3. EPIDEMIOLOGY AETIOLOGY PATHOLOGY
3.1. Epidemiology and Aetiology
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 [4]. The incidence of TC has increased during recent decades, predominantly in industrialised countries [5-8], and it continues to rise. At diagnosis, 1-2% are bilateral and 90-95% of cases are germ cell tumours (GCT) [4]. The peak incidence is in the third decade of life for non-seminomatous 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). Histologically and clinically, these are subdivided into seminomas and non-seminomas, the latter encompassing somatic and extra-embryonal elements of embryonal carcinoma, yolk sac, choriocarcinoma and post-pubertal teratoma (PPT) [10].
Non GCNIS derived tumours include pre-pubertal type teratoma and yolk sac tumour, which occur in early childhood, and spermatocytic tumours which usually occurs in older men. Although there is overlapping histology between the pre-pubertal type teratoma/yolk sac and the teratoma and yolk sac tumour elements in the GCNIS-derived NSGCT, these have a separate and independent pathogenesis [10].
Risk factors for GCNIS-derived GCTs are components of the testicular dysgenesis syndrome, which encompasses cryptorchidism, hypospadias, decreased spermatogenesis and impaired fertility [11-13] or disorders of sex development [14]. Additional risk factors include a family history of TC among first-degree relatives and the presence of a contralateral testicular tumour or GCNIS [15-23] although the risk was lower if TC patients previously had received platinum-based chemotherapy [24,25]. Genome-wide association studies revealed detectable susceptibility loci leading to an increased relative risk to develop TC [26].
3.2. Histological classification
General:The recommended pathological classification is based on the 2022 update of the World Health Organization (WHO) pathological classification [27]. This outlined in Appendix 1- Pathological classification.