Encyclopedia of Pathology

Living Edition
| Editors: J.H.J.M. van Krieken

Spermatocytic Tumor

  • Maurizio ColecchiaEmail author
  • Alessia Bertolotti
Living reference work entry
DOI: https://doi.org/10.1007/978-3-319-28845-1_4950-1



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).

Clinical Features

  • Incidence

    Spermatocytic tumor accounts for about 1% of testicular germ cell tumors.

  • Age

    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.

  • Sex


  • Site

    Bilateral involvement occurs in 9% of cases. Never ST has been reported in extragonadal sites.

  • Treatment


  • Outcome

    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.


ST is composed of a polymorphous population of tumor cells: medium-sized cells (diameter 15–20 μm) with regular, round nucleus having finely granular to filamentous chromatin and variably prominent nucleoli; small cells (diameter 6–8 μm) with round dense nuclei and scant cytoplasm resembling lymphocytes; and scattered mono or multinucleated giant cells (diameter 50–150 μm) (Fig. 1). Mitotic figures and many apoptotic tumor cells are frequently observed. ST shows an expansive growth pattern, and the surrounding tubules are greatly extended and filled with neoplastic cells (Fig. 2). Tubular rupture in more than one area explains the occurrence of multiple tumor nodules; the stroma is scant lacking lymphocytic infiltrates or granulomatous inflammation. Large edematous areas similar to those of microcystic seminomas are also often observed (Fig. 3). GCNIS is absent. Finally in uncommon cases, the polymorphous population of tumor cells, described above, is absent and there is a more uniform proliferation of intermediate sized cells, with huge nucleoli, many mitotic figures, and this morphology has been defined “anaplastic” spermatocytic tumor (Lombardi et al. 2011). So far, 18 cases of ST combined with sarcoma have been described: eight of these sarcomas were rhabdomyosarcomas, and the others were defined as “undifferentiated spindle.” All of these tumors showed high grade, with necrosis and numerous mitotic figures.
Fig. 1

Spermatocytic tumor. These cells have eosinophilic cytoplasm and round nuclei. The nuclei of the larger cells have a filamentous or spireme pattern similar to that seen in spermatocytes

Fig. 2

Spermatocytic tumor, intratubular growth. Frequently observed adjacent to spermatocytic tumor the intratubular growth shows a more homogenous cellularity. The adjacent tubules show normal spermatogenesis

Fig. 3

Spermatocytic tumor. Large edematous areas similar to those of microcystic seminomas, that give a macroscopically soft, mushy texture to the tumor


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).

Molecular Features

Gains of chromosome 9 and the absence of the i(12q) isochromosomes are almost specific for ST, less often of chromosomes 1 and 20, with partial loss of chromosome 22 (Rosenberg et al. 1998). Gain of chromosome 9 corresponds to additional copies of the DMRT1 gene (Looijenga et al. 2006).

Differential Diagnosis

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.

Malignant Lymphoma

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

  1. 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
  2. Kao, C. S., Badve, S. S., & Ulbright, T. M. (2014). The utility of immunostaining for NUT, GAGE7 and NY-ESO-1 in the diagnosis of spermatocytic seminoma. Histopathology, 65(1), 35–44.CrossRefGoogle Scholar
  3. Lombardi, M., Valli, M., Brisigotti, M., & Rosai, J. (2011). Spermatocytic seminoma: review of the literature and description of a new case of the anaplastic variant. International Journal of Surgical Pathology, 19(1), 5–10.CrossRefGoogle Scholar
  4. 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
  5. Masson, P. (1946). Etude sur le seminoma. Review Cancer Biology, 5(4), 361–387.Google Scholar
  6. Mikuz, G., Böhm, G. W., Behrend, M., Schäfer, G., Colecchia, M., & Verdorfer, I. (2014). Therapy-resistant metastasizing anaplastic spermatocytic seminoma: A cytogenetic hybrid: a case report. Analytical and Quantitative Cytopathology and Histopathology, 36(3), 177–182.PubMedGoogle Scholar
  7. 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
  8. 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

Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  1. 1.Uropathology Unit, Department of PathologyFondazione IRCCS Istituto Nazionale dei Tumori di MilanoMilanItaly
  2. 2.Department of PathologyFondazione IRCCS Istituto Nazionale dei Tumori di MilanoMilanItaly