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Guidelines

Testicular Cancer

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  1. Introduction
  2. Methods
  3. Epidemiology Aetiology Pathology
  4. Staging & Prognosis
  5. Diagnostic Evaluation
  6. Disease Management
  7. Follow Up After Curative Therapy
  8. Rare Adult Para And Testicular Tumours
  9. References
  10. Conflict Of Interest
  11. Citation Information
  12. Copyright And Terms Of Use
3. Epidemiology Aetiology Pathology
  • 1. Introduction
  • 2. Methods
  • 3. Epidemiology Aetiology Pathology
  • 4. Staging Prognosis
  • 5. Diagnostic Evaluation
  • 6. Disease Management
  • 7. Follow Up After Curative Therapy
  • 8. Rare Adult Para And Testicular Tumours
  • 9. References
  • 10. Conflict Of Interest
  • 11. Citation Information
  • 12. Copyright And Terms Of Use
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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.

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