ArticleNature communications2023
Genomic signatures of past and present chromosomal instability in Barrett's esophagus and early esophageal adenocarcinoma.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 29 citations in OpenAlex.
- Biomarker Use in Barrett's Esophagus Surveillance.The American journal of gastroenterology · 2026Review
- A tumor profiling resource for ovarian cancer: insights into chemotherapy-driven heterogeneity and personalized treatment strategy.Nature communications · 2026Article
- Integrated epidemiological and molecular data inform the relationship between precancer and cancer states of esophageal adenocarcinoma.Nature medicine · 2026Article
- Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026Review
- Comprehensive Overview of Gastric Cancer Immunohistochemistry: Key Biomarkers, Advanced Detection Methods, and Perspectives.Medicina (Kaunas, Lithuania) · 2026Review
- Molecular stratification of esophageal adenocarcinoma: implications for prognosis and treatment strategy.Oncogene · 2026Review
- Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026Review
- The biology and therapeutic implications of heterogeneity in Barrett oesophagus and oesophageal adenocarcinoma.Nature reviews. Clinical oncology · 2026Review
- Etiology and Pathophysiology of Barrett's Esophagus/Neoplasia.Digestion · 2026Review
- Current Concepts for Diagnosing Non-Dysplastic and Dysplastic Barrett's Esophagus.Gastrointestinal endoscopy clinics of North America · 2026Review
- Large-scale single-cell phylogenetic mapping of clonal evolution in the human aging esophagus.bioRxiv : the preprint server for biology · 2025Article
- Investigation of c-Fos/c-Jun Signaling Pathways in Periostracum Cicadae's Inhibition of EMT in Gastric Tissue.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Cell-cycle dependent DNA repair and replication unifies patterns of chromosome instability.Nature communications · 2025Article
- EMcnv: enhancing CNV detection performance through ensemble strategies with heterogeneous meta-graph neural networks.Briefings in bioinformatics · 2025Article
- Current status and perspectives of esophageal cancer: a comprehensive review.Cancer communications (London, England) · 2025Review
- Article
- Cancer phylogenetic inference using copy number alterations detected from DNA sequencing data.Cancer pathogenesis and therapy · 2025Review
- Reduction of chromosomal instability and inflammation is a common aspect of adaptation to aneuploidy.EMBO reports · 2024Article
- Article
- Patterns of Aneuploidy and Signaling Consequences in Cancer.Cancer research · 2024Review
Corrections and comments
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Authors and funding
18 authors at 10 institutions in 4 countries.
Funding
Abstract
The progression of precancerous lesions to malignancy is often accompanied by increasing complexity of chromosomal alterations but how these alterations arise is poorly understood. Here we perform haplotype-specific analysis of chromosomal copy-number evolution in the progression of Barrett's esophagus (BE) to esophageal adenocarcinoma (EAC) on multiregional whole-genome sequencing data of BE with dysplasia and microscopic EAC foci. We identify distinct patterns of copy-number evolution indicating multigenerational chromosomal instability that is initiated by cell division errors but propagated only after p53 loss. While abnormal mitosis, including whole-genome duplication, underlies chromosomal copy-number changes, segmental alterations display signatures of successive breakage-fusion-bridge cycles and chromothripsis of unstable dicentric chromosomes. Our analysis elucidates how multigenerational chromosomal instability generates copy-number variation in BE cells, precipitates complex alterations including DNA amplifications, and promotes their independent clonal expansion and transformation. In particular, we suggest sloping copy-number variation as a signature of ongoing chromosomal instability that precedes copy-number complexity. These findings suggest copy-number heterogeneity in advanced cancers originates from chromosomal instability in precancerous cells and such instability may be identified from the presence of sloping copy-number variation in bulk sequencing data.
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Registered trials
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.