ArticleNature genetics2016
Mutational signatures in esophageal adenocarcinoma define etiologically distinct subgroups with therapeutic relevance.
Article in Nature genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 247 papers, 1 of them a synthesis that pooled it.
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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
247 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Spectrum of mutational signatures in T-cell lymphoma reveals a key role for UV radiation in cutaneous T-cell lymphoma.Scientific reports · 2021Pooled it
- Molecular profiling of BRAF-V600E-mutant metastatic colorectal cancer in the phase 3 BEACON CRC trial.Nature medicine · 2024Trial
- Oxaliplatin/capecitabine or carboplatin/paclitaxel-based preoperative chemoradiation for resectable oesophageal adenocarcinoma (NeoSCOPE): Long-term results of a randomised controlled trial.European journal of cancer (Oxford, England : 1990) · 2021Trial
- Efficacy of Combined VEGFR1-3, PDGFα/β, and FGFR1-3 Blockade Using Nintedanib for Esophagogastric Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Trial
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- Variable latency between the founder genetic event and rhabdoid tumor expansion.bioRxiv : the preprint server for biology · 2026Article
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- Effects of ethanol and acetaldehyde on multi-organ genomic mutation landscapes.Cell biology and toxicology · 2026Article
- A recurrent sequencing artifact on Illumina sequencers with two-color fluorescent dye chemistry and its impact on somatic variant detection.Genome biology · 2026Article
- Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026Review
- BRAFJournal of experimental & clinical cancer research : CR · 2026Article
- Identification of isoform switching events linked with esophageal adenocarcinoma patient survival informs novel prognostic and therapeutic targets.Cell death & disease · 2026Article
- Mutational Signatures and Clonal Hematopoiesis in Intestinal Metaplasia across Countries with Varying Stomach Cancer Incidence.Cancer discovery · 2026Article
- SigRescueR: a pan-system framework for noise correction and mutational signature identification across sequencing platforms.Briefings in bioinformatics · 2026Article
- Molecular stratification of esophageal adenocarcinoma: implications for prognosis and treatment strategy.Oncogene · 2026Review
- Immunosuppressive tumor microenvironment and immunotherapy resistance of esophageal carcinoma.Frontiers in immunology · 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
- The neoantigen and associated tumour microenvironment in long-term survivors with oesophageal adenocarcinoma.Frontiers in immunology · 2026Article
187 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
27 authors.
Funding
Abstract
Esophageal adenocarcinoma (EAC) has a poor outcome, and targeted therapy trials have thus far been disappointing owing to a lack of robust stratification methods. Whole-genome sequencing (WGS) analysis of 129 cases demonstrated that this is a heterogeneous cancer dominated by copy number alterations with frequent large-scale rearrangements. Co-amplification of receptor tyrosine kinases (RTKs) and/or downstream mitogenic activation is almost ubiquitous; thus tailored combination RTK inhibitor (RTKi) therapy might be required, as we demonstrate in vitro. However, mutational signatures showed three distinct molecular subtypes with potential therapeutic relevance, which we verified in an independent cohort (n = 87): (i) enrichment for BRCA signature with prevalent defects in the homologous recombination pathway; (ii) dominant T>G mutational pattern associated with a high mutational load and neoantigen burden; and (iii) C>A/T mutational pattern with evidence of an aging imprint. These subtypes could be ascertained using a clinically applicable sequencing strategy (low coverage) as a basis for therapy selection.
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