- 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)
- 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
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)
- Testicular abnormalities
- Testicular atrophy
- Genetic abnormalities
- cKIT mutation is associated with bilateral testicular germ cell tumors
95% are germ cell tumors (Percentages taken from )
- 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
- 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)
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.
- 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.
- For risk of second malignancies, please see the second malignancies page
- 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.)
- 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.