Symposium 23A: Tumours of the testis

The diagnostic challenge posed by testicular tumours relates to their wide spectrum of histological appearance and their relative uncommonness compared to neoplasms of other organs. Many pathologists therefore have relatively little exposure to them, and the more rare forms of testicular tumours may, understandably, prove especially challenging. There is, unfortunately, no guarantee that the next tumour viewed under the microscope will not be an unusual type of testicular tumour. It is therefore prudent for the practicing pathologist to become familiar with these less common forms of testicular neoplasia; otherwise, patients may be subjected to inappropriate and potentially harmful therapies. Spermatocytic seminoma represents only about 3% of ‘seminomas’ and 1–2% of testicular tumours. It tends to occur in men who are, on average, 15–20 years older than those with ‘usual’ seminoma, with a mean age of occurrence of 55 years. A testicular mass and ⁄ or pain is the mode of presentation in all cases. Grossly these tumours are often multinodular, with a whitefleshy to tan-myxoid to haemorrhagic cut surface. They may rarely extend outside of the testis into the paratesticular structures. On microscopic examination, the tumour cells are typically arranged in sheets that may be interrupted by oedema that can sometimes induce a cystic, pseudoglandular or trabecular appearance. The tumour cells usually have a ‘tripartite’ appearance that includes small, smudged cells resembling lymphocytes, intermediate-sized cells and giant cells that may be multinucleated. The intermediate and giant cells may have a filamentous or ‘spireme’ chromatin that resembles that of primary spermatocytes. The nuclei, in contrast to those of ‘usual’ seminoma, have a round, symmetrical appearance. Unlike the other forms of germ cell tumour in adult patients, the seminiferous tubules consistently lack intratubular germ cell neoplasia of the unclassified type (IGCNU; so-called ‘carcinoma-in situ’), although prominent intratubular growth of spermatocytic seminoma is common. In addition, in contrast to many of the other forms of germ cell tumour, spermatocytic seminoma lacks placental alkaline phosphatase and has scant or absent cytokeratin reactivity. Most importantly, spermatocytic seminoma virtually never metastasizes and is therefore adequately treated by orchiectomy alone. Recently, Albores-Saavedra et al. described an ‘anaplastic’ variant of spermatocytic seminoma. These tumours had areas where there was a uniform population of cells with prominent nucleoli (Figure 1), potentially mimicking embryonal carcinoma. Other foci, however, had the typical polymorphous cell population, so generous sampling can usually resolve this differential diagnosis. The absence of IGCNU and lack of CD30 reactivity and cytokeratin reactivity are also helpful in problematic cases. Despite characterization of these tumours by Albores-Saavedra and coworkers as ‘anaplastic’ there was no evidence in their series or subsequently that spermatocytic seminomas with this appearance had a different behaviour than the excellent outcome of ‘non-anaplastic’ spermatocytic seminoma. Rarely, spermatocytic seminoma may develop a sarcomatous component. These tumours typically occurred in patients with a long-standing testicular mass that underwent rapid enlargement. The tumours have distinct foci of spermatocytic seminoma and sarcoma that intermix in areas. The sarcoma sometimes shows embryonal rhabdomyosarcomatous differentiation, but in other cases is an undifferentiated spindle cell sarcoma. In contrast to uncomplicated spermatocytic seminoma, the patients with these tumours have developed metastases in a high proportion of the cases, with the metastases occurring in a haematogenous distribution and consisting solely of the sarcomatous component.