Prospective analysis of low-level BCR-ABL1 T315I mutation in CD34+ cells of patients with de novo chronic myeloid leukemia

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F14%3A00078457" target="_blank" >RIV/00216224:14110/14:00078457 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/65269705:_____/14:00061685

Výsledek na webu

<a href="http://dx.doi.org/10.3109/10428194.2013.842988" target="_blank" >http://dx.doi.org/10.3109/10428194.2013.842988</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3109/10428194.2013.842988" target="_blank" >10.3109/10428194.2013.842988</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Prospective analysis of low-level BCR-ABL1 T315I mutation in CD34+ cells of patients with de novo chronic myeloid leukemia

Popis výsledku v původním jazyce

Th e detection of BCR ? ABL1 kinase domain (KD) mutations is frequently associated with resistance to tyrosine kinase inhibitors (TKIs), which results in an impaired prognosis for patients with chronic myeloid leukemia (CML) [1]. Early detection of thesemutations can potentially lead to early therapeutic intervention and optimization of an ongoing treatment strategy. Considering the hematopoiesis hierar- chy, it is expected that BCR ? ABL1 mutation clones expand directly from hematopoietic stem cells or early progenitor cells [2]. It has already been reported that BCR ? ABL1 KD mutations were detected in these cells before they occurred in bone marrow (BM) or peripheral blood (PB) [3]. Particu- lar focus should be given to the T315I mutation, which isresistant to all approved TKIs (imatinib, nilotinib and dasa- tinib) [4,5], meaning that early detection of this key BCR ? ABL1 KD mutation in ? source ? cells could have potential clinical benefits.

Název v anglickém jazyce

Prospective analysis of low-level BCR-ABL1 T315I mutation in CD34+ cells of patients with de novo chronic myeloid leukemia

Popis výsledku anglicky

Th e detection of BCR ? ABL1 kinase domain (KD) mutations is frequently associated with resistance to tyrosine kinase inhibitors (TKIs), which results in an impaired prognosis for patients with chronic myeloid leukemia (CML) [1]. Early detection of thesemutations can potentially lead to early therapeutic intervention and optimization of an ongoing treatment strategy. Considering the hematopoiesis hierar- chy, it is expected that BCR ? ABL1 mutation clones expand directly from hematopoietic stem cells or early progenitor cells [2]. It has already been reported that BCR ? ABL1 KD mutations were detected in these cells before they occurred in bone marrow (BM) or peripheral blood (PB) [3]. Particu- lar focus should be given to the T315I mutation, which isresistant to all approved TKIs (imatinib, nilotinib and dasa- tinib) [4,5], meaning that early detection of this key BCR ? ABL1 KD mutation in ? source ? cells could have potential clinical benefits.

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

8

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

3

Strana od-do

1915-1917

Kód UT WoS článku

000340224100035

EID výsledku v databázi Scopus

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