[Testicular tumors (germ cell tumors, Leydig cell tumors, Sertoli cell tumors)].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
An unusual case of a moderately well-differentiated, encapsulated, Sertoli Leydig cell tumor with heterologous elements recurring 3 years after a conservative unilateral oophorectomy in a 15-year-old female is reported. This is the first case report of a metastatic Sertoli Leydig cell tumor with mucinous heterologous elements. A relative lack of uniformly accepted histological criteria of these tumors makes prognosis difficult to access. The optimal therapy for recurrent Sertoli Leydig cell tumor is unknown. Initial plans of management of this rare neoplasm, follow-up, and current concepts of treatment of recurrences will be discussed.
Large cell calcifying Sertoli cell tumor of the testis is an extremely rare type of sex cord tumor with low malignant potential that occurs in the first and second ecades of life. Twenty-eight cases have been reported in the literature and, to our knowledge, only 2 had an aggressive behaviour. Patient age, tumor size, histological malignant patterns such as pleomorphism and high mitotic rate seem to heavy influence the future neoplasm malignancy. Ultrasonography imaging of the large cell calcifying has described in only 6 cases. We report an experience with a large cell calcifying Seroli cell tumor of the testis and point out the unusual sonographic findings. Moreover, if histologic examination suggests no malignant features, we suggest local excision as ideal therapy for the preservation of testicular parenchyma.
The spectrum of Sertoli cell tumors in children covers a wide range of testis and ovarian tumors classified as sex cord-stromal tumors. Sertoli cell tumor of the testis is extremely rare in the pediatric population. The American Academy of Pediatrics Section on Urology Prepubertal Testicular Tumor Registry has reported a total of six cases of Sertoli cell tumor of the testis, accounting for 1.3% of the 430 cases reported to the registry as of October 1996. Despite their rarity, Sertoli cell variants of sex cord-stromal tumors have generated keen interest because of their variable histologic appearance and biologic behavior, including endocrine activity. Because sex cord-stromal tumors occur in the ovary and testis, a primitive cellular origin to these tumors is likely in males and females.
A pure Sertoli cell tumor of the testis in a 26-year-old man is reported, with cytologic, histologic and ultrastructural findings. The preoperative cytological diagnosis allowed a conservative surgical approach.
Sertoli cell tumors are rare low-grade malignancies occurring in the testis and the ovary. No chromosome studies of this tumor type have yet been reported. We observed an extra i(1q) as the sole chromosome anomaly in an ovarian Sertoli cell tumor.
OBJECTIVES: A rare case of Sertoli cell tumor of the testis is described. The problems associated with this tumor type and the importance of the differential diagnosis are discussed. METHODS/RESULTS: The clinical features of a patient with Sertoli cell tumor in a cryptorchid testis are presented. CONCLUSIONS: It is recognized that there is a higher incidence of tumors in undescended testis and among these are Sertoli cell tumors.
Sertoli cell tumors (TCS) derivated from sex-cord estroma cells, are an uncommon variety of testicles neoplasms. A 66 year-old patient that came to the consultation for an increased scrotum of size present. Ultrasound viewed a hipoecoic nodule capable with testicular tumor, more secondary hidrocele. After undergoing the standard treatment, by means of groin radical orchiectomy, its pathologic analysis identified the lesion as Sertoli cell tumor conventional. The pathologic features that best correlate with a clinically benign course are as follows: a lower size tumor to 5 cm, mild nuclear atypia, a mitotic rate of less than 5 mitosis per 10 high power fields, and absent necrosis. Our case presented with these features. Follow-up of these neoplasms should be prolonged by the unusual of its presentation and a small percentage of cases are clinically malignant.
A case of infantile Sertoli cell tumor of the testis is presented. A 2-year-old child visited our hospital with the complaint of painless swelling of the left scrotal content. A solid tumor was demonstrated in the left testis by scrotal echography. Physical and laboratory examinations were within normal limits and alpha-fetoprotein and beta-HCG were not elevated. The left testis was removed. The tumor sized 3.0 x 3.0 x 2.2 cm and weighted 14.5 g. Pathohistological diagnosis was benign Sertoli cell tumor. Tumor cells were vimentin positive and TM-1 reactive antigen positive and revealed electronmicroscopically some features of Sertoli cells such as intermediated microfilament, rich lysosomes and interdigitation between adjacent cells. The patient was well with no evidence of diseases one and a half years after the operation.
This report describes the ultrastructural and hormonal characteristics of the recently described large-cell calcifying Sertoli cell tumor of the testis, a rare subtype of pure Sertoli cell tumor. The ultrastructural findings showed similarity to normal Sertoli cells, pure Sertoli cell tumors, Sertoli cells in azoospermic human testes, and the Sertoli cell component of Sertoli-Leydig cell tumors. Ultrastructure indicated features common to steroid-producing cells. Testosterone and estradiol were demonstrated in the tumor by immunocytochemical and biochemical methods.
This study concerns the immunohistochemical localization of S-100 alpha, S-100 beta, and whole brain S-100 (wbS-100) in testicular large-cell calcifying Sertoli cell tumor (LCCSCT). We examined 8 LCCSCTs (7 benign and 1 malignant), 6 Sertoli cell tumors not otherwise specified (SCTs-NOS), 6 Leydig cell tumors (LCTs), 5 ovarian Sertoli-Leydig cell tumors (SLCTs), and 7 gonadoblastomas (GBLs). The 8 LCCSCTs showed immunoreactivity for S-100 alpha, S-100 beta, and wbS-100. Five of the 6 LCTs and the Leydig cell components in the ovarian SLCTs stained positively for S-100 alpha and wbS-100 but were negative for S-100 beta. SCTs-NOS and the Sertoli cell components in the SLCTs occasionally showed focal and weak/moderate positivity for S-100 alpha, S-100 beta, and wbS-100. Sex cord cells of the GBLs were positive for S-100 beta and wbS-100 and negative for S-100 alpha. Germ cell elements of the GBLs were negative for S-100 alpha, S-100 beta, and wbS-100. In nonneoplastic testicular parenchyma adjacent to the above-mentioned tumors, there was S-100 alpha reactivity in Leydig cells, rete testis, and a few Sertoli cells. S-100 beta reactivity was seen in a few Sertoli cells, Schwann cells, and some endothelial cells. WbS-100 reactivity was present in Leydig cells, a few Sertoli cells, rete testis, Schwann cells, and some endothelial cells. The results indicate that S-100 alpha and S-100 beta can potentially be used as immunohistochemical markers for LCCSCT, especially when differentiating it from LCT, which may mimic LCCSCT on routine histopathology. Although the biological significance of both S-100 subunits expression in LCCSCT remains unknown, these notable calcium-binding proteins may be associated with the characteristic calcification in LCCSCT through regulation of calcium levels in the tumor cells.
The distinction of ovarian Sertoli cell tumor from other tumors in the histological differential diagnosis, particularly endometrioid carcinoma and carcinoid tumor, may be difficult. Many immunohistochemical markers have been studied for this differential diagnosis, but currently available markers are neither 100% sensitive nor specific. Sox9 is a transcription factor involved in Sertoli cell differentiation in the testis. The role that this molecule plays in the pathogenesis of ovarian Sertoli cell tumors and the potential use as an immunohistochemical marker for differential diagnosis have not been investigated. Immunohistochemical staining for Sox9 was performed in 152 ovarian tumors: pure Sertoli cell tumor (n = 36), endometrioid borderline tumor (n = 38), well-differentiated endometrioid carcinoma (n = 26), sertoliform endometrioid carcinoma (n = 13), and carcinoid tumor (n = 39). Nuclear expression was considered positive. Extent and intensity of staining were semiquantitatively scored. In addition, immunohistochemical composite scores in positive cases (ranging from 1 to 12) were calculated based on the extent score multiplied by the intensity score. Sox9 was expressed in 44% of Sertoli cell tumors, 55% of endometrioid borderline tumors, 65% of well-differentiated endometrioid carcinomas, 39% of sertoliform endometrioid carcinomas, and 10% of carcinoid tumors. The mean Sox9 immunohistochemical composite scores in positive cases were 6.3 for Sertoli cell tumor, 5.3 for endometrioid borderline tumor, 8.0 for well-differentiated endometrioid carcinoma, 2.8 for sertoliform endometrioid carcinoma, and 6.8 for carcinoid tumor. The differences in the mean Sox9 composite scores between Sertoli cell tumor and the other tumor categories were not statistically significant (p values ranged from 0.092 to 0.523). We conclude that Sox9 is variably expressed in ovarian Sertoli cell tumor and other tumors that are in the differential diagnosis and, thus, is not helpful for immunohistochemical distinction. Understanding the role of Sox9 in the pathogenesis of ovarian Sertoli cell tumor requires further study.
We report on six boys with intratubular Sertoli cell proliferations (ISCPs), studied by routine histologic methods, electron microscopy, and immunohistochemistry of anti-müllerian hormone (AMH), inhibin alpha-subunit, 3beta-hydroxysteroid dehydrogenase (3beta-HSD), proliferative cellular nuclear antigen, and p53, and carefully followed for extended periods with periodic clinical examinations, testicular ultrasonographies, and determinations of serum levels of AMH and inhibin B. Peutz-Jeghers syndrome was found in four of six patients, and gynecomastia occurred in five of six patients. One boy had isosexual pseudoprecocity. ISCPs were observed as multiple foci of seminiferous tubules with large and proliferated Sertoli cells replacing germ cells and limited by the basement membrane. Mitotic figures, atypia, and/or interstitial invasion were not observed. Bilateral ISCPs were the only pathologic finding in three patients (patient nos. 1-3) and were associated with a microscopic tumor that resembled a large-cell calcifying Sertoli cell tumor (LCCSCT) in a fourth patient (patient no. 4). In the two remaining patients (patient nos. 5 and 6) ISCPs and LCCSCT were found in both testes. Ultrastructural examination showed large Sertoli cells, with round nuclei, sparse organelles, and some glycogen. Inhibin alpha-subunit immunolocalization was positive in the five patients in whom it was determined (patient nos. 2-6), AMH was positive in those ISCPs associated with tumors (patient nos. 4-6) and negative in isolated ISCPs (patient nos. 2 and 3); 3beta-HSD and PCNA were variable, and p53 was negative in all ISCPs. Patient nos. 1-4 have been followed for 2-19 years. One of them is currently entering puberty, the other two have already completed puberty and have testes of normal size, and the remaining one is an adult with clinically normal testes and sperm production. None of these patients had evidence of tumor development during follow-up as shown by serial ultrasonographies and serum levels of AMH and inhibin B. Patient nos. 5 and 6 who had bilateral ISCPs and LCCSCT were orchidectomized and evolved for 2-10 years after surgery without tumor recurrence. The prognostic significance of ISCPs, particularly when they are the only pathologic finding in a testicular biopsy, is a matter of controversy. Based on the long normal evolution, we recommend a conservative approach to therapy. The bilateral and multicentric character of ISCPs and their association with Sertoli tumors and Peutz-Jeghers syndrome suggest that they represent either proliferative lesions with tumorigenic potential or the intraepithelial stage in the evolution of some testicular Sertoli cell tumors.
OBJECTIVE: Immunohistochemical staining is reported to be useful in distinguishing ovarian Sertoli-stromal cell tumors from carcinosarcomas. To assess Sertoli cell differentiation in a rare malignant biphasic testicular tumor, we compared the immunophenotypic profile of the tumor with that of Sertoli cell nodules and adenomas and mullerian carcinosarcomas. DESIGN: Immunohistochemical staining was performed on 6 testes (4 with hyperplastic Sertoli cell nodules, 2 with Sertoli cell adenomas) and 7 carcinosarcomas (6 involving the uterus, 1 involving the uterus and ovary) using primary monoclonal antibodies AE1/AE3, CAM 5.2, CA 19.9, and antibodies directed against epithelial membrane antigen, carcinoembryonic antigen (monoclonal and polyclonal), S100, placental alkaline phosphatase, and inhibin. These staining results were compared with those of the index case. RESULTS: All testes showed positive staining for inhibin and vimentin in the Sertoli cells of the nodules and adenomas. One Sertoli cell nodule showed focal staining with AE1/AE3 and CAM 5.2. Both adenomas showed focal positive staining for S100. All nodules and adenomas were negative for epithelial membrane antigen, monoclonal and polyclonal carcinoembryonic antigen, CA 19.9, and placental alkaline phosphatase. In contrast, the carcinomatous areas of the carcinosarcomas were all negative for inhibin but exhibited positive staining for AE1/AE3, CAM 5.2, and epithelial membrane antigen. The carcinosarcomas showed variable expression of vimentin, S100, carcinoembryonic antigen, CA 19.9, and placental alkaline phosphatase. The epithelial component of the tumor from the index case showed strong diffuse staining for inhibin and vimentin and only very faint focal staining with AE1/AE3 and CAM 5.2. The epithelial component was negative for epithelial membrane antigen, monoclonal and polyclonal carcinoembryonic antigen, S100, CA 19.9, and placental alkaline phosphatase. CONCLUSIONS: The immunohistochemical findings in the index case support the diagnosis of Sertoli cell tumor with a heterologous sarcomatous component over carcinosarcoma. Inhibin seems to be the best single marker for Sertoli cell differentiation. To our knowledge, only 1 other case of this rare testicular tumor has been reported in the literature.
Thirty-three cases of Sertoli cell tumor, occurring in dogs of different breeds and ages, were studied histologically. Ectopic testes showed a particularly high tendency to develop the tumor. Metastases were not detected in regularly autopsied dogs nor reported or later ascertained for the bioptic consignments. According to Nielsen and Lein's classification (1974) our findings were divided as follows: 27 intratubular Sertoli cell tumors, 19 with stromal invasion and 8 without invasion; 2 diffuse tumors; 4 multiple primary tumors (3 Sertoli-seminoma cell tumor and 1 Sertoli-Leydig cell tumor). The above classification is discussed and proposed tentatively for revision.
Explore the source record for details and available documents.
We report a case of Sertoli cell tumor. A 33-year-old man visited our clinic with a complaint of painless left scrotal swelling on September 29th, 2003. An elastic firm induration larger than a hen's egg in size was palpable on the surface of the left testis. Tumor markers for testicular tumor such as human chorionic gonadotropin-beta, alpha fetoprotein, and lactate dehydrogenase were not elevated. However, ultrasound showed a low echoic mass in the left testis. Therefore, we performed left high orchiectomy under the diagnosis of left testicular tumor. Its histology showed Sertoli cell tumor. Neither recurrence nor metastasis has been detected for about 8 months after the operation.