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dc.contributor.author허정원*
dc.contributor.author문영철*
dc.date.accessioned2016-08-28T12:08:39Z-
dc.date.available2016-08-28T12:08:39Z-
dc.date.issued2011*
dc.identifier.issn0732-183X*
dc.identifier.otherOAK-8261*
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/222186-
dc.description.abstractPurpose: This study attempted to analyze the prognostic role of single nucleotide polymorphism array (SNP-A) -based karyotying in 133 patients with acute myeloid leukemia with normal karyotype (AML-NK), which presents with diverse clinical outcomes, thus requiring further stratification of patient subgroups according to their prognoses. Patients and Methods: A total of 133 patients with AML-NK confirmed by metaphase cytogenetics (MC) and fluorescent in situ hybridization analysis were included in this study. Analysis by Genome-Wide Human SNP 6.0 Array was performed by using DNAs derived from marrow samples at diagnosis. Results: Forty-three patients (32.3%) had at least one abnormal SNP lesion that was not detected by MC. One hundred thirteen abnormal SNP lesions included 55 losses, 23 gains, and 35 copy-neutral losses of heterozygosity. Multivariate analyses showed that detection of abnormal SNP lesions by SNP-A karyotyping results in an unfavorable prognostic value for overall survival (hazard ratio [HR], 2.69; 95% CI, 1.50 to 4.82; P = .001); other significant prognostic factors included secondary AML (HR, 5.55; 95% CI, 1.80 to 17.14; P = .003), presence of the FLT3 mutation (HR, 3.17; 95% CI, 1.71 to 5.87; P < .001), and age (HR, 1.03; 95% CI, 1.01 to 1.05; P = .020). Conclusion: Our data demonstrated that abnormal SNP lesions detected by SNP-A karyotyping might indicate an adverse prognosis in patients with AML-NK, thus requiring a more sophisticated treatment strategy for improvement of treatment outcomes. © 2011 by American Society of Clinical Oncology.*
dc.languageEnglish*
dc.titleAdverse prognostic impact of abnormal lesions detected by genome-wide single nucleotide polymorphism array-based karyotyping analysis in acute myeloid leukemia with normal karyotype*
dc.typeArticle*
dc.relation.issue35*
dc.relation.volume29*
dc.relation.indexSCI*
dc.relation.indexSCIE*
dc.relation.indexSCOPUS*
dc.relation.startpage4702*
dc.relation.lastpage4708*
dc.relation.journaltitleJournal of Clinical Oncology*
dc.identifier.doi10.1200/JCO.2011.35.5719*
dc.identifier.wosidWOS:000298141700025*
dc.identifier.scopusid2-s2.0-83255164849*
dc.author.googleYi J.H.*
dc.author.googleHuh J.*
dc.author.googleKim H.-J.*
dc.author.googleKim S.-H.*
dc.author.googleKim Y.-K.*
dc.author.googleSohn S.K.*
dc.author.googleMoon J.H.*
dc.author.googleKim S.H.*
dc.author.googleKim K.H.*
dc.author.googleWon J.H.*
dc.author.googleMun Y.C.*
dc.author.googleKim H.*
dc.author.googlePark J.*
dc.author.googleJung C.W.*
dc.author.googleKim D.H.*
dc.contributor.scopusid허정원(7102258576)*
dc.contributor.scopusid문영철(7003363716)*
dc.date.modifydate20240422115947*
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의과대학 > 의학과 > Journal papers
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