title: Less advanced testicular dysgenesis is associated by a higher prevalence of germ cell neoplasia.
abstract: There is a theory that the more evident clinical signs of testicular dysgenesis, the more frequent the neoplastic lesions are. The aim of this study was to relate the incidence of testicular germ cell neoplastic lesions (overt germ cell tumours--GCT or testicular carcinoma in situ) to the intensity of testicular organogenesis disturbances (dysgenesis). Biopsies were taken from 154 testes of the following patients: 23 patients with GCT in the contralateral gonad (CGCT), 41 patients with undescended testes operated in childhood (UDT), 90 with azoo-/oligozoospermia (A/O) diagnosed because of infertility. Assessment of seminiferous epithelium, number of Leydig cells, areal fraction of intertubular space (IS), morphometric analysis of seminiferous tubules diameter and thickness of tubular wall were performed. Monoclonal antibodies against placental like alkaline phosphatase and cytokeratin 18 were applied. Germ cell neoplastic lesions were detected in 7.1% of testes and were associated with disturbed spermatogenesis. Among testes with disturbed spermatogenesis they were found the most frequently in CGCT (22.2% vs. 11.1% in UDT and 3.8% in A/O), where spermatogenesis had the highest score (5.7 +/- 3.8 points vs. 4.2 +/- 2.7 in UDT and 4.6 +/- 2.9 in A/O). In CGCT, signs of testicular dysgenesis were less advanced: the highest tubular diameter was 164.4 +/- 32.3 microm vs. 163.5 +/- 28.6 in UDT and 161.4 +/- 31.5 in A/O, the lowest thickness of tubular wall was 8.9 +/- 3.2 microm vs. 10.2 +/- 3.6 in UDT and 10.2 +/- 3.2 in A/O, lowest IS was 36.9 +/- 14.9% vs. 47.9 +/- 18.0 in UDT and 46.5 +/- 18.5 in A/O, and the lowest percentage of tubules with immature Sertoli cells was 0.1 +/- 0.4% vs. 4.9 +/- 7.0 in UDT and 5.2 +/- 9.7 in A/O. Results indicate that neoplastic lesions appear only in testes with disturbed spermatogenesis. Worse condition of spermatogenesis is associated by the presence of other dysgenetic features, but neoplastic lesions appear more frequently in testes with the less advanced features of testicular dysgenesis.
authors.affiliation: Division of Reproductive Endocrinology, Department of Andrology and Reproductive Endocrinology, Medical University of Lodz, Lodz, Poland.
authors.forename: A
authors.initials: A
authors.lastname: Guminska
authors.forename: E
authors.initials: E
authors.lastname: Oszukowska
authors.forename: W
authors.initials: W
authors.lastname: Kuzanski
authors.forename: M
authors.initials: M
authors.lastname: Sosnowski
authors.forename: J K
authors.initials: JK
authors.lastname: Wolski
authors.forename: R
authors.initials: R
authors.lastname: Walczak-Jedrzejowska
authors.forename: K
authors.initials: K
authors.lastname: Marchlewska
authors.forename: J
authors.initials: J
authors.lastname: Niedzielski
authors.forename: K
authors.initials: K
authors.lastname: Kula
authors.forename: J
authors.initials: J
authors.lastname: Slowikowska-Hilczer
mesh_terms: D000293:Adolescent; D000328:Adult; D001706:Biopsy; D003456:Cryptorchidism / Q000473:pathology / Q000601:surgery; D005854:Germ Cells / Q000473:pathology; D006059:Gonadal Dysgenesis / Q000473:pathology*; D006801:Humans; D007985:Leydig Cells / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009369:Neoplasms / Q000473:pathology; D009373:Neoplasms, Germ Cell and Embryonal / Q000473:pathology*; D009845:Oligospermia / Q000473:pathology; D012671:Seminiferous Tubules / Q000473:pathology; D012708:Sertoli Cells / Q000473:pathology; D013091:Spermatogenesis / Q000502:physiology; D013733:Testicular Diseases / Q000473:pathology; D013736:Testicular Neoplasms / Q000473:pathology*; D013737:Testis / Q000473:pathology*; D055815:Young Adult