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Yolk sac tumors (YSTs) are a major histological subtype of malignant ovarian germ cell tumors with a relatively poor prognosis. The molecular basis of this disease has not been thoroughly characterized at the genomic level. Here we perform whole-exome and RNA sequencing on 41 clinical tumor samples from 30 YST patients, with distinct responses to cisplatin-based chemotherapy. We show that microsatellite instability status and mutational signatures are informative of chemoresistance. We identify somatic driver candidates, including significantly mutated genes  KRAS  and  KIT  and copy-number alteration drivers, including deleted  ARID1A  and  PARK2 , and amplified  ZNF217 ,  CDKN1B , and  KRAS . YSTs have very infrequent  TP53  mutations, whereas the tumors from patients with abnormal gonadal development contain both  KRAS  and  TP53  mutations. We further reveal a role of  OVOL2  overexpression in YST resistance to cisplatin. This study lays a critical foundation for understanding key molecular aberrations in YSTs and developing related therapeutic strategies.

Analysis of the genomic landscape of yolk sac tumors reveals mechanisms of evolution and chemoresistance