Please use this identifier to cite or link to this item: https://doi.org/10.1097/PAT.0b013e32835c7645
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dc.titleKIT gene mutation analysis in solid tumours: Biology, clincial applications and trends in diagnostic reporting
dc.contributor.authorTay, C.M.
dc.contributor.authorOng, C.W.
dc.contributor.authorLee, V.K.M.
dc.contributor.authorPang, B.
dc.date.accessioned2014-12-12T07:37:11Z
dc.date.available2014-12-12T07:37:11Z
dc.date.issued2013-02
dc.identifier.citationTay, C.M., Ong, C.W., Lee, V.K.M., Pang, B. (2013-02). KIT gene mutation analysis in solid tumours: Biology, clincial applications and trends in diagnostic reporting. Pathology 45 (2) : 127-137. ScholarBank@NUS Repository. https://doi.org/10.1097/PAT.0b013e32835c7645
dc.identifier.issn00313025
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/116172
dc.description.abstractGain-of-function mutations involving c-kit protein, a cellsurface transmembrane receptor for stem cell factor, have been identified as a key oncogenic driver in a variety of solid tumours. Coupled with the development of tyrosine kinase inhibitors such as imatinib, c-kit has emerged as a viable drug target in what seems to be a validated therapeutic concept. This review will focus on gastrointestinal stromal tumours and melanomas, two types of solid tumours most closely associated with KIT gene mutations. The biology of KIT mutations in both conditions, as well as the value of KIT mutation testing in predicting disease and treatment outcomes are discussed. Since initial response to imatinib is largely influenced by mutation status, genotyping these tumours serves to facilitate personalised oncology. We also summarise our experience with diagnostic reporting of KIT mutation analysis over a period of 3 years, and briefly survey future developments in treatment, which indeed look very promising. © 2013 Royal College of Pathologists of Australasia.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1097/PAT.0b013e32835c7645
dc.sourceScopus
dc.subjectGISTs
dc.subjectKIT mutation
dc.subjectMelanomas
dc.subjectPDGFRA mutation
dc.subjectPersonalised oncology
dc.subjectTyrosine kinase inhibitor
dc.typeReview
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.description.doi10.1097/PAT.0b013e32835c7645
dc.description.sourcetitlePathology
dc.description.volume45
dc.description.issue2
dc.description.page127-137
dc.description.codenPTLGA
dc.identifier.isiut000313063300004
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