dc.contributor.author | Ryan, CJ | |
dc.contributor.author | Bajrami, I | |
dc.contributor.author | Lord, CJ | |
dc.date.accessioned | 2018-09-24T09:21:18Z | |
dc.date.issued | 2018-10-01 | |
dc.identifier.citation | Trends in cancer, 2018, 4 (10), pp. 671 - 683 | |
dc.identifier.issn | 2405-8033 | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/2811 | |
dc.identifier.eissn | 2405-8025 | |
dc.identifier.doi | 10.1016/j.trecan.2018.08.003 | |
dc.description.abstract | Synthetic 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.format | Print-Electronic | |
dc.format.extent | 671 - 683 | |
dc.language | eng | |
dc.language.iso | eng | |
dc.publisher | CELL PRESS | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0 | |
dc.subject | Humans | |
dc.subject | Neoplasms | |
dc.subject | Computational Biology | |
dc.subject | RNA Interference | |
dc.subject | Penetrance | |
dc.subject | Oncogenes | |
dc.subject | Molecular Targeted Therapy | |
dc.subject | Genetic Therapy | |
dc.subject | CRISPR-Cas Systems | |
dc.subject | Gene Editing | |
dc.subject | Synthetic Lethal Mutations | |
dc.title | Synthetic Lethality and Cancer - Penetrance as the Major Barrier. | |
dc.type | Journal Article | |
dcterms.dateAccepted | 2018-08-22 | |
rioxxterms.versionofrecord | 10.1016/j.trecan.2018.08.003 | |
rioxxterms.licenseref.uri | https://creativecommons.org/licenses/by/4.0 | |
rioxxterms.licenseref.startdate | 2018-10 | |
rioxxterms.type | Journal Article/Review | |
dc.relation.isPartOf | Trends in cancer | |
pubs.issue | 10 | |
pubs.notes | Not 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-status | Published | |
pubs.volume | 4 | |
pubs.embargo.terms | Not known | |
icr.researchteam | Gene Function | |
dc.contributor.icrauthor | Lord, Christopher | |