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Association of MGMT Gene Promoter Methylation With Clinicopathological Parameters in Patients With Wild-type IDH Glioblastoma

DC Field Value Language
dc.contributor.author김세훈-
dc.contributor.author유지환-
dc.contributor.author장종희-
dc.date.accessioned2022-03-11T05:55:02Z-
dc.date.available2022-03-11T05:55:02Z-
dc.date.issued2022-01-
dc.identifier.issn0250-7005-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/187862-
dc.description.abstractBackground: The methylation status of the O6-methylguanine-DNA methyltransferase (MGMT) promoter plays a key role in response to temozolomide chemotherapy and disease prognosis in patients with wild-type isocitrate dehydrogenase (IDH) glioblastoma (GBM). Patients and methods: The MGMT promoter methylation status and its association with clinicopathological parameters were retrospectively analysed in a cohort of 316 patients with GBM with wild-type IDH. Results: MGMT methylation was significantly associated with ATRX chromatin remodeler (ATRX) loss and completion of the standard Stupp protocol. The median durations of overall and progression-free survival for the unmethylated, low-methylated (10-39%), and hypermethylated (≥40%) groups were 15, 23, and 30 months and 11, 18, and 21 months, respectively. However, the improvement in the survival of the hypermethylated group was not statistically significant. Conclusion: We suggest a possible association between MGMT methylation status and ATRX mutations in GBM with wild-type IDH.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherInternational Institute of Anticancer Research-
dc.relation.isPartOfANTICANCER RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleAssociation of MGMT Gene Promoter Methylation With Clinicopathological Parameters in Patients With Wild-type IDH Glioblastoma-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pathology (병리학교실)-
dc.contributor.googleauthorMoonsik Kim-
dc.contributor.googleauthorJihwan Yoo-
dc.contributor.googleauthorJong Hee Chang-
dc.contributor.googleauthorSe Hoon Kim-
dc.identifier.doi10.21873/anticanres.15490-
dc.contributor.localIdA00610-
dc.contributor.localIdA05158-
dc.contributor.localIdA03470-
dc.relation.journalcodeJ00188-
dc.identifier.eissn1791-7530-
dc.identifier.pmid34969742-
dc.identifier.urlhttps://ar.iiarjournals.org/content/42/1/335.long-
dc.subject.keywordATRX loss-
dc.subject.keywordMGMT-
dc.subject.keywordglioblastoma-
dc.subject.keywordhypermethylation-
dc.subject.keywordlow methylation-
dc.subject.keywordmethylation status-
dc.subject.keywordtemozolomide chemotherapy-
dc.subject.keywordwild-type IDH-
dc.contributor.alternativeNameKim, Se Hoon-
dc.contributor.affiliatedAuthor김세훈-
dc.contributor.affiliatedAuthor유지환-
dc.contributor.affiliatedAuthor장종희-
dc.citation.volume42-
dc.citation.number1-
dc.citation.startPage335-
dc.citation.endPage341-
dc.identifier.bibliographicCitationANTICANCER RESEARCH, Vol.42(1) : 335-341, 2022-01-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurosurgery (신경외과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers

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