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Depositordc.contributorTaylor, Martin
Funderdc.contributor.otherCRUK - Cancer Research UKen_UK
Funderdc.contributor.otherMRC - Medical Research Councilen_UK
Data Creatordc.creatorAitken, Sarah
Data Creatordc.creatorAnderson, Craig
Data Creatordc.creatorFrances, Connor
Data Creatordc.creatorRayner, Tim
Data Creatordc.creatorLukk, Margus
Data Creatordc.creatorFeng, Christine
Data Creatordc.creatorSemple, Colin
Data Creatordc.creatorLopez-Bigas, Nuria
Data Creatordc.creatorFlicek, Paul
Data Creatordc.creatorOdom, Duncan
Data Creatordc.creatorTaylor, Martin
Date Accessioneddc.date.accessioned2020-08-24T16:17:29Z
Date Availabledc.date.available2020-08-24T16:17:29Z
Citationdc.identifier.citationAitken, Sarah; Anderson, Craig; Frances, Connor; Rayner, Tim; Lukk, Margus; Feng, Christine; Semple, Colin; Lopez-Bigas, Nuria; Flicek, Paul; Odom, Duncan; Taylor, Martin. (2020). Pervasive lesion segregation shapes cancer genome evolution, [dataset]. https://doi.org/10.7488/ds/2910.en
Persistent Identifierdc.identifier.urihttp://hdl.handle.net/10283/3742
Persistent Identifierdc.identifier.urihttps://doi.org/10.7488/ds/2910
Dataset Description (abstract)dc.description.abstractCancers arise through the acquisition of oncogenic mutations and grow by clonal expansion. Here we reveal that most mutagenic DNA lesions are not resolved into a mutated DNA base pair within a single cell cycle. Instead, DNA lesions segregate, unrepaired, into daughter cells for multiple cell generations, resulting in the chromosome-scale phasing of subsequent mutations. We characterize this process in mutagen-induced mouse liver tumours and show that DNA replication across persisting lesions can produce multiple alternative alleles in successive cell divisions, thereby generating both multiallelic and combinatorial genetic diversity. The phasing of lesions enables accurate measurement of strand-biased repair processes, quantification of oncogenic selection and fine mapping of sister-chromatid-exchange events. Finally, we demonstrate that lesion segregation is a unifying property of exogenous mutagens, including UV light and chemotherapy agents in human cells and tumours, which has profound implications for the evolution and adaptation of cancer genomes. The data submitted here is analysis output based on primary data submitted to the EBI under the indicated accession PRJEB37808.en_UK
Dataset Description (TOC)dc.description.tableofcontentsSee README.txt file in data submission for a description of the data.en_UK
Languagedc.language.isoengen_UK
Relation (Is Referenced By)dc.relation.isreferencedbyhttps://doi.org/10.1038/s41586-020-2435-1en_UK
Relation (Is Referenced By)dc.relation.isreferencedbyhttps://doi.org/10.1101/868679en_UK
Rightsdc.rightsCreative Commons Attribution 4.0 International Public Licenseen
Sourcedc.sourcehttps://www.ebi.ac.uk/ena/browser/view/PRJEB37808en_UK
Subjectdc.subjectCanceren_UK
Subjectdc.subjectMutationen_UK
Subjectdc.subjectDNA damageen_UK
Subjectdc.subjectLesion segregationen_UK
Subject Classificationdc.subject.classificationMedicine and Dentistryen_UK
Titledc.titlePervasive lesion segregation shapes cancer genome evolutionen_UK
Typedc.typedataseten_UK

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