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dc.contributor.authorNoujaim, J
dc.contributor.authorGonzalez, D
dc.contributor.authorThway, K
dc.contributor.authorJones, RL
dc.contributor.authorJudson, I
dc.date.accessioned2016-09-20T13:06:00Z
dc.date.issued2016-05
dc.identifier.citationCancer biology & therapy, 2016, 17 (5), pp. 543 - 545
dc.identifier.issn1538-4047
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/114
dc.identifier.eissn1555-8576
dc.identifier.doi10.1080/15384047.2016.1156263
dc.description.abstractExon 11 KIT mutations are found in a majority of gastrointestinal stromal tumors (GIST) and are usually predictive of response to imatinib, a KIT, PDGFRA and ABL inhibitor. Exon 11 mutations with poor sensitivity to imatinib and poor outcome can be observed on rare occasions, including p.(L576P). In silico and in vitro studies suggested a decreased binding affinity for imatinib in p.(L576P) KIT mutations, thereby offering an explanation for their poor outcome and poor response to standard therapy. These observations were further corroborated with anecdotal case reports of refractoriness or non-durable response to imatinib therapy. However, we describe the favorable response to imatinib and outcome in 5 p.(L576P)-KIT mutant GIST patients treated at a tertiary sarcoma referral center. The sensitivity of p.(L576P)-KIT mutations to imatinib, and the prognostic impact of this mutation need to be further evaluated in a larger cohort. Based on our observations, p.(L576P) mutated GISTs should be treated with standard first line imatinib therapy.
dc.formatPrint-Electronic
dc.format.extent543 - 545
dc.languageeng
dc.language.isoeng
dc.subjectHumans
dc.subjectGastrointestinal Stromal Tumors
dc.subjectPrognosis
dc.subjectMutation
dc.subjectFemale
dc.subjectMale
dc.subjectImatinib Mesylate
dc.titlep.(L576P) -KIT mutation in GIST: Favorable prognosis and sensitive to imatinib?
dc.typeJournal Article
rioxxterms.funderThe Institute of Cancer Research
rioxxterms.identifier.projectUnspecified
rioxxterms.versionofrecord10.1080/15384047.2016.1156263
rioxxterms.licenseref.startdate2016-05
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfCancer biology & therapy
pubs.issue5
pubs.notes12 months
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/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Sarcoma Clinical Trials
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Sarcoma Clinical Trials (R Jones)
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Sarcoma Clinical Trials (R Jones)/Sarcoma Clinical Trials (R Jones) (hon.)
pubs.organisational-group/ICR/Primary Group/Royal Marsden Clinical Units
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/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Sarcoma Clinical Trials
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Sarcoma Clinical Trials (R Jones)
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Sarcoma Clinical Trials (R Jones)/Sarcoma Clinical Trials (R Jones) (hon.)
pubs.organisational-group/ICR/Primary Group/Royal Marsden Clinical Units
pubs.publication-statusPublished
pubs.volume17
pubs.embargo.terms12 months
icr.researchteamSarcoma Clinical Trials (R Jones)en_US
dc.contributor.icrauthorGonzalez de Castro, Daviden
dc.contributor.icrauthorJudson, Ianen
dc.contributor.icrauthorJones, Robinen
dc.contributor.icrauthorThway, Khinen


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