Local Androgenic Effect of Interstitial Cell Tumor of the Testis

Gittes, Ruben F.; Smith, Graham W.; Conn, Coulson A.; Smith, Fred. J.

doi:10.1016/s0022-5347(17)61835-4

Cited by 32 publications

(10 citation statements)

References 6 publications

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“…The oestradiol response to hCG is apparent later. On the other hand, the very rare Leydig cell tumours observed in prepubertal boys are characterized by an exclusive secretion of T (Weill et ul., 1978;Gittes et al, 1970). The role of endogenous LH in aromatizing activity should be evaluated by in-vitro studies using tumoral Leydig cells in culture with serum of both untreated and GnRH agonist treated patients.…”

Section: Clinical Endocrinology (1992) 37mentioning

confidence: 99%

Oestrogen secreting Leydig cell tumour and GnRH agonist in‐vivo and in‐vitro studies

Kerlan

Nahoul

Abalain

et al. 1992

Clinical Endocrinology

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The kinetics of E2 response to hCG administration would suggest a modification of the regulation of the aromatase activity in this type of oestrogen secreting tumour. A certain endogenous LH level may be necessary to supply a sufficient quantity of T substrate, and to maintain aromatase activity of such Leydig cell tumours secreting oestrogens. These tumours seem to be responsive to endogenous LH levels.

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Section: Clinical Endocrinology (1992) 37mentioning

confidence: 99%

Oestrogen secreting Leydig cell tumour and GnRH agonist in‐vivo and in‐vitro studies

Kerlan

Nahoul

Abalain

et al. 1992

Clinical Endocrinology

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“…Key words: Testis, Leydig cell tumor, Histoculture, Testosterone, Immunohistochemistry (Endocrine Journal 43: 73-78, 1996) LEYDIG cell tumors of the testis are rare but the majority are associated with various steroid biosynthetic abnormalities including testosterone and estrogen overproduction [1][2][3][4][5]. Clinical hormonal analysis of testicular Leydig cell tumor has been extensively performed [1][2][3][4][5], but no detailed analysis of steroidogenesis of a Leydig cell tumor itself including in vitro studies has been reported.…”

Section: Introductionmentioning

confidence: 99%

“…Clinical hormonal analysis of testicular Leydig cell tumor has been extensively performed [1][2][3][4][5], but no detailed analysis of steroidogenesis of a Leydig cell tumor itself including in vitro studies has been reported. We had the opportunity to examine an 11-yearold boy with a Leydig cell tumor of the testis with increased plasma androstenedione and testosterone concentrations and pseudoprecocious puberty.…”

Section: Introductionmentioning

confidence: 99%

Leydig Cell Tumor of the Testis: Analysis of Testosterone Production and Secretion by Three-Dimensional Histoculture.

et al. 1996

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Abstract.We treated an 11-year-old boy with a testicular Leydig cell tumor. We analyzed the testosterone production of this tumor by immunolocalization of steroidogenic enzymes and in vitro three-dimensional histoculture. Spermatic venous blood from the tumor bearing testis had noticeably high concentrations of testosterone and androstenedione. The tumor had the characteristic ultrastructural features of steroid producing cells and was immunoreactive for P450scc (side chain cleavage), 3I3HSD (hydroxysteroid dehydrogenase) and P450c17 (17a-hydroxylase).Three-dimensional collagengel-supported histoculture demonstrated that the tumor tissue in the culture maintained its histologic architecture, expression of steroidogenic enzymes, and secretion of testosterone into the medium for up to 7 days in culture. Histoculture preserved in vitro testosterone production in this case of testicular Leydig cell tumor.Key words: Testis, Leydig cell tumor, Histoculture, Testosterone, Immunohistochemistry (Endocrine Journal 43: 73-78, 1996) LEYDIG cell tumors of the testis are rare but the majority are associated with various steroid biosynthetic abnormalities including testosterone and estrogen overproduction [1][2][3][4][5]. Clinical hormonal analysis of testicular Leydig cell tumor has been extensively performed [1][2][3][4][5], but no detailed analysis of steroidogenesis of a Leydig cell tumor itself including in vitro studies has been reported. We had the opportunity to examine an 11-yearold boy with a Leydig cell tumor of the testis with increased plasma androstenedione and testosterone concentrations and pseudoprecocious puberty. Pathological analysis of the resected specimens including electron microscopy and immuno- The patient was an 11-year-old Japanese boy. His parents noticed linear and skeletal growth acceleration and virilization at the age of 9 years, but he did not receive medical attention at that time. He presented to the pediatrician with complaints of testicular enlargement and premature puberty at the age of 11 years and was referred to Tohoku University Hospital, Sendai, Japan for evaluation of a testicular mass.His height was 160.05 cm and his weight was 58.0 kg on admission, both greater than the 95

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“…As sexual precocity can be differentiated into two major subgroups (gonadotropin-dependent precocious puberty and gonadotropin-independent pseudo-precocious puberty, the latter resulting from autonomous sex steroid production or exposure to exogenous sex steroid) hormonal assessment for the different possibilities is important [12,13,14]. For correct comparison of hormonal profiles in infants and children it is important to define laboratory specific normal values, which are adjusted for age, sex and pubertal stage.…”

Section: Methodsmentioning

confidence: 99%

Leydig-Cell Tumour in Children: Variable Clinical Presentation, Diagnostic Features, Follow-Up and Genetic Analysis of Four Cases

Petkovic

Salemi²,

Vassella³

et al. 2006

Horm Res Paediatr

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Background: Testicular tumours are relatively uncommon in infants and children, accounting for only 1–2 % of all paediatric solid tumours. Of these approximately 1.5% are Leydig-cell tumours. Further, activating mutations of the luteinizing hormone receptor gene (LHR), as well as of the G protein genes, such as G_salpha (gsp) and G_ialpha (gip2) subunits, and cyclin-dependent kinase gene 4(CDK4) have been associated with the development of several endocrine neoplasms. Aims/Methods: In this report, the clinical variability of Leydig-cell tumours in four children is described. The LHR-, gsp-, gip2- and CDK4 genes were investigated to establish the possible molecular pathogenesis of the variable phenotype of the Leydig-cell tumours. Results: No activating mutations in these genes were found in the four Leydig-cell tumours studied. Therefore, the absence of activating mutations in LHR, as well as in both the ‘hot spot’ regions for activating mutations within the G-alpha subunits and in the regulatory ‘hot spot’ on the CDK4 genes in these tumours indicates molecular heterogeneity among Leydig-cell tumours. Conclusion: Four children with a variable phenotype caused by Leydig-cell tumours are described. A molecular analysis of all the ‘activating’ genes and mutational regions known so far was performed, but no abnormalities were found. The lessons learnt from these clinically variable cases are: perform ultrasound early and most importantly, consider discrepancies between testicular swelling, tumour size and androgen production.

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Local Androgenic Effect of Interstitial Cell Tumor of the Testis

Cited by 32 publications

References 6 publications

Oestrogen secreting Leydig cell tumour and GnRH agonist in‐vivo and in‐vitro studies

Oestrogen secreting Leydig cell tumour and GnRH agonist in‐vivo and in‐vitro studies

Leydig Cell Tumor of the Testis: Analysis of Testosterone Production and Secretion by Three-Dimensional Histoculture.

Leydig-Cell Tumour in Children: Variable Clinical Presentation, Diagnostic Features, Follow-Up and Genetic Analysis of Four Cases

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