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dc.contributor.authorRyan, CJ
dc.contributor.authorBajrami, I
dc.contributor.authorLord, CJ
dc.date.accessioned2018-09-24T09:21:18Z
dc.date.issued2018-10
dc.identifier.citationTrends in cancer, 2018, 4 (10), pp. 671 - 683
dc.identifier.issn2405-8033
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2811
dc.identifier.eissn2405-8025
dc.identifier.doi10.1016/j.trecan.2018.08.003
dc.description.abstractSynthetic lethality has long been proposed as an approach for targeting genetic defects in tumours. Despite a decade of screening efforts, relatively few robust synthetic lethal targets have been identified. Improved genetic perturbation techniques, including CRISPR/Cas9 gene editing, have resulted in renewed enthusiasm for searching for synthetic lethal effects in cancer. An implicit assumption behind this enthusiasm is that the lack of reproducibly identified targets can be attributed to limitations of RNAi technologies. We argue here that a bigger hurdle is that most synthetic lethal interactions (SLIs) are not highly penetrant, in other words they are not robust to the extensive molecular heterogeneity seen in tumours. We outline strategies for identifying and prioritising SLIs that are most likely to be highly penetrant.
dc.formatPrint-Electronic
dc.format.extent671 - 683
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.subjectHumans
dc.subjectNeoplasms
dc.subjectComputational Biology
dc.subjectRNA Interference
dc.subjectPenetrance
dc.subjectOncogenes
dc.subjectMolecular Targeted Therapy
dc.subjectGenetic Therapy
dc.subjectCRISPR-Cas Systems
dc.subjectGene Editing
dc.subjectSynthetic Lethal Mutations
dc.titleSynthetic Lethality and Cancer - Penetrance as the Major Barrier.
dc.typeJournal Article
dcterms.dateAccepted2018-08-22
rioxxterms.versionofrecord10.1016/j.trecan.2018.08.003
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2018-10
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfTrends in cancer
pubs.issue10
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Gene Function
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Gene Function
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Breast Cancer Research/Gene Function
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Gene Function
pubs.publication-statusPublished
pubs.volume4
pubs.embargo.termsNot known
icr.researchteamGene Functionen_US
dc.contributor.icrauthorLord, Christopheren


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