Testicular cancer represents 1% of adult neoplasms and 5% of urological tumours, with three to ten new cases per 100,000 males/per year in Western societies.

Testicular cancer has increased during recent decades, predominantly in industrialised countries, and it continues to rise. At diagnosis, 1-2% are bilateral and 90-95% of cases are germ cell tumours (GCT). The peak incidence is in the third decade of life for nonseminomatous germ cell tumour (NSGCT) and mixed GCT patients, and in the fourth decade for seminoma testis (ST) patients.

In 5% of GCT patients, the primary site is at an extragonadal location [9]. There are two fundamental categories of GCTs based on their development and epigenetic features. Most malignant post-pubertal GCTs originate from germ cell neoplasia “in situ” (GCNIS).

Clinically and histologically, these are subdivided into seminomas and non-seminomas, the later encompassing somatic and extraembryonal elements of embryonal carcinoma, yolk sac, choriocarcinoma and teratoma. Non-GCNIS related tumours include pre-pubertal type teratoma and yolk sac, diagnosed in early childhood, and spermatocytic tumours in elderly men.

Although there is overlapping histology between the pre-pubertal teratoma/yolk sac and the teratoma and yolk sac elements in the GCNIS-related non-seminomas, these have a separate and independent pathogenesis.

TESTICULAR CANCER

Epidemiological risk factors for TC are components of the testicular dysgenesis syndrome, which encompasses cryptorchidism, hypospadias, decreased spermatogenesis and impaired fertility or disorders/differences of sex development. Additional risk factors include a family history of TC among first-degree relatives and the presence of a contralateral testicular tumour or GCNIS. Recent genome-wide association studies revealed detectable susceptibility loci leading to an increased relative risk to develop TC.