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dc.contributor.authorSimons, Benjaminen
dc.date.accessioned2015-11-24T16:51:23Z
dc.date.available2015-11-24T16:51:23Z
dc.date.issued2015-12-22en
dc.identifier.citationSimons. Proceedings of the National Academy of Sciences (2015) Vol. 113 Issue 1, pp. 128–133. doi:10.1073/pnas.1516123113en
dc.identifier.issn0027-8424
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/252727
dc.description.abstractUsing deep sequencing technology, methods based on the sporadic acquisition of somatic DNA mutations in human tissues have been used to trace the clonal evolution of progenitor cells in diseased states. However, the potential of these approaches to explore cell fate behavior of normal tissues and the initiation of preneoplasia remain underexploited. Focusing on the results of a recent deep sequencing study of eyelid epidermis, we show that the quantitative analysis of mutant clone size provides a general method to resolve the pattern of normal stem cell fate, and to detect and characterize the mutational signature of rare field transformations in human tissues, with implications for the early detection of preneoplasia.
dc.description.sponsorshipWe are indebted to Peter Campbell, Phil Jones and Inigo Martincorena for sharing information on the sizes of the biopsies used in their study, and for making their sequencing data publically available. We are also grateful to Trevor Graham, Philip Greulich and Anna Philpott for valuable discussions, and we acknowledge the financial support of the Wellcome Trust (grant number 098357/Z/12/Z).
dc.languageEnglishen
dc.language.isoenen
dc.publisherNational Academy of Sciences
dc.rightsAttribution-NonCommercial 2.0 UK: England & Wales*
dc.rights.urihttp://creativecommons.org/licenses/by-nc/2.0/uk/*
dc.subjectstem cellsen
dc.subjectDNA sequencingen
dc.subjectepidermisen
dc.subjectcanceren
dc.titleDeep sequencing as a probe of normal stem cell fate and preneoplasia in human epidermisen
dc.typeArticle
dc.description.versionThis is the author accepted manuscript. The final version is available from PNAS via http://dx.doi.org/10.1073/pnas.1516123113en
prism.endingPage133
prism.publicationDate2015en
prism.publicationNameProceedings of the National Academy of Sciencesen
prism.startingPage128
prism.volume113en
dc.rioxxterms.funderWellcome Trust
dc.rioxxterms.projectid098357/Z/12/Z
rioxxterms.versionofrecord10.1073/pnas.1516123113en
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2015-12-22en
dc.contributor.orcidSimons, Benjamin [0000-0002-3875-7071]
dc.identifier.eissn1091-6490
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idWELLCOME TRUST (098357/Z/12/Z)
rioxxterms.freetoread.startdate2016-06-22


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Attribution-NonCommercial 2.0 UK: England & Wales
Except where otherwise noted, this item's licence is described as Attribution-NonCommercial 2.0 UK: England & Wales