ArticleCommunications biology2022
Rearrangement processes and structural variations show evidence of selection in oesophageal adenocarcinomas.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Long-term exposure to the ethanol-derived metabolite acetaldehyde elevates structural genomic alterations but not base substitutions.Communications biology · 2026Article
- Global Hypomethylation as Minimal Residual Disease (MRD) Biomarker in Esophageal and Esophagogastric Junction Adenocarcinoma.Cancers · 2025Article
- Context-dependent effects of CDKN2A and other 9p21 gene losses during the evolution of esophageal cancer.Nature cancer · 2025Article
- Disentangling oncogenic amplicons in esophageal adenocarcinoma.Nature communications · 2024Article
- Article
- Dysregulation of lysine acetylation in the pathogenesis of digestive tract cancers and its clinical applications.Frontiers in cell and developmental biology · 2024Review
- The transcriptional landscape of endogenous retroelements delineates esophageal adenocarcinoma subtypes.NAR cancer · 2023Article
- Oncogenic structural aberration landscape in gastric cancer genomes.Nature communications · 2023Article
- Article
- Article
- Article
- Extrachromosomal DNA (ecDNA) in cancer: mechanisms, functions, and clinical implications.Frontiers in oncology · 2023Review
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Authors and funding
14 authors.
Funding
Abstract
Oesophageal adenocarcinoma (OAC) provides an ideal case study to characterize large-scale rearrangements. Using whole genome short-read sequencing of 383 cases, for which 214 had matched whole transcriptomes, we observed structural variations (SV) with a predominance of deletions, tandem duplications and inter-chromosome junctions that could be identified as LINE-1 mobile element (ME) insertions. Complex clusters of rearrangements resembling breakage-fusion-bridge cycles or extrachromosomal circular DNA accounted for 22% of complex SVs affecting known oncogenes. Counting SV events affecting known driver genes substantially increased the recurrence rates of these drivers. After excluding fragile sites, we identified 51 candidate new drivers in genomic regions disrupted by SVs, including ETV5, KAT6B and CLTC. RUNX1 was the most recurrently altered gene (24%), with many deletions inactivating the RUNT domain but preserved the reading frame, suggesting an altered protein product. These findings underscore the importance of identification of SV events in OAC with implications for targeted therapies.
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Registered trials
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