Please use this identifier to cite or link to this item: https://doi.org/10.1038/ncomms7999
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dc.titleChip-based analysis of exosomal mRNA mediating drug resistance in glioblastoma
dc.contributor.authorShao, H
dc.contributor.authorChung, J
dc.contributor.authorLee, K
dc.contributor.authorBalaj, L
dc.contributor.authorMin, C
dc.contributor.authorCarter, B.S
dc.contributor.authorHochberg, F.H
dc.contributor.authorBreakefield, X.O
dc.contributor.authorLee, H
dc.contributor.authorWeissleder, R
dc.date.accessioned2020-10-26T09:07:45Z
dc.date.available2020-10-26T09:07:45Z
dc.date.issued2015
dc.identifier.citationShao, H, Chung, J, Lee, K, Balaj, L, Min, C, Carter, B.S, Hochberg, F.H, Breakefield, X.O, Lee, H, Weissleder, R (2015). Chip-based analysis of exosomal mRNA mediating drug resistance in glioblastoma. Nature Communications 6 : 6999. ScholarBank@NUS Repository. https://doi.org/10.1038/ncomms7999
dc.identifier.issn2041-1723
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/180471
dc.description.abstractReal-time monitoring of drug efficacy in glioblastoma multiforme (GBM) is a major clinical problem as serial re-biopsy of primary tumours is often not a clinical option. MGMT (O 6 -methylguanine DNA methyltransferase) and APNG (alkylpurine-DNA-N-glycosylase) are key enzymes capable of repairing temozolomide-induced DNA damages and their levels in tissue are inversely related to treatment efficacy. Yet, serial clinical analysis remains difficult, and, when done, primarily relies on promoter methylation studies of tumour biopsy material at the time of initial surgery. Here we present a microfluidic chip to analyse mRNA levels of MGMT and APNG in enriched tumour exosomes obtained from blood. We show that exosomal mRNA levels of these enzymes correlate well with levels found in parental cells and that levels change considerably during treatment of seven patients. We propose that if validated on a larger cohort of patients, the method may be used to predict drug response in GBM patients.
dc.publisherNature Publishing Group
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectmessenger RNA
dc.subjectmethylated DNA protein cysteine methyltransferase
dc.subjectdacarbazine
dc.subjectmessenger RNA
dc.subjecttemozolomide
dc.subjecttumor marker
dc.subjectdisease treatment
dc.subjectdrug resistance
dc.subjectenzyme activity
dc.subjectgene expression
dc.subjectmethylation
dc.subjectRNA
dc.subjecttumor
dc.subjectArticle
dc.subjectblood brain barrier
dc.subjectcancer resistance
dc.subjectcell culture
dc.subjectcohort analysis
dc.subjectcontrolled study
dc.subjectDNA methylation
dc.subjectdrug efficacy
dc.subjectdrug response
dc.subjectexosome
dc.subjectgene product
dc.subjectglioblastoma
dc.subjecthuman
dc.subjecthuman cell
dc.subjectmethylation
dc.subjectmicrofluidics
dc.subjectpromoter region
dc.subjectradiotherapy
dc.subjectreverse transcription
dc.subjectRNA analysis
dc.subjectRNA extraction
dc.subjecttherapy
dc.subjecttreatment outcome
dc.subjecttreatment response
dc.subjecttumor biopsy
dc.subjectanalogs and derivatives
dc.subjectanimal
dc.subjectBrain Neoplasms
dc.subjectdrug effects
dc.subjectdrug resistance
dc.subjectfemale
dc.subjectgene expression profiling
dc.subjectgene expression regulation
dc.subjectgenetics
dc.subjectglioblastoma
dc.subjectimmunomagnetic separation
dc.subjectmetabolism
dc.subjectnude mouse
dc.subjectprocedures
dc.subjecttumor cell line
dc.subjectAnimals
dc.subjectBiomarkers, Tumor
dc.subjectBrain Neoplasms
dc.subjectCell Line, Tumor
dc.subjectDacarbazine
dc.subjectDrug Resistance, Neoplasm
dc.subjectExosomes
dc.subjectFemale
dc.subjectGene Expression Profiling
dc.subjectGene Expression Regulation, Neoplastic
dc.subjectGlioblastoma
dc.subjectHumans
dc.subjectImmunomagnetic Separation
dc.subjectMice, Nude
dc.subjectMicrofluidics
dc.subjectRNA, Messenger
dc.subjectTreatment Outcome
dc.typeArticle
dc.contributor.departmentBIOMEDICAL ENGINEERING
dc.description.doi10.1038/ncomms7999
dc.description.sourcetitleNature Communications
dc.description.volume6
dc.description.page6999
dc.published.statepublished
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