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Statements

Subject Item
n2:RIV%2F00064203%3A_____%2F11%3A7050%21RIV12-MZ0-00064203
rdf:type
n12:Vysledek skos:Concept
rdfs:seeAlso
http://www.ncbi.nlm.nih.gov/pubmed/21551233
dcterms:description
We previously demonstrated that outcome of pediatric 11q23/MLL-rearranged AML depends on the translocation partner (TP). In this multicenter international study on 733 children with 11q23/MLL-rearranged AML, we further analyzed which additional cytogenetic aberrations (ACA) had prognostic significance. ACAs occurred in 344 (47%) of 733 and were associated with unfavorable outcome (5-year overall survival [OS] 47% vs 62%, P < .001). Trisomy 8, the most frequent specificACA(n = 130/344, 38%), independently predicted favorable outcome within the ACAs group (OS 61% vs 39%, P = .003; Cox model for OS hazard ratio (HR) 0.54, P = .03), on the basis of reduced relapse rate (26% vs 49%, P < .001). Trisomy 19 (n = 37/344, 11%) independently predicted poor prognosis in ACAs cases, which was partly caused by refractory disease (remission rate 74% vs 89%, P = .04; OS 24% vs 50%, P < .001; HR 1.77, P = .01). Structural ACAs had independent adverse prognostic value for event-free survival (HR 1.36, P = .01). Complex karyotype, defined as >= 3 abnormalities, was present in 26% (n = 192/733) and showed worse outcome than those without complex karyotype (OS 45% vs 59%, P = .003) in univariate analysis only. In conclusion, like TP, specific ACAs have independent prognostic significance in pediatric 11q23/MLL-rearranged AML, and the mechanism underlying these prognostic differences should be studied. (Blood. 2011;117(26):7102-7111) We previously demonstrated that outcome of pediatric 11q23/MLL-rearranged AML depends on the translocation partner (TP). In this multicenter international study on 733 children with 11q23/MLL-rearranged AML, we further analyzed which additional cytogenetic aberrations (ACA) had prognostic significance. ACAs occurred in 344 (47%) of 733 and were associated with unfavorable outcome (5-year overall survival [OS] 47% vs 62%, P < .001). Trisomy 8, the most frequent specificACA(n = 130/344, 38%), independently predicted favorable outcome within the ACAs group (OS 61% vs 39%, P = .003; Cox model for OS hazard ratio (HR) 0.54, P = .03), on the basis of reduced relapse rate (26% vs 49%, P < .001). Trisomy 19 (n = 37/344, 11%) independently predicted poor prognosis in ACAs cases, which was partly caused by refractory disease (remission rate 74% vs 89%, P = .04; OS 24% vs 50%, P < .001; HR 1.77, P = .01). Structural ACAs had independent adverse prognostic value for event-free survival (HR 1.36, P = .01). Complex karyotype, defined as >= 3 abnormalities, was present in 26% (n = 192/733) and showed worse outcome than those without complex karyotype (OS 45% vs 59%, P = .003) in univariate analysis only. In conclusion, like TP, specific ACAs have independent prognostic significance in pediatric 11q23/MLL-rearranged AML, and the mechanism underlying these prognostic differences should be studied. (Blood. 2011;117(26):7102-7111)
dcterms:title
Prognostic significance of additional cytogenetic aberrations in 733 de novo pediatric 11q23/MLL-rearranged AML patients: results of an international study Prognostic significance of additional cytogenetic aberrations in 733 de novo pediatric 11q23/MLL-rearranged AML patients: results of an international study
skos:prefLabel
Prognostic significance of additional cytogenetic aberrations in 733 de novo pediatric 11q23/MLL-rearranged AML patients: results of an international study Prognostic significance of additional cytogenetic aberrations in 733 de novo pediatric 11q23/MLL-rearranged AML patients: results of an international study
skos:notation
RIV/00064203:_____/11:7050!RIV12-MZ0-00064203
n12:predkladatel
n13:ico%3A00064203
n4:aktivita
n9:I n9:V
n4:aktivity
I, V
n4:cisloPeriodika
26
n4:dodaniDat
n14:2012
n4:domaciTvurceVysledku
n7:4977939
n4:druhVysledku
n5:J
n4:duvernostUdaju
n17:S
n4:entitaPredkladatele
n11:predkladatel
n4:idSjednocenehoVysledku
224378
n4:idVysledku
RIV/00064203:_____/11:7050
n4:jazykVysledku
n15:eng
n4:klicovaSlova
acute myeloid-leukemia; acute myeloblastic-leukemia; oncology-group; myelodysplastic syndrome; complex karyotype; up-regulation; childrens-cancer; poor-prognosis; gene-mutations; trials
n4:klicoveSlovo
n6:myelodysplastic%20syndrome n6:gene-mutations n6:acute%20myeloid-leukemia n6:trials n6:oncology-group n6:up-regulation n6:acute%20myeloblastic-leukemia n6:complex%20karyotype n6:childrens-cancer n6:poor-prognosis
n4:kodStatuVydavatele
US - Spojené státy americké
n4:kontrolniKodProRIV
[0EE4076B9DBA]
n4:nazevZdroje
Blood
n4:obor
n18:FD
n4:pocetDomacichTvurcuVysledku
1
n4:pocetTvurcuVysledku
34
n4:rokUplatneniVysledku
n14:2011
n4:svazekPeriodika
117
n4:tvurceVysledku
Rubnitz, J. E Perot, C. Harrison, CJ Chang, M. Pieters, R. Beverloo, H. B. Kaspers, GJL Alonzo, TA Tomizawa, D. Forestier, E. Dworzak, MN Gibson, B. Starý, Jan Raimondi, SC Lo Nigro, L. Hasle, H. Strehl, S. Morimoto, A. Reinhardt, D. Zimmermann, M. Taga, T. Zwaan, CM Smith, FO Creutzig, U. Auvrignon, A. Coenen, E. A. Stasevich, I. Harbott, J. Webb, D. Zemanová, Z. Litvinko, N. Leszl, A. van den Heuvel-Eibrink, MM Heerema, NA
n4:wos
000292244000019
s:issn
0006-4971
s:numberOfPages
10