dc.contributor.author | Dhillon, KK | |
dc.contributor.author | Bajrami, I | |
dc.contributor.author | Taniguchi, T | |
dc.contributor.author | Lord, CJ | |
dc.date.accessioned | 2017-03-06T15:49:18Z | |
dc.date.issued | 2016-10-01 | |
dc.identifier.citation | Endocrine-related cancer, 2016, 23 (10), pp. T39 - T55 | |
dc.identifier.issn | 1351-0088 | |
dc.identifier.uri | https://repository.icr.ac.uk/handle/internal/475 | |
dc.identifier.eissn | 1479-6821 | |
dc.identifier.doi | 10.1530/erc-16-0228 | |
dc.description.abstract | When the BRCA1 and BRCA2 tumour suppressor genes were identified in the early 1990s, the immediate implications of mapping, cloning and delineating the sequence of these genes were that individuals in families with a BRCA gene mutation could be tested for the presence of a mutation and their risk of developing cancer could be predicted. Over time though, the discovery of BRCA1 and BRCA2 has had a much greater influence than many might have imagined. In this review, we discuss how the discovery of BRCA1 and BRCA2 has not only provided an understanding of the molecular processes that drive tumourigenesis but also reignited an interest in therapeutically exploiting loss-of-function alterations in tumour suppressor genes. | |
dc.format | Print-Electronic | |
dc.format.extent | T39 - T55 | |
dc.language | eng | |
dc.language.iso | eng | |
dc.publisher | BIOSCIENTIFICA LTD | |
dc.subject | Animals | |
dc.subject | Humans | |
dc.subject | Breast Neoplasms | |
dc.subject | Genetic Predisposition to Disease | |
dc.subject | Therapies, Investigational | |
dc.subject | Genes, Lethal | |
dc.subject | Female | |
dc.subject | Molecular Targeted Therapy | |
dc.subject | Synthetic Lethal Mutations | |
dc.title | Synthetic lethality: the road to novel therapies for breast cancer. | |
dc.type | Journal Article | |
dcterms.dateAccepted | 2016-08-15 | |
rioxxterms.versionofrecord | 10.1530/erc-16-0228 | |
rioxxterms.licenseref.startdate | 2016-10 | |
rioxxterms.type | Journal Article/Review | |
dc.relation.isPartOf | Endocrine-related cancer | |
pubs.issue | 10 | |
pubs.notes | No embargo | |
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 | 23 | |
pubs.embargo.terms | No embargo | |
icr.researchteam | Gene Function | |
dc.contributor.icrauthor | Lord, Christopher | |