Please use this identifier to cite or link to this item: https://doi.org/10.18632/oncotarget.2194
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dc.titleThe NF1 gene revisited -from bench to bedside
dc.contributor.authorYap, Y.-S
dc.contributor.authorMcPherson, J.R
dc.contributor.authorOng, C.-K
dc.contributor.authorRozen, S.G
dc.contributor.authorTeh, B.-T
dc.contributor.authorLee, A.S.G
dc.contributor.authorCallen, D.F
dc.date.accessioned2020-09-09T02:57:58Z
dc.date.available2020-09-09T02:57:58Z
dc.date.issued2014
dc.identifier.citationYap, Y.-S, McPherson, J.R, Ong, C.-K, Rozen, S.G, Teh, B.-T, Lee, A.S.G, Callen, D.F (2014). The NF1 gene revisited -from bench to bedside. Oncotarget 5 (15) : 5873-5892. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.2194
dc.identifier.issn19492553
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/174999
dc.description.abstractNeurofibromatosis type 1 (NF1) is a relatively common tumour predisposition syndrome related to germline aberrations of NF1, a tumour suppressor gene. The gene product neurofibromin is a negative regulator of the Ras cellular proliferation pathway, and also exerts tumour suppression via other mechanisms. Recent next-generation sequencing projects have revealed somatic NF1 aberrations in various sporadic tumours. NF1 plays a critical role in a wide range of tumours. NF1 alterations appear to be associated with resistance to therapy and adverse outcomes in several tumour types. Identification of a patient's germline or somatic NF1 aberrations can be challenging, as NF1 is one of the largest human genes, with a myriad of possible mutations. Epigenetic factors may also also contribute to inadequate levels of neurofibromin in cancer cells. Clinical trials of NF1-based therapeutic approaches are currently limited. Preclinical studies on neurofibromin-deficient malignancies have mainly been on malignant peripheral nerve sheath tumour cell lines or xenografts derived from NF1 patients. However, the emerging recognition of the role of NF1 in sporadic cancers may lead to the development of NF1-based treatments for other tumour types. Improved understanding of the implications of NF1 aberrations is critical for the development of novel therapeutic strategies.
dc.publisherImpact Journals LLC
dc.sourceUnpaywall 20200831
dc.subject2 (2 chloro 4 iodoanilino) n cyclopropylmethoxy 3,4 difluorobenzamide
dc.subjectalisertib
dc.subjectalpha2a interferon
dc.subjecterlotinib
dc.subjecteverolimus
dc.subjectimatinib
dc.subjectisotretinoin
dc.subjectn (2,3 dihydroxypropoxy) 3,4 difluoro 2 (2 fluoro 4 iodoanilino)benzamide
dc.subjectneurofibromin
dc.subjectpirfenidone
dc.subjectplacebo
dc.subjectrapamycin
dc.subjectretaspimycin
dc.subjectselumetinib
dc.subjectsorafenib
dc.subjectthalidomide
dc.subjecttipifarnib
dc.subjectneurofibromin
dc.subjectarticle
dc.subjectbrain tumor
dc.subjectbreast tumor
dc.subjectcancer inhibition
dc.subjectcolorectal carcinoma
dc.subjectdown regulation
dc.subjectdrug potentiation
dc.subjectdrug targeting
dc.subjectepigenetics
dc.subjectgene deletion
dc.subjectgene mutation
dc.subjectgene sequence
dc.subjectgenetic association
dc.subjectgenetic procedures
dc.subjecthematologic malignancy
dc.subjecthuman
dc.subjectlung cancer
dc.subjectmalignant peripheral nerve sheath tumor
dc.subjectmelanoma
dc.subjectmolecular diagnosis
dc.subjectneurofibroma
dc.subjectneurofibromatosis
dc.subjectnext generation sequencing
dc.subjectNF1 gene
dc.subjectnonhuman
dc.subjectovary carcinoma
dc.subjectphase 1 clinical trial (topic)
dc.subjectphase 2 clinical trial (topic)
dc.subjectprotein function
dc.subjectsomatic mutation
dc.subjecttumor suppressor gene
dc.subjectanimal
dc.subjectgenetics
dc.subjectneoplasm
dc.subjecttumor suppressor gene
dc.subjectAnimals
dc.subjectGenes, Neurofibromatosis 1
dc.subjectHumans
dc.subjectNeoplasms
dc.subjectNeurofibromin 1
dc.typeArticle
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.contributor.departmentDEPT OF MICROBIOLOGY & IMMUNOLOGY
dc.description.doi10.18632/oncotarget.2194
dc.description.sourcetitleOncotarget
dc.description.volume5
dc.description.issue15
dc.description.page5873-5892
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