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dc.contributor.authorNagel, Zachary D.
dc.contributor.authorBrenner, David J.
dc.contributor.authorBegley, Thomas J.
dc.contributor.authorSobol, Robert W.
dc.contributor.authorBielas, Jason H.
dc.contributor.authorStambrook, Peter J.
dc.contributor.authorWei, Qingyi
dc.contributor.authorHu, Jennifer J.
dc.contributor.authorTerry, Mary Beth
dc.contributor.authorDilworth, Caroline
dc.contributor.authorMcAllister, Kimberly A.
dc.contributor.authorReinlib, Les
dc.contributor.authorWorth, Leroy
dc.contributor.authorShaughnessy, Daniel T.
dc.contributor.authorEngelward, Bevin P
dc.date.accessioned2018-09-13T14:36:14Z
dc.date.available2018-09-13T14:36:14Z
dc.date.issued2017-04
dc.date.submitted2017-02
dc.identifier.issn0027-5107
dc.identifier.urihttp://hdl.handle.net/1721.1/117738
dc.description.abstractThe rise of advanced technologies for characterizing human populations at the molecular level, from sequence to function, is shifting disease prevention paradigms toward personalized strategies. Because minimization of adverse outcomes is a key driver for treatment decisions for diseased populations, developing personalized therapy strategies represent an important dimension of both precision medicine and personalized prevention. In this commentary, we highlight recently developed enabling technologies in the field of DNA damage, DNA repair, and mutagenesis. We propose that omics approaches and functional assays can be integrated into population studies that fuse basic, translational and clinical research with commercial expertise in order to accelerate personalized prevention and treatment of cancer and other diseases linked to aberrant responses to DNA damage. This collaborative approach is generally applicable to efforts to develop data-driven, individualized prevention and treatment strategies for other diseases. We also recommend strategies for maximizing the use of biological samples for epidemiological studies, and for applying emerging technologies to clinical applications. Keywords: DNA damage; Comet; H2AX; Host cell reactivation; DNA repair; DNA damage response; Precision medicineen_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Grant ES02116)en_US
dc.publisherElsevier BVen_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/J.MRFMMM.2017.03.007en_US
dc.rightsCreative Commons Attribution-NonCommercial-NoDerivs Licenseen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en_US
dc.sourceElsevieren_US
dc.titleTowards precision prevention: Technologies for identifying healthy individuals with high risk of diseaseen_US
dc.typeArticleen_US
dc.identifier.citationNagel, Zachary D. et al. “Towards Precision Prevention: Technologies for Identifying Healthy Individuals with High Risk of Disease.” Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 800–802 (August 2017): 14–28 © 2017 Elsevier B.V.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biological Engineeringen_US
dc.contributor.mitauthorEngelward, Bevin P
dc.relation.journalMutation Research/Fundamental and Molecular Mechanisms of Mutagenesisen_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dc.date.updated2018-08-28T17:52:00Z
dspace.orderedauthorsNagel, Zachary D.; Engelward, Bevin P.; Brenner, David J.; Begley, Thomas J.; Sobol, Robert W.; Bielas, Jason H.; Stambrook, Peter J.; Wei, Qingyi; Hu, Jennifer J.; Terry, Mary Beth; Dilworth, Caroline; McAllister, Kimberly A.; Reinlib, Les; Worth, Leroy; Shaughnessy, Daniel T.en_US
dspace.embargo.termsNen_US
dc.identifier.orcidhttps://orcid.org/0000-0003-4322-3573
mit.licensePUBLISHER_CCen_US


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