ArticleNature genetics2020
Interplay between whole-genome doubling and the accumulation of deleterious alterations in cancer evolution.
Article in Nature genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers.
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Who cites it
156 citing papers in PubMed.
- Whole genome duplication through mitotic slippage causes nuclear instability.The EMBO journal · 2026Article
- Charting intratumor heterogeneity from bench to bedside.Nature cancer · 2026Review
- LeafRank: A phylodynamic framework for inferring relative fitness from single-cell phylogenies in chromosomally unstable tumors.bioRxiv : the preprint server for biology · 2026Article
- Genomic Catastrophe Defines the Evolutionary Trajectory of Adrenocortical Carcinoma.Endocrine pathology · 2026Article
- Ploidy shapes gemcitabine response through altered potency and delayed cell death.bioRxiv : the preprint server for biology · 2026Article
- Somatic copy number variation as a prognostic marker for recurrence in never-smokers with early-stage lung adenocarcinoma.International journal of cancer · 2026Article
- Pervasive chromosomal instability drives the karyotypic evolution of hypodiploid tumours.Genome medicine · 2026Article
- Integrated genomic analyses identify oncogenic pathway interplay in hepatocarcinogenesis defining specific molecular subtypes.Nature communications · 2026Article
- Cell and Nuclear Size Is Associated with Chromosomal Instability and Tumorigenicity in Cancer Cells That Undergo Whole Genome Doubling.Cancer research · 2026Article
- Article
- Genomic Characterization of Lung Cancer in Never-Smokers Using Deep Learning.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2026Article
- Spontaneous whole genome duplication renders mouse embryonic fibroblasts resistant to reprogramming.Cell & bioscience · 2026Article
- Gene duplication is associated with gene diversification and potential neofunctionalization in lung cancer evolution.Genome research · 2026Article
- Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer.Cancer discovery · 2026Article
- Biological clocks keep a watch on mitosis.Nature cell biology · 2026Review
- Genomic Reshuffling After Cell Fusion: Catalyst for Cancer Evolution and Progression.Advances in experimental medicine and biology · 2026Review
- AutoEpiCollect 2.0: A Web-Based Machine Learning Tool for Personalized Peptide Cancer Vaccine Design.Molecules (Basel, Switzerland) · 2025Article
- Genome doubling as a dynamic driver of ovarian cancer evolution: insights from single-cell sequencing.Journal of ovarian research · 2025Review
- Energetics of whole genome doubling and genomic instability.Cancer letters · 2025Review
- Allelic Imbalance and Chromothripsis Lead to Diversity in Japanese Tumor Genomes With Whole-Genome Duplication.Cancer science · 2025Article
96 more citing papers are in PubMed but not listed here.
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17 authors.
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Abstract
Whole-genome doubling (WGD) is a prevalent event in cancer, involving a doubling of the entire chromosome complement. However, despite its prevalence and prognostic relevance, the evolutionary selection pressures for WGD in cancer have not been investigated. Here, we combine evolutionary simulations with an analysis of cancer sequencing data to explore WGD during cancer evolution. Simulations suggest that WGD can be selected to mitigate the irreversible, ratchet-like, accumulation of deleterious somatic alterations, provided that they occur at a sufficiently high rate. Consistent with this, we observe an enrichment for WGD in tumor types with extensive loss of heterozygosity, including lung squamous cell carcinoma and triple-negative breast cancers, and we find evidence for negative selection against homozygous loss of essential genes before, but not after, WGD. Finally, we demonstrate that loss of heterozygosity and temporal dissection of mutations can be exploited to identify novel tumor suppressor genes and to obtain a deeper characterization of known cancer genes.
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