{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1361699996083994880.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1182/blood.v97.1.89"}},{"identifier":{"@type":"URI","@value":"http://ashpublications.org/blood/article-pdf/97/1/89/1670662/89.pdf"}},{"identifier":{"@type":"NAID","@value":"30022492666"}}],"dc:title":[{"@value":"Prevalence and prognostic significance of Flt3 internal tandem duplication in pediatric acute myeloid leukemia"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>Abstract</jats:title><jats:p>The Flt3 gene encodes a tyrosine kinase receptor that regulates proliferation and differentiation of hematopoietic stem cells. An internal tandem duplication of the Flt3 gene (Flt3/ITD) has been reported in acute myelogenous leukemia (AML) and may be associated with poor prognosis. We analyzed diagnostic bone marrow specimens from 91 pediatric patients with AML treated on Children's Cancer Group (CCG)-2891 for the presence of the Flt3/ITD and correlated its presence with clinical outcome. Fifteen of 91 samples (16.5%) were positive for the Flt3/ITD. Flt3/ITD-positive patients had a median diagnostic white count of 73 800 compared with 28 400 for the Flt3/ITD-negative patients (P = .05). The size of the duplication ranged from 21 to 174 base pairs (bp). Nucleotide sequencing of the abnormal polymerase chain reaction products demonstrated that all duplications involved exon 11 of theFlt3 gene and also preserved the reading frame. Lineage restriction analysis revealed that Flt3/ITD was not present in the lymphocytes, suggesting a lack of stem cell involvement for this mutation. None of the Flt3/ITD-positive patients had unfavorable cytogenetic markers, and there was no predominance of a particular FAB class. The remission induction rate was 40% in Flt3/ITD-positive patients compared with 74% in Flt3/ITD-negative ones (P = .005). The Kaplan-Meier estimates of event-free survival at 8 years for patients with and without Flt3/ITD were 7% and 44%, respectively (P = .002). Multivariate analysis demonstrated that presence of the Flt3/ITD was the single most significant, independent prognostic factor for poor outcome (P = .009) in pediatric AML.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1381699996083994882","@type":"Researcher","foaf:name":[{"@value":"Soheil Meshinchi"}],"jpcoar:affiliationName":[{"@value":"From The Fred Hutchinson Cancer Research Center, and University of Washington Medical Center, Seattle, WA; South Carolina Cancer Center, Columbia, SC; University of Southern California School of Medicine, Los Angeles, CA; National Childhood Cancer Foundation, Arcadia, CA; and Children's Cancer Group, Pasadena, CA."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996083994883","@type":"Researcher","foaf:name":[{"@value":"William G. Woods"}],"jpcoar:affiliationName":[{"@value":"From The Fred Hutchinson Cancer Research Center, and University of Washington Medical Center, Seattle, WA; South Carolina Cancer Center, Columbia, SC; University of Southern California School of Medicine, Los Angeles, CA; National Childhood Cancer Foundation, Arcadia, CA; and Children's Cancer Group, Pasadena, CA."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996083994880","@type":"Researcher","foaf:name":[{"@value":"Derek L. Stirewalt"}],"jpcoar:affiliationName":[{"@value":"From The Fred Hutchinson Cancer Research Center, and University of Washington Medical Center, Seattle, WA; South Carolina Cancer Center, Columbia, SC; University of Southern California School of Medicine, Los Angeles, CA; National Childhood Cancer Foundation, Arcadia, CA; and Children's Cancer Group, Pasadena, CA."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996083995008","@type":"Researcher","foaf:name":[{"@value":"David A. Sweetser"}],"jpcoar:affiliationName":[{"@value":"From The Fred Hutchinson Cancer Research Center, and University of Washington Medical Center, Seattle, WA; South Carolina Cancer Center, Columbia, SC; University of Southern California School of Medicine, Los Angeles, CA; National Childhood Cancer Foundation, Arcadia, CA; and Children's Cancer Group, Pasadena, CA."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996083994884","@type":"Researcher","foaf:name":[{"@value":"Jonathan D. Buckley"}],"jpcoar:affiliationName":[{"@value":"From The Fred Hutchinson Cancer Research Center, and University of Washington Medical Center, Seattle, WA; South Carolina Cancer Center, Columbia, SC; University of Southern California School of Medicine, Los Angeles, CA; National Childhood Cancer Foundation, Arcadia, CA; and Children's Cancer Group, Pasadena, CA."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996083994885","@type":"Researcher","foaf:name":[{"@value":"Thomas K. Tjoa"}],"jpcoar:affiliationName":[{"@value":"From The Fred Hutchinson Cancer Research Center, and University of Washington Medical Center, Seattle, WA; South Carolina Cancer Center, Columbia, SC; University of Southern California School of Medicine, Los Angeles, CA; National Childhood Cancer Foundation, Arcadia, CA; and Children's Cancer Group, Pasadena, CA."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996083994881","@type":"Researcher","foaf:name":[{"@value":"Irwin D. Bernstein"}],"jpcoar:affiliationName":[{"@value":"From The Fred Hutchinson Cancer Research Center, and University of Washington Medical Center, Seattle, WA; South Carolina Cancer Center, Columbia, SC; University of Southern California School of Medicine, Los Angeles, CA; National Childhood Cancer Foundation, Arcadia, CA; and Children's Cancer Group, Pasadena, CA."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699996083994886","@type":"Researcher","foaf:name":[{"@value":"Jerald P. Radich"}],"jpcoar:affiliationName":[{"@value":"From The Fred Hutchinson Cancer Research Center, and University of Washington Medical Center, Seattle, WA; South Carolina Cancer Center, Columbia, SC; University of Southern California School of Medicine, Los Angeles, CA; National Childhood Cancer Foundation, Arcadia, CA; and Children's Cancer Group, Pasadena, CA."}]}],"publication":{"publicationIdentifier":[{"@type":"EISSN","@value":"15280020"},{"@type":"PISSN","@value":"00064971"}],"prism:publicationName":[{"@value":"Blood"}],"dc:publisher":[{"@value":"American Society of Hematology"}],"prism:publicationDate":"2001-01-01","prism:volume":"97","prism:number":"1","prism:startingPage":"89","prism:endingPage":"94"},"reviewed":"false","url":[{"@id":"http://ashpublications.org/blood/article-pdf/97/1/89/1670662/89.pdf"}],"createdAt":"2002-07-27","modifiedAt":"2024-12-09","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050282810812299392","@type":"Article","resourceType":"学術雑誌論文(journal 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Disorders"},{"@value":"小児造血器疾患におけるチロシンキナーゼの臨床的意義とその阻害剤による治療"}]},{"@id":"https://cir.nii.ac.jp/crid/1390282680007614720","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isCitedBy"],"jpcoar:relatedTitle":[{"@language":"ja","@value":"小児白血病発症の分子機構"},{"@value":"教育講演 小児白血病発症の分子機構"},{"@language":"ja-Kana","@value":"キョウイク コウエン ショウニ ハッケツビョウ ハッショウ ノ ブンシ キコウ"},{"@language":"en","@value":"[Mechanism of molecular leukemogenesis in childhood leukemia]."}]},{"@id":"https://cir.nii.ac.jp/crid/1390282680009670656","@type":"Article","relationType":["isCitedBy"],"jpcoar:relatedTitle":[{"@language":"ja","@value":"FLT3分子を標的とした白血病治療の可能性"},{"@language":"ja-Kana","@value":"FLT3 ブンシ オ ヒョウテキ ト シタ ハッケツビョウ チリョウ ノ カノウセイ"}]},{"@id":"https://cir.nii.ac.jp/crid/1570291225084395648","@type":"Article","relationType":["isCitedBy"],"jpcoar:relatedTitle":[{"@language":"ja","@value":"急性骨髄性白血病における遺伝子異常と予後"},{"@language":"en","@value":"Correlation between Aberrations of Genes and Prognosis in Pediatric Acute Myeloid Leukemia"}]},{"@id":"https://cir.nii.ac.jp/crid/1570854175245976448","@type":"Article","relationType":["isCitedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Biology, Clinical Relevance, and Molecularly Targeted Therapy in Acute Leukemia with FLT3 Mutation"}]},{"@id":"https://cir.nii.ac.jp/crid/1573668924810347392","@type":"Article","relationType":["isCitedBy"],"jpcoar:relatedTitle":[{"@language":"ja","@value":"cDNA array を用いた浸潤性乳管癌における遺伝子発現解析"}]},{"@id":"https://cir.nii.ac.jp/crid/1573950399608157952","@type":"Article","relationType":["isCitedBy"],"jpcoar:relatedTitle":[{"@language":"ja","@value":"小児白血病の予後因子 : 新しい展開"},{"@language":"en","@value":"Prognostic factors in Children with Acute Leukemia:Recent 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