ArticleNature communications2025
Divergent trajectories to structural diversity impact patient survival in high grade serous ovarian cancer.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Unraveling CD4Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Evaluation of quantitative polymerase chain reaction for detecting BRCA1 or BRCA2 copy number loss in high-grade serous ovarian cancer.Scientific reports · 2026Article
- Spectrum and Impact of Mitochondrial DNA Mutations in Ovarian Cancer.International journal of molecular sciences · 2025Review
- Long read sequencing reveals novel genomic and epigenomic alterations in repetitive regions of high grade serous ovarian cancer.Scientific reports · 2025Article
- Article
- Targeting SUMOylation in ovarian cancer: Sensitivity, resistance, and the role of MYC.iScience · 2025Article
- Pathogenic mitochondrial DNA variants are associated with response to anti-VEGF therapy in ovarian cancer PDX models.Journal of experimental & clinical cancer research : CR · 2024Article
- A novel ITGB8 transcript variant sustains ovarian cancer cell survival through genomic instability and altered ploidy on a mutant p53 background.Journal of ovarian research · 2024Article
- Ovarian carcinosarcoma is highly aggressive compared to other ovarian cancer histotypes.Frontiers in oncology · 2024Article
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Authors and funding
40 authors.
Funding
Abstract
Deciphering the structural variation across tumour genomes is crucial to determine the events driving tumour progression and better understand tumour adaptation and evolution. High grade serous ovarian cancer (HGSOC) is an exemplar tumour type showing extreme, but poorly characterised structural diversity. Here, we comprehensively describe the mutational landscape driving HGSOC, exploiting a large (N = 324), deeply whole genome sequenced dataset. We reveal two divergent evolutionary trajectories, affecting patient survival and involving differing genomic environments. One involves homologous recombination repair deficiency (HRD) while the other is dominated by whole genome duplication (WGD) with frequent chromothripsis, breakage-fusion-bridges and extra-chromosomal DNA. These trajectories contribute to structural variation hotspots, containing candidate driver genes with significantly altered expression. While structural variation predominantly drives tumorigenesis, we find high mtDNA mutation loads associated with shorter patient survival. We show that a combination of mutations in the mitochondrial and nuclear genomes impact prognosis, suggesting strategies for patient stratification.
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