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Chapter 6: Genitourinary oncology 281

iv Chemotherapy is not as effective and is used mainly Aetiology
for non-responsive disease. Maldescent of the testis has a 10–15-fold risk. Ten per
Throughout treatment a multidisciplinary approach cent of all testicular tumours develop in testes which

is needed with regard to palliation of symptoms. Bis- are or were cryptorchid, some contra-laterally. A family
phosphonates are used for bone pain and to prevent history is also a known risk factor as is infertility.
fractures. Localised radiation is used for bone pain
and recently bone-targeting radioisotopes have been
Pathophysiology
developed for those with multiple metastases.
It is currently thought that the precursor of most germ
cell tumours is intratubular germ cell neoplasia (some-
Prognosis times called testicular carcinoma in situ), where the sem-
Depends on grade, volume of primary and TNM stag- iniferous tubules have atypical germ cells.
ing; 50% present with incurable disease. If confined to It appears that these atypical cells are formed early
prostate: 80% have 5-year survival and 60% have 10- in gestation and may be influenced by events in utero.
year survival. If metastases are present: 20% have 5-year They then lie dormant, until puberty, when they spread
survival and 10% have 10-year survival. non-invasively. In some individuals, they become ma-
lignant and either develop along the seminomatous or
teratomatous line.
Introduction to testicular tumours

Definition
Classification
Tumours of the testis may be classified broadly into those
The main components of the testis are the germ cells
arising from the germ-cell line and those arising from
(spermatogonia), the sex cords or seminiferous tubules
non-germ cells.
(Sertoli cells) and stroma (Leydig cells). Germ cell tu-
mours are the most common (90–95%) testicular tu-
Incidence mours. Germ cells are multipotent, i.e. can form many
Relatively uncommon (∼3–6/100,000 per annum), but tissue types, as normally they are involved in reproduc-
stillthemostcommonsolidorgantumourinyoungmen tionandmayformbothembryonicandextra-embryonic
and increasing in recent years. tissue. Therefore many different cell types may coexist
in a germ cell tumour (see Fig. 6.10).
Non-germ cell tumours (see Fig. 6.11) include those
Age
arising from Sertoli and Leydig cells, of which only
Depends on type, peak 25–40 years.
∼10% behave malignantly. Leydig cells normally pro-
ducetestosterone,soLeydigcelltumourshavethepoten-
Sex tial to produce steroid hormones at levels high enough
Males to have systemic effects. Both Leydig cell and Sertoli cell

Germ Cell Tumours

Seminoma (40%) Teratoma (32%) Mixed (14%)
Arise from
germ cells in the Embryonic Extraembryonic
seminiferous tubules Tissue Tissue
Figure 6.10 The British Testicular and show Trophoblast
Tumour Panel Classification of Germ cell spermatocytic Yolk Sac
tumours (% are as a proportion of all differentiation
testicular tumours).