ArticleNature genetics2019
The landscape of selection in 551 esophageal adenocarcinomas defines genomic biomarkers for the clinic.
Article in Nature genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
139 citing papers in PubMed, 1 synthesis or guideline pooled it, 231 citations in OpenAlex.
- A novel meta-analysis based on data augmentation and elastic data shared lasso regularization for gene expression.BMC bioinformatics · 2022Pooled it
- Phase II Trial of Palbociclib in Patients with Advanced Esophageal or Gastric Cancer.The oncologist · 2020Trial
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- Article
- Patterns, Timing, and Survival of Recurrence After Surgery for Esophageal and Junctional Adenocarcinoma in the European Multicentre ENSURE Study.Annals of surgical oncology · 2026Article
- Clinical implications of lactylation modification in digestive system tumors (Review).Oncology letters · 2026Review
- Whole genome sequencing in oesophageal adenocarcinoma unmasks potential precision therapies.BMC cancer · 2026Article
- Integrated epidemiological and molecular data inform the relationship between precancer and cancer states of esophageal adenocarcinoma.Nature medicine · 2026Article
- Intestinal metaplasia is the only precursor to esophageal adenocarcinoma.Nature medicine · 2026Article
- Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026Review
- Emerging Biomarkers for Managing Barrett's Esophagus.Gastrointestinal endoscopy clinics of North America · 2026Review
- The biology and therapeutic implications of heterogeneity in Barrett oesophagus and oesophageal adenocarcinoma.Nature reviews. Clinical oncology · 2026Review
- Gastrointestinal cancer: molecular pathogenesis and targeted therapy.Molecular biomedicine · 2025Review
- Single-cell analysis of Barrett's esophagus and carcinoma reveals cell types conferring risk via genetic predisposition.Cell genomics · 2025Article
- NRF2-mediated persistent adaptation of oesophageal adenocarcinoma cells to HER2 inhibition.Oncogene · 2025Article
- Cancer-associated fibroblasts are associated with neo-adjuvant treatment response in oesophageal adenocarcinoma.British journal of cancer · 2025Article
- Metabolic Profiling of DistinctInternational journal of molecular sciences · 2025Article
- Evolutionary and immune microenvironment dynamics during neoadjuvant treatment of esophageal adenocarcinoma.Nature cancer · 2025Article
- Nanopore-based consensus sequencing enables accurate multimodal tumor cell-free DNA profiling.Genome research · 2025Article
- Gastroesophageal circulating tumor cell crosstalk with peripheral immune system guides CTC survival and proliferation.Cell death & disease · 2025Article
79 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
Esophageal adenocarcinoma (EAC) is a poor-prognosis cancer type with rapidly rising incidence. Understanding of the genetic events driving EAC development is limited, and there are few molecular biomarkers for prognostication or therapeutics. Using a cohort of 551 genomically characterized EACs with matched RNA sequencing data, we discovered 77 EAC driver genes and 21 noncoding driver elements. We identified a mean of 4.4 driver events per tumor, which were derived more commonly from mutations than copy number alterations, and compared the prevelence of these mutations to the exome-wide mutational excess calculated using non-synonymous to synonymous mutation ratios (dN/dS). We observed mutual exclusivity or co-occurrence of events within and between several dysregulated EAC pathways, a result suggestive of strong functional relationships. Indicators of poor prognosis (SMAD4 and GATA4) were verified in independent cohorts with significant predictive value. Over 50% of EACs contained sensitizing events for CDK4 and CDK6 inhibitors, which were highly correlated with clinically relevant sensitivity in a panel of EAC cell lines and organoids.
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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.