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Genomic Landscape, Evolution and Chemoresistance of Yolk Sac Tumors

ABSTRACT: Yolk sac tumors (YSTs) are a major histological subtype of malignant ovarian germ cell tumors, and compared to other subtypes, patients with YST have a worse prognosis. The molecular basis of this disease has not been characterized at the genomic level. Here we characterized 41 clinical tumor samples (and related normal samples) from 30 YST patients, with distinct responses to cisplatin-based chemotherapy.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Homo Sapiens

SUBMITTER: Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College

PROVIDER: PRJEB44264 | EVA | 2021-04-16

REPOSITORIES: EVA

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			Action	DRS
	P01-P.vcf.csi	Other
	P01-P.vcf.gz	Vcf
	P01-P.vcf.gz.csi	Vcf
	P02-P.vcf.csi	Other
	P02-P.vcf.gz	Vcf

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Genomic Landscape, Evolution and Chemoresistance of Yolk Sac Tumors

Project description:Yolk sac tumors (YSTs) are a major histological subtype of malignant ovarian germ cell tumors, and compared to other subtypes, patients with YST have a worse prognosis. The molecular basis of this disease has not been characterized at the genomic level. Here we characterized 41 clinical tumor samples (and related normal samples) from 30 YST patients, with distinct responses to cisplatin_x001f__x001F_-based chemotherapy, through a combination of whole-exome and RNA sequencing. We show that microsatellite instability status and mutational signature are informative of chemoresistance. We identify somatic driver candidates, including significantly mutated genes KRAS and KIT and copy-number alteration drivers, such as deleted ARID1A and PARK2, and amplified ZNF217, CDKN1B, and KRAS. Interestingly, YSTs appear to have very infrequent TP53 mutations, whereas the tumors from patients with abnormal gonadal development are characterized by both KRAS and TP53 mutations as well as abnormal sex-specific genes. The differential expression analysis of primary sensitive tumors versus relapsed tumors and in vitro experiments suggest a role of OVOL2 overexpression in YST resistance to cisplatin. Our study lays a critical foundation for understanding key molecular aberrations and developing novel therapeutic strategies for this disease.

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