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Times Cited: 296
Times Cited: 296
Times Cited
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Similarity
Extrachromosomal oncogene amplification drives tumour evolution and genetic heterogeneity.
Kristen M Turner, Viraj Deshpande, Doruk Beyter, Tomoyuki Koga, Jessica Rusert, Catherine Lee, Bin Li, Karen Arden, Bing Ren, David A Nathanson,[...]. Nature 2017
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Extrachromosomal oncogene amplification in tumour pathogenesis and evolution.
Roel G W Verhaak, Vineet Bafna, Paul S Mischel. Nat Rev Cancer 2019
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Circular ecDNA promotes accessible chromatin and high oncogene expression.
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Discordant inheritance of chromosomal and extrachromosomal DNA elements contributes to dynamic disease evolution in glioblastoma.
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Functional Enhancers Shape Extrachromosomal Oncogene Amplifications.
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Extrachromosomal circular DNA drives oncogenic genome remodeling in neuroblastoma.
Richard P Koche, Elias Rodriguez-Fos, Konstantin Helmsauer, Martin Burkert, Ian C MacArthur, Jesper Maag, Rocio Chamorro, Natalia Munoz-Perez, Montserrat Puiggròs, Heathcliff Dorado Garcia,[...]. Nat Genet 2020
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Extrachromosomal DNA is associated with oncogene amplification and poor outcome across multiple cancers.
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The somatic genomic landscape of glioblastoma.
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MINUTE CHROMATIN BODIES IN MALIGNANT TUMOURS OF CHILDHOOD.
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Gene amplification as double minutes or homogeneously staining regions in solid tumors: origin and structure.
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Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1.
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Massive genomic rearrangement acquired in a single catastrophic event during cancer development.
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Exploring the landscape of focal amplifications in cancer using AmpliconArchitect.
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Double minute chromosomes can be produced from precursors derived from a chromosomal deletion.
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Circular DNA elements of chromosomal origin are common in healthy human somatic tissue.
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Extrachromosomal microDNAs and chromosomal microdeletions in normal tissues.
Yoshiyuki Shibata, Pankaj Kumar, Ryan Layer, Smaranda Willcox, Jeffrey R Gagan, Jack D Griffith, Anindya Dutta. Science 2012
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Normal and Cancerous Tissues Release Extrachromosomal Circular DNA (eccDNA) into the Circulation.
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Single-cell RNA-seq highlights intratumoral heterogeneity in primary glioblastoma.
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Oncogenic extrachromosomal DNA functions as mobile enhancers to globally amplify chromosomal transcription.
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Genomic organization and evolution of double minutes/homogeneously staining regions with MYC amplification in human cancer.
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Tumor Evolution of Glioma-Intrinsic Gene Expression Subtypes Associates with Immunological Changes in the Microenvironment.
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Chromothripsis from DNA damage in micronuclei.
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Production of Extrachromosomal MicroDNAs Is Linked to Mismatch Repair Pathways and Transcriptional Activity.
Laura W Dillon, Pankaj Kumar, Yoshiyuki Shibata, Yuh-Hwa Wang, Smaranda Willcox, Jack D Griffith, Yves Pommier, Shunichi Takeda, Anindya Dutta. Cell Rep 2015
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Extrachromosomal circular DNA is common in yeast.
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Extrachromosomal DNA-relieving heredity constraints, accelerating tumour evolution.
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An Integrative Model of Cellular States, Plasticity, and Genetics for Glioblastoma.
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15
Inhibiting homologous recombination decreases extrachromosomal amplification but has no effect on intrachromosomal amplification in methotrexate-resistant colon cancer cells.
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Transposition and amplification of oncogene-related sequences in human neuroblastomas.
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Comprehensive genomic characterization defines human glioblastoma genes and core pathways.
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Elimination of extrachromosomally amplified MYC genes from human tumor cells reduces their tumorigenicity.
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The 2016 World Health Organization Classification of Tumors of the Central Nervous System: a summary.
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Small extrachromosomal circular DNAs, microDNA, produce short regulatory RNAs that suppress gene expression independent of canonical promoters.
Teressa Paulsen, Yoshiyuki Shibata, Pankaj Kumar, Laura Dillon, Anindya Dutta. Nucleic Acids Res 2019
Teressa Paulsen, Yoshiyuki Shibata, Pankaj Kumar, Laura Dillon, Anindya Dutta. Nucleic Acids Res 2019
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MOLECULAR SIZE AND CIRCULARITY OF DNA IN CELLS OF MAMMALS AND HIGHER PLANTS.
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Enhancer hijacking determines extrachromosomal circular MYCN amplicon architecture in neuroblastoma.
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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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Unstable amplification of an altered dihydrofolate reductase gene associated with double-minute chromosomes.
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ATAC-seq identifies thousands of extrachromosomal circular DNA in cancer and cell lines.
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Pankaj Kumar, Shashi Kiran, Shekhar Saha, Zhangli Su, Teressa Paulsen, Ajay Chatrath, Yoshiyuki Shibata, Etsuko Shibata, Anindya Dutta. Sci Adv 2020
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Structure and evolution of double minutes in diagnosis and relapse brain tumors.
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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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MYC-containing double minutes in hematologic malignancies: evidence in favor of the episome model and exclusion of MYC as the target gene.
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Chromothripsis drives the evolution of gene amplification in cancer.
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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.