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Ethnic delineation of primary glioblastoma genome

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dc.contributor.authorKoo, Harim-
dc.contributor.authorChoi, Seung Won-
dc.contributor.authorCho, Hee Jin-
dc.contributor.authorLee, In-Hee-
dc.contributor.authorKong, Doo-Sik-
dc.contributor.authorSeol, Ho Jun-
dc.contributor.authorLee, Jung-Il-
dc.contributor.authorChoi, Jung-Won-
dc.contributor.authorSa, Jason K.-
dc.contributor.authorNam, Do-Hyun-
dc.date.accessioned2021-08-30T12:56:00Z-
dc.date.available2021-08-30T12:56:00Z-
dc.date.created2021-06-19-
dc.date.issued2020-10-
dc.identifier.issn2045-7634-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/52608-
dc.description.abstractGlioblastoma (GBM) is the most malignant primary brain tumor in adults with substantial genomic alterations. The median survival is approximately 14.6 months, despite aggressive therapeutic intervention, which comprised of surgical resection, radiotherapy, and chemotherapy. Recent studies on cancer genomic have revealed crucial insights into dynamic molecular subgroups within GBM, which govern distinct clinical response and sensitivity of each individual to therapy. In the present study, we analyzed genomic composition of primary GBMs between two ethnic groups [IRCR (Institute of Refractory Cancer Research), and TCGA (The Cancer Genome Atlats)] to explore genomic and molecular features that constitute malignant behavior of glioblastoma based on distinct ethnicity. We identified enrichments of MAPK and p53 pathways in IRCR patients, while aberrant activation of Receptor Tyrosine Kinases (RTKs) were predominant in TCGA cohort. We also discovered differential clinical prognosis between two groups and explored essential features that present such diversity.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherWILEY-
dc.subjectMUTATIONS-
dc.subjectLANDSCAPE-
dc.subjectIDH1-
dc.subjectEGFR-
dc.subjectPROGRESSION-
dc.subjectEVOLUTION-
dc.subjectPATHWAYS-
dc.subjectSUBTYPES-
dc.subjectPDGFRA-
dc.subjectTUMORS-
dc.titleEthnic delineation of primary glioblastoma genome-
dc.typeArticle-
dc.contributor.affiliatedAuthorSa, Jason K.-
dc.identifier.doi10.1002/cam4.3370-
dc.identifier.scopusid2-s2.0-85089362101-
dc.identifier.wosid000559451100001-
dc.identifier.bibliographicCitationCANCER MEDICINE, v.9, no.19, pp.7352 - 7359-
dc.relation.isPartOfCANCER MEDICINE-
dc.citation.titleCANCER MEDICINE-
dc.citation.volume9-
dc.citation.number19-
dc.citation.startPage7352-
dc.citation.endPage7359-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaOncology-
dc.relation.journalWebOfScienceCategoryOncology-
dc.subject.keywordPlusMUTATIONS-
dc.subject.keywordPlusLANDSCAPE-
dc.subject.keywordPlusIDH1-
dc.subject.keywordPlusEGFR-
dc.subject.keywordPlusPROGRESSION-
dc.subject.keywordPlusEVOLUTION-
dc.subject.keywordPlusPATHWAYS-
dc.subject.keywordPlusSUBTYPES-
dc.subject.keywordPlusPDGFRA-
dc.subject.keywordPlusTUMORS-
dc.subject.keywordAuthorethnic-
dc.subject.keywordAuthorgenetics-
dc.subject.keywordAuthorgenomics-
dc.subject.keywordAuthorglioblastoma-
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