ArticleCancer cell2018
The Tandem Duplicator Phenotype Is a Prevalent Genome-Wide Cancer Configuration Driven by Distinct Gene Mutations.
Article in Cancer cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
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Who cites it
112 citing papers in PubMed, 181 citations in OpenAlex.
- Molecular and clinical determinants of response and resistance to rucaparib for recurrent ovarian cancer treatment in ARIEL2 (Parts 1 and 2).Nature communications · 2021Trial
- The BRCA1 coiled-coil domain is dispensable for suppression of tandem duplications and tolerance of FANCM loss.The EMBO journal · 2026Article
- Article
- Insights from three decades of BRCA1/2 modeling in mice.Nature genetics · 2026Review
- 53BP1-independent Shieldin-BRCA1 antagonism at replication-coupled double-strand breaks.Nature communications · 2026Article
- Cis-regulatory and long noncoding RNA alterations in breast cancer - current insights, biomarker utility, and the critical need for functional validation.Molecular oncology · 2026Review
- TONSOKU prevents the formation of large tandem duplications and restrains ATR-WEE1 checkpoint activation.Nature communications · 2026Article
- TONSL suppresses polymerase theta-dependent tandem duplications through chromatin-guided repair.Nature communications · 2026Article
- CDK12 Inactivation Attenuates Prostate Cancer Progression by Inhibiting BNIP3-Mediated Mitophagy.Cell proliferation · 2026Article
- New twist on BRCA1-mediated DNA recombination repair and tumor suppression.Trends in cell biology · 2026Review
- Assessing the Detection Power of Genome-Wide Copy Number Variation Profiles in Prostate Cancer Using Simulated Shallow Whole-Genome Sequencing Data.JCO clinical cancer informatics · 2026Article
- Decoding the Genomic and Functional Landscape of Emerging Subtypes in Ovarian Cancer.Cancer discovery · 2025Article
- Late steps of allelic break-induced replication suppress tandem duplication associated with BRCA1 deficiency.Nucleic acids research · 2025Article
- Functional impact of the hyperduplication genomophenotype in high copy number endometrial cancer.iScience · 2025Article
- New insights into the dule roles CDK12 in human cancers: Mechanisms and interventions for cancer therapy.Journal of pharmaceutical analysis · 2025Review
- Divergent trajectories to structural diversity impact patient survival in high grade serous ovarian cancer.Nature communications · 2025Article
- Molecular consequences of acute versus chronic CDK12 loss in prostate carcinoma nominates distinct therapeutic strategies.bioRxiv : the preprint server for biology · 2025Article
- The Slx4-Rad1-Rad10 nuclease differentially regulates deletions and duplications induced by a replication fork barrier.PLoS genetics · 2025Article
- The tandem duplicator phenotype may be a novel targetable subgroup in pancreatic cancer.NPJ precision oncology · 2025Article
- Patterns and variations of copy number alterations in acute myeloid leukemia: insights from the LeukAtlas database.Leukemia · 2025Article
52 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
The tandem duplicator phenotype (TDP) is a genome-wide instability configuration primarily observed in breast, ovarian, and endometrial carcinomas. Here, we stratify TDP tumors by classifying their tandem duplications (TDs) into three span intervals, with modal values of 11 kb, 231 kb, and 1.7 Mb, respectively. TDPs with ∼11 kb TDs feature loss of TP53 and BRCA1. TDPs with ∼231 kb and ∼1.7 Mb TDs associate with CCNE1 pathway activation and CDK12 disruptions, respectively. We demonstrate that p53 and BRCA1 conjoint abrogation drives TDP induction by generating short-span TDP mammary tumors in genetically modified mice lacking them. Lastly, we show how TDs in TDP tumors disrupt heterogeneous combinations of tumor suppressors and chromatin topologically associating domains while duplicating oncogenes and super-enhancers.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.