Tumors arising from germ cells, which may differentiate along gonadal lines (seminoma), extra-embryonic lines (yolk sac tumor or choriocarcinoma) or transform to totipotential cells (undifferentiated: embryonal carcinoma or differentiated: teratoma).
Either pure (60%) or mixed (40%; >2 histology) tumors.
Predisposing factors: cryptorchidism, testicular dysgenesis (e.g. testicular feminization and Klinefelter syndrome), prior or family history of GCT.
Caucasian > African Americans.
Secrete serum markers valuable in diagnosis and management:
AFP (yolk sac tumor), HCG (choriocarcinoma) and LDH (not specific, level provides a tool to assess tumor burden).
Painless testicular enlargement.
Unilateral (only 2% bilateral).
From clinical standpoint, most important distinction is between seminomas and non-seminomatous GCTs.
Seminomas tend to remain localized for a longer time (70% stage 1) and metastasize via lymph nodes.
Non-seminomatous GCTs metastasize earlier (60% stages II and III) via hematogenous spread.
Seminoma is extremely radiosensitive whereas NSGCTs are relatively radioresistant.
Seminoma occurs at age range 35-45 years; non-seminomatous GCT occurs in patients 10 years younger.
GCTs in postpubertal men typically have 1 or > copies of chr 12p [most commonly i(12p)]; ~80% GCTs have at least 1 i(12p).
Infantile teratoma often diploid, infantile yolk sac tumors often aneuploid and spermatocytic seminoma either diploid or aneuploidy.
Immunohistochemistry: all GCTs are PLAP+ and SALL4+