Radiation Oncology/Testis/Overview

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Testes Overview


Epidemiology[edit | edit source]

  • 7000 cases/yr.
  • Most common neoplasm in men ages 15-35.
  • Highest incidence among white males especially from northern Europe.
  • ~2/3 are clinical Stage I
  • Most common testicular cancer in men >50 is lymphoma
  • GCTs sometimes present in extragonadal sites: mediastinum, brain and sacrococcygeal region (often midline)

Anatomy[edit | edit source]

  • Surrounded by tunica albuginea
  • Seminiferous tubules lead to rete testis, epididymis, vas efferens and finally to urethra
  • Seminiferous tubules
    • Spermatogonia participate in sperm production (~67 days)
    • Sertoli cells are epithelial cells lining seminiferous tubules
      • Nurture and support the developing sperm cells through the stages of spermatogenesis
      • Produce several hormones, including estradiol to regulate spermatogenesis and androgen-binding protein to transport androgens
      • Form blood-testis barrier
    • Leydig cells are interstitial cells
      • Responsible for endocrine function, primarily via production of testosterone
      • Controlled by LH (testosterone synthesis) and FSH (increase in number of LH receptors)
  • Rete testis = anastamosing network of tubules in the testicular hilum; sperm are concentrated
  • Epididymis = sperm maturation and storage

Natural history[edit | edit source]

10% of germ cell tumors may arise in non-gonadal sites, in which case it is usually an anterior mediastinal mass (as opposed to a posterior mediastinal mass, which is usually metastatic) or centrally located retroperitoneal (as opposed to lateralized masses seen in metastatic disease)


Risk Factors[edit | edit source]

  • Testicular abnormalities
    • Cryptorchism
    • Testicular atrophy
    • Infertility
  • Genetic abnormalities
    • cKIT mutation is associated with bilateral testicular germ cell tumors


Pathology[edit | edit source]

95% are germ cell tumors (Percentages taken from [1])

  • Germ cell:
    • Seminoma (50%)
    • Non-seminoma (50%)
      • Pure (15%): Embryonal (10%), teratoma (3-5%), choriocarcinoma (<1%), yolk-sac tumor (<1%)
      • Mixed (35%)
  • Sex-cord stroma:
    • Leydig cell, Sertoli cell, granulosa cell
  • Lymphoma:
    • Common in men > 50


If the tumor has any component of a non-seminoma, it should be classified as a non-seminoma.
If there is an elevated AFP even if the histology shows a pure seminoma, it should be classified as a non-seminoma.

  • Seminoma - no differentiation; retains some aspects of spermatogenesis
  • NSGCT - undergo some differentiation to totipotential cells
    • Embryonic tissue differentiation - embryonal carcinoma and teratoma
    • Extra-embryonic tissue differentiation - choriocarcinoma and yolk sac tumors


  • Teratoma is not sensitive to chemotherapy. Requires resection. Does not metastasize.
  • Choriocarcinoma is one of few tumors that metastasize more frequently hematogenously (also follicular carcinoma of the thyroid, renal cell carcinoma)

Tumor markers[edit | edit source]

Check AFP, B-HCG, and LDH.

  • AFP - yolk sac, embryonal. Half-life is 5-7 days.
    • Elevated in 70% of patients with teratocarcinomas and embryonal carcinomas.
    • Never elevated in Seminomas
  • B-HCG - choriocarcinoma, embryonal. Half-life is 18-36 hrs.
    • Elevated in 40-60% of nonseminomas and ~10% of seminomas
  • Placental Alk Phos - most sensitive for surveillance of pure seminomas with ~50% sensitivity for metastatic disease
  • LDH - Surveillance marker with slight rise in ~80% of advanced seminomas and 60% of nonseminomas

1 in 5 pts with pure seminoma will have minimal B-HCG elevation (<100 mIU/mL).
Tumor markers not elevated in pure teratomas.

Prognostic factors[edit | edit source]

Risk stratification:

  • Tumors can be classified as good risk, intermediate risk, or poor risk using the IGCCCG system.
  • For details see at Seminoma or Non-seminoma

Radiation technique[edit | edit source]

  • Para-aortic field borders - Designed to cover the potential drainage areas of the para-aortic region, remember testicular vein returns at L2.
    • Top border - At or near the crura of the diaphram to cover insertions of the renal vein and antegrade flow
    • Inferior border - Bifurcation of the common iliacs
    • Lateral borders- Transverse processes of the vertebral bodies to cover LNs. Keep in mind L renal hilum.


Toxicity[edit | edit source]


Review[edit | edit source]

  • Erasmus, 2006 (Netherlands) PMID 17158533 -- "Controversies in the management of clinical stage I testis cancer." (de Wit R, J Clin Oncol. 2006 Dec 10;24(35):5482-92.)


References[edit | edit source]

  1. Ulbright TM, Amin MB, Young RH. Tumors of the testis, adnexa, spermatic cord, and scrotum. Atlas of tumor pathology. 3rd series. Fascicle 25. Washington, DC: Armed Forces Institute of Pathology, 1999.