Skip to content
Home » Oncology » Oncology – Testis » Testis cancer pathology / subtypes

Testis cancer pathology / subtypes

Seminoma vs NSGCT:

  • Seminoma tends to stay organ confined for longer – NSGCT more likely to present advanced
  • Seminoma tends to spread to nodes only more often than NSGCT which is more likely than seminoma to have haematogenous spread
  • Overall NSGCT more aggressive

 

Extra-gonadal germ cell tumours:

  • Approx 5 %, mostly in midline locations retroperitoneum and mediastinum
  • ? error in migration of germ cells during development
  • Primary mediastinal NSGCTs are less sensitive to chemo – 5 year survival around 45 %
  • Primary mediastinal seminoma similar prognosis to testicular seminoma
  • Primary retroperitoneal GCTs are biologically indistinct from testicular GCTs with same prognosis

 

Classic seminoma

  • Most common type
  • Most common 30s and 40s
  • Clear cytoplasm (“fried egg”)
  • About 15 % have syncitiotrophoblasts which produce b-HCG (therefore 15 % seminomas will have raised b-HCG)
  • Arises from GCNIS and may be a precursor to other NSGCT subtypes
  • Anaplastic seminoma was a previously described subtype but had no clinical relevance so is no longer described
  • Exquisitely radiosensitive
  • Tends to be more homogenous and hypoechoic on ultrasound, cf. NSGCT more heterogenous

 

Spermatocytic tumour (formerly spermatocytic seminoma)

  • Rare, tending to be in older men
  • Metastasis is very rare – tends to be cured with orchidectomy alone
  • Does not arise from GCNIS

Embryonal carcinoma

  • Aggressive with high rates metastasis
  • Occasional syncitiotrophoblasts and b-HCG production
  • Most undifferentiated cell type of NSGCT – and can differentiate to other types including teratoma, within the primary or mets
  • Can be smaller tumours but often more invasive

 

Choriocarcinoma

  • Rare, aggressive, and haematogenous metastasis is common
  • Typically produce very high levels of b-HCG (which can rarely cause other endocrinological disturbances)
  • Widespread metastasis to lungs and other unusual sites not uncommon

 

Yolk sac tumours

  • Pure yolk sac tumours are rare in adults, usually being mixed with other NSGCT
  • More common in pre-pubertal kids and mediastinal GCT
  • Roughly half have characteristic Schiller-Duval bodies
  • Almost always produce AFP, only rarely produce b-HCG

 

Teratomas

  • Contain cells from at least 2 of endoderm, mesoderm or ectoderm, in varying states of differentiation
  • Roughly translates to “monster tumour” in Greek
  • Pure teratomas are uncommon, but reasonably common in mixed NSGCT
  • Generally normal tumour markers (rarely produce AFP)
  • Teratoma is resistant to chemotherapy – therefore often residual masses post chemo may have teratoma
  • Teratomas can grow aggressively and become large, and can transform to somatic malignancies like rhabdomyosarcoma or adenocarcinoma (teratoma with malignant transformation) – usually at metastatic sites

 

 

Sex cord stromal tumours:

  • 90 % benign ; 10 % malignant
  • Histological criteria to help distinguish malignancy
    • Tumour > 5 cm
    • Necrosis
    • Vascular invasion
    • Nuclear atypia
    • High mitotic index
    • Increased MIB-1 expression
    • Infiltrative margins
    • DNA ploidy
  • Most malignant cases have at least 2 of these features – but the presence of metastatic disease is the only reliable criteria to distinguish

 

Leydig cell tumours

  • Most common sex cord stromal tumour
  • May present with symptoms due to excess androgens being converted peripherally to oestrogen – gynaecomastia, impotence, decreased libido
  • May contain histologic Reinke’s crystals
  • Chemoresistant and radioresistant – therefore need RPLND if metastatic

 

Sertoli cell tumours

  • Rare < 1 %
  • Assoc with Peutz-Jeghers syndrome
  • Frequently bilateral
  • Often associated with gynaecomastia
  • Diagnostic work up and treatment/surveillance similar to Leydig cell tumours

 

Gonadoblastoma

  • Usually in cases of DSD / phenotypically females
  • Can progress to malignant GCT
  • Bilateral orchidectomy generally recommended (up to 40 % bilateral involvement)

 

 

Follow up for sex-cord stromal tumours:

  • No clear guidelines or evidence
  • Metastatic Leydig/Sertoli tumours = poorer prognosis cf. germ cell tumour
  • ?CT follow up for a few years
  • RPLND if nodal metastases, no current role for chemotherapy
  • Consider endocrinological follow up as well