ArticleNature communications2023
Mutational signature dynamics shaping the evolution of oesophageal 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 20 papers.
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Who cites it
20 citing papers in PubMed.
- The role of cytotoxicity in the process of carcinogenesis.Archives of toxicology · 2026Article
- Effects of ethanol and acetaldehyde on multi-organ genomic mutation landscapes.Cell biology and toxicology · 2026Article
- Integrated epidemiological and molecular data inform the relationship between precancer and cancer states of esophageal adenocarcinoma.Nature medicine · 2026Article
- A signature-agnostic test for differences between tumor mutation spectra reveals carcinogen and ancestry effects.Communications biology · 2026Article
- Genomics Define Malignant Transformation in Myeloma Precursor Conditions.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2026Article
- Ultra-deep duplex sequencing reveals unique features of somatic evolution in the normal tissues of a family with Li-Fraumeni syndrome.bioRxiv : the preprint server for biology · 2026Article
- The biology and therapeutic implications of heterogeneity in Barrett oesophagus and oesophageal adenocarcinoma.Nature reviews. Clinical oncology · 2026Review
- Leveraging data-driven insights for esophageal and gastric cancer diagnosis.BMC medical informatics and decision making · 2025Article
- Genome-scale multi-organ analysis of mutagenic effects of ethanol and acetaldehyde in Sprague Dawley rats.bioRxiv : the preprint server for biology · 2025Article
- Monitoring the rate and variability of somatic genomic alterations using long-read sequencing.Scientific reports · 2025Article
- Novel prognostic biomarkers in small cell lung cancer reveal mutational signatures, genomic mutations, and immune implications.Scientific reports · 2025Article
- Evolutionary and immune microenvironment dynamics during neoadjuvant treatment of esophageal adenocarcinoma.Nature cancer · 2025Article
- APOBEC3B Does Not Promote Tumor Progression in Tp53 Hemizygous Mice.Cancer reports (Hoboken, N.J.) · 2025Article
- Exosomes in esophageal cancer: function and therapeutic prospects.Medical oncology (Northwood, London, England) · 2024Review
- Pan-cancer analysis of the interplay between mutational signatures and cellular signaling.iScience · 2024Article
- Tumor initiation and early tumorigenesis: molecular mechanisms and interventional targets.Signal transduction and targeted therapy · 2024Review
- Metformin in Esophageal Carcinoma: Exploring Molecular Mechanisms and Therapeutic Insights.International journal of molecular sciences · 2024Review
- 8-Oxoadenine: A «New» Player of the Oxidative Stress in Mammals?International journal of molecular sciences · 2024Review
- Gastro-Esophageal Junction Precancerosis: Histological Diagnostic Approach and Pathogenetic Insights.Cancers · 2023Review
- Mutational signature dynamics shaping the evolution of oesophageal adenocarcinoma.Nature communications · 2023Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
A variety of mutational processes drive cancer development, but their dynamics across the entire disease spectrum from pre-cancerous to advanced neoplasia are poorly understood. We explore the mutagenic processes shaping oesophageal adenocarcinoma tumorigenesis in 997 instances comprising distinct stages of this malignancy, from Barrett Oesophagus to primary tumours and advanced metastatic disease. The mutational landscape is dominated by the C[T > C/G]T substitution enriched signatures SBS17a/b, which are linked with TP53 mutations, increased proliferation, genomic instability and disease progression. The APOBEC mutagenesis signature is a weak but persistent signal amplified in primary tumours. We also identify prevalent alterations in DNA damage repair pathways, with homologous recombination, base and nucleotide excision repair and translesion synthesis mutated in up to 50% of the cohort, and surprisingly uncoupled from transcriptional activity. Among these, the presence of base excision repair deficiencies show remarkably poor prognosis in the cohort. In this work, we provide insights on the mutational aetiology and changes enabling the transition from pre-neoplastic to advanced oesophageal adenocarcinoma.
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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.