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Ng, Alvin Wei Tian; McClurg, Dylan Peter; Wesley, Ben; Zamani, Shahriar A; Black, Emily; Miremadi, Ahmad; Giger, Olivier; Hoopen, Rogier Ten; Devonshire, Ginny; Redmond, Aisling M; Grehan, Nicola; Jammula, Sriganesh; Blasko, Adrienn; Li, Xiaodun; Aparicio, Samuel; Tavaré, Simon; Nowicki-Osuch, Karol; Fitzgerald, Rebecca C
Nature communications, 05/2024, Letnik: 15, Številka: 1Journal Article
Esophageal adenocarcinoma is a prominent example of cancer characterized by frequent amplifications in oncogenes. However, the mechanisms leading to amplicons that involve breakage-fusion-bridge cycles and extrachromosomal DNA are poorly understood. Here, we use 710 esophageal adenocarcinoma cases with matched samples and patient-derived organoids to disentangle complex amplicons and their associated mechanisms. Short-read sequencing identifies ERBB2, MYC, MDM2, and HMGA2 as the most frequent oncogenes amplified in extrachromosomal DNAs. We resolve complex extrachromosomal DNA and breakage-fusion-bridge cycles amplicons by integrating of de-novo assemblies and DNA methylation in nine long-read sequenced cases. Complex amplicons shared between precancerous biopsy and late-stage tumor, an enrichment of putative enhancer elements and mobile element insertions are potential drivers of complex amplicons' origin. We find that patient-derived organoids recapitulate extrachromosomal DNA observed in the primary tumors and single-cell DNA sequencing capture extrachromosomal DNA-driven clonal dynamics across passages. Prospectively, long-read and single-cell DNA sequencing technologies can lead to better prediction of clonal evolution in esophageal adenocarcinoma.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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