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dc.contributor.authorOchs, Michael F.
dc.contributor.authorGaykalova, Daria A.
dc.contributor.authorZizkova, Veronika
dc.contributor.authorGuo, Theresa
dc.contributor.authorTiscareno, Ilse
dc.contributor.authorWei, Yingying
dc.contributor.authorVatapalli, Rajita
dc.contributor.authorHennessey, Patrick T.
dc.contributor.authorAhn, Julie
dc.contributor.authorDanilova, Ludmila V.
dc.contributor.authorKhan, Zubair
dc.contributor.authorBishop, Justin A.
dc.contributor.authorGutkind, J. Silvio
dc.contributor.authorKoch, Wayne M.
dc.contributor.authorWestra, William H.
dc.contributor.authorFertig, Elana J.
dc.contributor.authorCalifano, Joseph A.
dc.date.accessioned2018-04-21T14:23:08Z
dc.date.available2018-04-21T14:23:08Z
dc.date.issued2017
dc.identifier.citationGaykalova, D. A., Zizkova, V., Guo, T., Tiscareno, I., Vatapalli, R., Hennessey, P. T., & ... Gutkind, J. S. (n.d). Integrative computational analysis of transcriptional and epigenetic alterations implicates DTX1 as a putative tumor suppressor gene in HNSCC. Oncotarget, 8(9), 15349-15363.en_US
dc.identifier.urihttps://dx.doi.org/10.18632/oncotarget.14856
dc.description.abstractOver a half million new cases of Head and Neck Squamous Cell Carcinoma (HNSCC) are diagnosed annually worldwide, however, 5 year overall survival is only 50% for HNSCC patients. Recently, high throughput technologies have accelerated the genome-wide characterization of HNSCC. However, comprehensive pipelines with statistical algorithms that account for HNSCC biology and perform independent confirmatory and functional validation of candidates are needed to identify the most biologically relevant genes. We applied outlier statistics to high throughput gene expression data, and identified 76 top-scoring candidates with significant differential expression in tumors compared to normal tissues. We identified 15 epigenetically regulated candidates by focusing on a subset of the genes with a negative correlation between gene expression and promoter methylation. Differential expression and methylation of 3 selected candidates (BANK1, BIN2, and DTX1) were confirmed in an independent HNSCC cohorts from Johns Hopkins and TCGA (The Cancer Genome Atlas). We further performed functional evaluation of NOTCH regulator, DTX1, which was downregulated by promoter hypermethylation in tumors, and demonstrated that decreased expression of DTX1 in HNSCC tumors maybe associated with NOTCH pathway activation and increased migration potential.en_US
dc.language.isoen_USen_US
dc.publisherImpact Journalsen_US
dc.subjectHNSCCen_US
dc.subjectDTX1en_US
dc.subjectexpressionen_US
dc.subjectmethylationen_US
dc.subjectintegrationen_US
dc.titleIntegrative computational analysis of transcriptional and epigenetic alterations implicates DTX1 as a putative tumor suppressor gene in HNSCCen_US
dc.typeArticleen_US
dc.typeTexten_US
prism.publicationNameOncotarget
prism.volume8
prism.issueIdentifier9
prism.publicationDate2017
prism.startingPage15349
prism.endingPage15363
dc.identifier.handlehttps://dr.tcnj.edu/handle/2900/2276


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