ArticleNature genetics2015
Paired exome analysis of Barrett's esophagus and adenocarcinoma.
Article in Nature genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 225 papers, 1 of them a synthesis that pooled it.
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Who cites it
225 citing papers in PubMed, 1 synthesis or guideline pooled it, 373 citations in OpenAlex.
- Genomic Heterogeneity and Exceptional Response to Dual Pathway Inhibition in Anaplastic Thyroid Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Pooled it
- Genomic and transcriptomic correlates of immunotherapy response within the tumor microenvironment of leptomeningeal metastases.Nature communications · 2021Trial
- Phase II Multicenter Study of Enzalutamide in Metastatic Castration-Resistant Prostate Cancer to Identify Mechanisms Driving Resistance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Trial
- Loss of PTEN Is Associated with Resistance to Anti-PD-1 Checkpoint Blockade Therapy in Metastatic Uterine Leiomyosarcoma.Immunity · 2017Trial
- GSTT2 Switches from a Homeostatic Antioxidant to a Cell-Cycle-Coupled Factor in Therapy-Resistant Esophageal Adenocarcinoma.Cancers · 2026Article
- Trajectory of Lymph Node Metastasis Reflects the Molecular Features of Esophageal Squamous Cell Carcinoma.Cancer research and treatment · 2026Article
- Biomarker Use in Barrett's Esophagus Surveillance.The American journal of gastroenterology · 2026Review
- Tumor transcriptional state predicts survival in immune-checkpoint-blockade-treated glioblastoma.Nature cancer · 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
- Harnessing genomics for early cancer detection, risk stratification and prevention.Nature genetics · 2026Review
- Chromosomal instability shapes the tumor microenvironment of esophageal adenocarcinoma via a cGAS-chemokine-myeloid axis.Science advances · 2026Article
- The biology and therapeutic implications of heterogeneity in Barrett oesophagus and oesophageal adenocarcinoma.Nature reviews. Clinical oncology · 2026Review
- Current Concepts for Diagnosing Non-Dysplastic and Dysplastic Barrett's Esophagus.Gastrointestinal endoscopy clinics of North America · 2026Review
- Emerging Biomarkers for Managing Barrett's Esophagus.Gastrointestinal endoscopy clinics of North America · 2026Review
- Detection of heterogeneous resistance mechanisms to tyrosine kinase inhibitors from cell-free DNA.Cell genomics · 2025Article
- Clonal cell states link gastroesophageal junction tissues with metaplasia and cancer.Nature communications · 2025Article
- Gastric (Foveolar)-Type Dysplasia in Barrett's Esophagus: A Clinical, Molecular, and Long-Term Outcome Study.The American journal of gastroenterology · 2025Article
- Genomic and transcriptomic dynamics in the stepwise progression of lung adenocarcinoma.Cell research · 2025Article
- The Interplay Between Esophageal Adenocarcinoma and Its Tumor Microenvironment: Toward Innovative Therapies.Cells · 2025Review
165 more citing papers are in PubMed but not listed here.
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Authors and funding
23 authors at 6 institutions in 1 country.
Funding
Abstract
Barrett's esophagus is thought to progress to esophageal adenocarcinoma (EAC) through a stepwise progression with loss of CDKN2A followed by TP53 inactivation and aneuploidy. Here we present whole-exome sequencing from 25 pairs of EAC and Barrett's esophagus and from 5 patients whose Barrett's esophagus and tumor were extensively sampled. Our analysis showed that oncogene amplification typically occurred as a late event and that TP53 mutations often occurred early in Barrett's esophagus progression, including in non-dysplastic epithelium. Reanalysis of additional EAC exome data showed that the majority (62.5%) of EACs emerged following genome doubling and that tumors with genomic doubling had different patterns of genomic alterations, with more frequent oncogenic amplification and less frequent inactivation of tumor suppressors, including CDKN2A. These data suggest that many EACs emerge not through the gradual accumulation of tumor-suppressor alterations but rather through a more direct path whereby a TP53-mutant cell undergoes genome doubling, followed by the acquisition of oncogenic amplifications.
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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.