Germ cell tumours arise from the germinal epithelium and both semi-nomas and teratomas are thought to arise from pre-existing carcinomas in situ. In the UK, the British classification is still the most commonly used.

The natural history of seminoma and teratoma differs and these differences largely dictate the variation in management between the two. The majority of seminomas (75%) present with Stage I disease— that is with no evidence of metastases. Spread tends to be predictable, to the para-aortic lymph nodes in the first instance and, subsequently, to the supra-diaphragmatic lymph nodes and thereafter to other metastatic sites.

Table 22.6 Pathological classification of testicular cancers





Spermatocyte seminona

Spermatocyte serinoma


Non-seminomatous germ

cell tumour

Teratoma differentiated (TD)

Mature teratoma

Malignant teratoma intermediate (MTI)

Embryonal carcinoma with

teratoma (teratocarcinoma)

Malignant teratoma undifferentiated (MTU)

Yolk sac tumour,embryonal


Malignant teratoma trophoblastic (MTT)

Yolk sac tumour;


Only about half of testicular teratomas present as Stage I disease and spread tends to be less predictable, with blood-borne metastases occurring earlier than with seminoma. In addition to this, teratomas produce markers in the form of the human chorioric gondotrophin (HCG) and/or alpha feta protein (AFP) in 75% of cases. Seminomas on the other hand have no reliable tumour marker to monitor disease, although the HCG may be raised in about 25% of cases. The lactate dehydrogenase (LDH) may be raised in both tumours and is useful for defining a prognostic group, but is not a reliable marker for monitoring response to treatment or subsequent relapse.

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