Pathogenetic role of ETV6 fusion gene in leukemic transformation of myelodysplastic syndrome refractory anemia with excess blasts-1 with a new, rare translocation t(11;19)(q24.3;q13.12) and insertion ins(6;12)(p22.3p13)

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F14%3A33145790" target="_blank" >RIV/61989592:15110/14:33145790 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00098892:_____/14:#0000661

Výsledek na webu

<a href="http://dx.doi.org/10.3109/10428194.2013.814127" target="_blank" >http://dx.doi.org/10.3109/10428194.2013.814127</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3109/10428194.2013.814127" target="_blank" >10.3109/10428194.2013.814127</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Pathogenetic role of ETV6 fusion gene in leukemic transformation of myelodysplastic syndrome refractory anemia with excess blasts-1 with a new, rare translocation t(11;19)(q24.3;q13.12) and insertion ins(6;12)(p22.3p13)

Popis výsledku v původním jazyce

Myelodysplastic syndrome (MDS) refers to a group of clonal disorders originating from hematopoietic stem cells, and is characterized by ineff ective diff erentiation of hematopoietic progenitors, bone marrow dysplasia, genetic instability and, often, a propensity to develop acute myeloid leukemia (AML). Th e molecular pathogenesis of MDS and the main cause for its progression to AML remain largely undefi ned. Early mutations in stem cells may cause diff erentiation arrest, leading to dysplasia, whereassubsequent defects aff ecting myeloid cell proliferation may cause the clonal expansion of aberrant cells and frank AML [1]. Although many chromosomal abnormalities have been detected in MDS, the genes involved in the pathogenesis have yet to be identified. According to a recently published new scoring system proposal, a total of fi ve prognostic subgroups were confi rmed, with 19 cytogenetic categories being defi ned [2]. With the exception of a complex karyotype, all detected chromoso

Název v anglickém jazyce

Pathogenetic role of ETV6 fusion gene in leukemic transformation of myelodysplastic syndrome refractory anemia with excess blasts-1 with a new, rare translocation t(11;19)(q24.3;q13.12) and insertion ins(6;12)(p22.3p13)

Popis výsledku anglicky

Myelodysplastic syndrome (MDS) refers to a group of clonal disorders originating from hematopoietic stem cells, and is characterized by ineff ective diff erentiation of hematopoietic progenitors, bone marrow dysplasia, genetic instability and, often, a propensity to develop acute myeloid leukemia (AML). Th e molecular pathogenesis of MDS and the main cause for its progression to AML remain largely undefi ned. Early mutations in stem cells may cause diff erentiation arrest, leading to dysplasia, whereassubsequent defects aff ecting myeloid cell proliferation may cause the clonal expansion of aberrant cells and frank AML [1]. Although many chromosomal abnormalities have been detected in MDS, the genes involved in the pathogenesis have yet to be identified. According to a recently published new scoring system proposal, a total of fi ve prognostic subgroups were confi rmed, with 19 cytogenetic categories being defi ned [2]. With the exception of a complex karyotype, all detected chromoso

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

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2014

Kód důvěrnosti údajů

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

Název periodika

Leukemia & Lymphoma

ISSN

1042-8194

e-ISSN

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Svazek periodika

55

Číslo periodika v rámci svazku

4

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

4

Strana od-do

950-953

Kód UT WoS článku

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EID výsledku v databázi Scopus

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