Seminoma (SEM)

Overview

Seminoma is a histologically pure testicular germ cell tumor composed of primordial germ cells. It sits under TESTIS in OncoTree, with typically favorable cisplatin sensitivity compared with nonseminomatous subtypes. Molecularly, seminoma is characterized by high KIT and KRAS mutation rates, in contrast to the TP53 enrichment seen in cisplatin-resistant nonseminomas.

Cohorts in the corpus

  • gct_msk_2016 — 54 seminoma patients (30% of the 180-patient MSK GCT cohort); profiled by whole-exome sequencing and MSK-IMPACT targeted sequencing PMID:27646943.

Recurrent alterations

  • KIT — mutations in 29.6% of seminomas versus 4% in nonseminoma (P<.001); predominantly exon 17 hotspots associated with imatinib-resistance patterns distinct from GIST PMID:27646943.
  • KRAS — enriched in seminomas overall (20% vs 8.7% in nonseminoma, P=.045); G12 hotspot dominant PMID:27646943.
  • TP53 — exclusively absent in seminoma in this cohort; none of the 4 primary mediastinal seminomas harbored TP53 mutations PMID:27646943.
  • 12p gain — present in 74% of discovery GCT tumors overall; characteristic of both seminoma and nonseminoma PMID:27646943.
  • Very low somatic mutation rate — mean 0.9 mutations/Mb in the combined cohort PMID:27646943.

Subtypes

  • Pure seminoma is treated differently from mixed/nonseminomatous GCT; pure mediastinal seminoma has a better prognosis than mediastinal nonseminoma (0 of 4 primary mediastinal seminomas had TP53 alterations vs 13 of 18 nonseminomas) PMID:27646943.

Therapeutic landscape

  • Cisplatin-based chemotherapy — seminoma is generally more sensitive to cisplatin than nonseminoma; the absence of TP53/MDM2 alterations in seminoma is consistent with its relatively favorable prognosis PMID:27646943.
  • Imatinib/sunitinib — potential candidates for KIT-mutant seminoma, though KIT mutations in testicular GCT have an imatinib-resistance hotspot pattern distinct from GIST exon 11/9 mutations PMID:27646943.

Sources

  • PMID:27646943 — Bagrodia et al. 2016 (JCO). 54 seminomas in MSK GCT cohort; KIT mutations 29.6%, KRAS enriched; no TP53 alterations in seminoma consistent with cisplatin sensitivity.

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