase chain reaction showed Wilms tumor 1 messenger ribonucleic acid expression in the testicular nubbins of both seminiferous tubule-positive and tubule-negative patients.
  
  
  CONCLUSIONS
  The presence of Wilms tumor 1-positive cells in the interstitium of vanishing testis lacking seminiferous tubules suggests that the disturbance of testicular development after Sertoli cell differentiation and during testicular tubule formation might be involved in the etiology of vanishing testis.
authors.affiliation: Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, Japan. kmizuno@med.nagoya-cu.ac.jp
authors.forename: Kentaro
authors.initials: K
authors.lastname: Mizuno
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Kojima
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Kamisawa
authors.forename: Satoshi
authors.initials: S
authors.lastname: Kurokawa
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Moritoki
authors.forename: Hidenori
authors.initials: H
authors.lastname: Nishio
authors.forename: Yutaro
authors.initials: Y
authors.lastname: Hayashi
authors.forename: Kenjiro
authors.initials: K
authors.lastname: Kohri
mesh_terms: D000293:Adolescent; D018797:Cell Cycle Proteins; D002648:Child; D003456:Cryptorchidism; D006061:Gonadal Dysgenesis, 46,XY / Q000209:etiology*; D006801:Humans; D007150:Immunohistochemistry; D007564:Japan; D008297:Male; D009687:Nuclear Proteins / Q000378:metabolism*; D000072260:RNA Splicing Factors; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012671:Seminiferous Tubules / Q000473:pathology*; D012708:Sertoli Cells; D013733:Testicular Diseases / Q000473:pathology*; D013737:Testis / Q000002:abnormalities / Q000098:blood supply / Q000166:cytology / Q000473:pathology*
chemical_list: D018797:Cell Cycle Proteins; D009687:Nuclear Proteins; D000072260:RNA Splicing Factors; C419554:WTAP protein, human