A tumor composed of cells with filamentous nuclear chromatin resembling spermatocytes: initially named spermatocytic seminoma (Masson 1946). In the 2016 WHO classification, the name has been changed to spermatocytic tumor (ST), being derived from postpubertal type germ cells, most commonly spermatogonia or early primary spermatocytes (Moch et al. 2016). Nowadays, both the synonyms are used (Hu et al. 2019).
Spermatocytic tumor accounts for about 1% of testicular germ cell tumors.
The more frequently reported age of incidence is the sixth decade of life (age range 19–92 years), a significantly more advanced age than that of all the other germ cell tumors.
Bilateral involvement occurs in 9% of cases. Never ST has been reported in extragonadal sites.
ST is only rarely reported with metastases, unless there is tumor dedifferentiation to form a sarcoma. The cases of metastatic spermatocytic tumor spread to the retroperitoneum, with one case involving the lungs (Mikuz et al. 2014). All patients with ST combined with sarcoma died of sarcoma metastases.
The tumors are usually 3–5 cm in diameter, but sizes up to 15 cm have been reported. Because of the gelatinous and mucinous cut surface and the presence of small mucoid cysts, the macroscopic appearance is typical. The consistency is soft with typical multinodular pattern, while growth into the epididymis and foci of necrosis may be seen. Sarcomatous foci may be fleshy or firm with necrotic areas.
STs are negative for the classical markers of GCTs: PLAP, OCT 3/4, α-feto-protein, β-HCG, and CD30. STs stain positively for protein expressed in spermatogonia (i.e., SALL4, CD 117, MAGE A 4, and DMRT1), and the cytoplasm of single cells shows a dot-like reaction for pancytokeratin. The novel markers NUT, GAGE7, and NY-ESO-1 are variably sensitive to ST, and high specificity is attained when there is multifocal and strong nuclear staining (Kao et al. 2014).
Seminoma (Solid Pattern)
Seminoma shows a monotous cell population with fibrovascular septa, and lymphoplasmacytic and/or granulomatous inflammation. The immunoreactivity for OCT 3/4, PLAP, and podoplanin are distinctive for seminoma, negative in ST.
The polymorphous and harmful-looking tumor cells and the lack of stroma make the tumor similar to malignant lymphoma, but typical interstitial growth pattern with more uniform cell population address to malignant lymphoma as well as the immunohistochemical test with CD45, CD20, or CD3.
References and Further Reading
- Hu, R., Ulbright, T. M., & Young, R. H. (2019). Spermatocytic Seminoma: A Report of 85 Cases Emphasizing Its Morphologic Spectrum Including Some Aspects Not Widely Known. The American Journal of Surgical Pathology, 43(1), 1–11.Google Scholar
- Looijenga, L. H., Hersmus, R., Gillis, A. J., Pfundt, R., Stoop, H. J., van Gurp, R. J., Veltman, J., Beverloo, H. B., van Drunen, E., van Kessel, A. G., Pera, R. R., Schneider, D. T., Summersgill, B., Shipley, J., McIntyre, A., van der Spek, P., Schoenmakers, E., & Oosterhuis, J. W. (2006). Genomic and expression profiling of human spermatocytic seminomas: primary spermatocyte as tumorigenic precursor and DMRT1 as candidate chromosome 9 gene. Cancer Research, 66(1), 290–302.CrossRefGoogle Scholar
- Masson, P. (1946). Etude sur le seminoma. Review Cancer Biology, 5(4), 361–387.Google Scholar
- Moch, H., Humphrey, P. A., Ulbright, T. M., & Reuter, V. E. (2016). WHO classification of tumours of the urinary system and male genital organs (4th ed.). Lyon.Google Scholar
- Rosenberg, C., Mostert, M. C., Schut, T. B., van de Pol, M., van Echten, J., de Jong, B., Raap, A. K., Tanke, H., Oosterhuis, J. W., & Looijenga, L. H. (1998). Chromosomal constitution of human spermatocytic seminomas: Comparative genomic hybridization supported by conventional and interphase cytogenetics. Genes, Chromosomes & Cancer, 23(4), 286–291.CrossRefGoogle Scholar