Clinical significance of genetic aberrations in secondary acute myeloid leukemia

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F12%3A00060868" target="_blank" >RIV/00216224:14110/12:00060868 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/65269705:_____/12:#0001872

Výsledek na webu

<a href="http://dx.doi.org/10.1002/ajh.23309" target="_blank" >http://dx.doi.org/10.1002/ajh.23309</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1002/ajh.23309" target="_blank" >10.1002/ajh.23309</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Clinical significance of genetic aberrations in secondary acute myeloid leukemia

Popis výsledku v původním jazyce

The study aimed to identify genetic lesions associated with secondary acute myeloid leukemia (sAML) in AQ1 comparison with AML arising de novo (dnAML) and assess their impact on patients? overall survival (OS). Genes TP53, AQ2 RUNX1, CBL, IDH1/2, NRAS, NPM1, and FLT3 were analyzed for mutations in all patients. We identified 36 recurrent cytogenetic aberrations (more than five events). Mutations in TP53, 9pUPD, and del7q were significantly associated with sAML, while NPM1 and FLT3 mutations associated with dnAML. Patients with sAML carrying TP53 mutations demonstrated lower 1-year OS rate than those with wild-type TP53 while complex karyotype, del7q (CUX1) and del7p (IKZF1) showed no significant effect on OS. Multivariate analysis confirmed that mutantTP53 was the only independent adverse prognostic factor for OS in sAML (hazard ratio 2.67; 95% CI: 1.33?5.37; P 5 0.006). Patients with dnAML and complex karyotype carried sAML-associated defects (TP53 defects in 54.

Název v anglickém jazyce

Clinical significance of genetic aberrations in secondary acute myeloid leukemia

Popis výsledku anglicky

The study aimed to identify genetic lesions associated with secondary acute myeloid leukemia (sAML) in AQ1 comparison with AML arising de novo (dnAML) and assess their impact on patients? overall survival (OS). Genes TP53, AQ2 RUNX1, CBL, IDH1/2, NRAS, NPM1, and FLT3 were analyzed for mutations in all patients. We identified 36 recurrent cytogenetic aberrations (more than five events). Mutations in TP53, 9pUPD, and del7q were significantly associated with sAML, while NPM1 and FLT3 mutations associated with dnAML. Patients with sAML carrying TP53 mutations demonstrated lower 1-year OS rate than those with wild-type TP53 while complex karyotype, del7q (CUX1) and del7p (IKZF1) showed no significant effect on OS. Multivariate analysis confirmed that mutantTP53 was the only independent adverse prognostic factor for OS in sAML (hazard ratio 2.67; 95% CI: 1.33?5.37; P 5 0.006). Patients with dnAML and complex karyotype carried sAML-associated defects (TP53 defects in 54.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FD - Onkologie a hematologie

OECD FORD obor

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Projekt

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Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2012

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

American Journal of Hematology

ISSN

0361-8609

e-ISSN

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Svazek periodika

87

Číslo periodika v rámci svazku

11

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

7

Strana od-do

1010-1016

Kód UT WoS článku

000310246100013

EID výsledku v databázi Scopus

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