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Times Cited: 88
Times Cited: 88
Times Cited
Times Co-cited
Similarity
Circular ecDNA promotes accessible chromatin and high oncogene expression.
Sihan Wu, Kristen M Turner, Nam Nguyen, Ramya Raviram, Marcella Erb, Jennifer Santini, Jens Luebeck, Utkrisht Rajkumar, Yarui Diao, Bin Li,[...]. Nature 2019
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Extrachromosomal oncogene amplification drives tumour evolution and genetic heterogeneity.
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Extrachromosomal circular DNA drives oncogenic genome remodeling in neuroblastoma.
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Targeted therapy resistance mediated by dynamic regulation of extrachromosomal mutant EGFR DNA.
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Extrachromosomal oncogene amplification in tumour pathogenesis and evolution.
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Extrachromosomal DNA is associated with oncogene amplification and poor outcome across multiple cancers.
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Discordant inheritance of chromosomal and extrachromosomal DNA elements contributes to dynamic disease evolution in glioblastoma.
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Normal and Cancerous Tissues Release Extrachromosomal Circular DNA (eccDNA) into the Circulation.
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Extrachromosomal microDNAs and chromosomal microdeletions in normal tissues.
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Circular DNA elements of chromosomal origin are common in healthy human somatic tissue.
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Discoveries of Extrachromosomal Circles of DNA in Normal and Tumor Cells.
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Inhibiting homologous recombination decreases extrachromosomal amplification but has no effect on intrachromosomal amplification in methotrexate-resistant colon cancer cells.
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Genomic organization and evolution of double minutes/homogeneously staining regions with MYC amplification in human cancer.
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Oncogenic extrachromosomal DNA functions as mobile enhancers to globally amplify chromosomal transcription.
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MOLECULAR SIZE AND CIRCULARITY OF DNA IN CELLS OF MAMMALS AND HIGHER PLANTS.
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Enhancer hijacking activates GFI1 family oncogenes in medulloblastoma.
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Small extrachromosomal circular DNAs, microDNA, produce short regulatory RNAs that suppress gene expression independent of canonical promoters.
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Extrachromosomal driver mutations in glioblastoma and low-grade glioma.
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Novel role for non-homologous end joining in the formation of double minutes in methotrexate-resistant colon cancer cells.
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Double-strand breakage in the extrachromosomal double minutes triggers their aggregation in the nucleus, micronucleation, and morphological transformation.
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Pan-cancer analysis of somatic copy-number alterations implicates IRS4 and IGF2 in enhancer hijacking.
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Extrachromosomal DNA-relieving heredity constraints, accelerating tumour evolution.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.