Analysis of gene expression in CD26 CML leukemic stem cell population

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F65269705%3A_____%2F19%3A00071828" target="_blank" >RIV/65269705:_____/19:00071828 - isvavai.cz</a>

Výsledek na webu

<a href="https://dev18-admin.morbo.puxdesign.cz/Amca-CSAC/media/content/2019/book-of-abstracts-CSAC2019.pdf" target="_blank" >https://dev18-admin.morbo.puxdesign.cz/Amca-CSAC/media/content/2019/book-of-abstracts-CSAC2019.pdf</a>

DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Analysis of gene expression in CD26 CML leukemic stem cell population

Popis výsledku v původním jazyce

Nowadays, chronic myeloid leukemia (CML) has become a well manageable disease and majority of the patients achieve remission on tyrosine kinase inhibitor (TKI) treatment. However, the disease usually shows a low-level persistence during therapy that arises from putative leukemic stem cells (LSC), which are, despite BCR-ABL1 positivity, resistant to TKI treatment. LSC can be identified and isolated based on a surface expression of specific surface markers of which CD26 is perhaps the best described with high positive correlation with the occurrence of BCR-ABL1. Our aim was to compare gene expression (GE) profiles of CD26+ LSC, CD26- HSC and CD38+ progenitor cells (PC) from CML patients and identify potential novel CML LSC markers or disrupted pathways. In summary, we identified consistent changes of gene expression in CD26+ LSC as well as CD38+ progenitor populations, with only 3% gene overlap showing specificity of these patterns for selected populations.These results were successfully verified using highthroughput real-time PCR. The involvement of identified candidate genes and pathways, which could provide important insights into the CML stem cell biology, are currently evaluated.

Název v anglickém jazyce

Analysis of gene expression in CD26 CML leukemic stem cell population

Popis výsledku anglicky

Nowadays, chronic myeloid leukemia (CML) has become a well manageable disease and majority of the patients achieve remission on tyrosine kinase inhibitor (TKI) treatment. However, the disease usually shows a low-level persistence during therapy that arises from putative leukemic stem cells (LSC), which are, despite BCR-ABL1 positivity, resistant to TKI treatment. LSC can be identified and isolated based on a surface expression of specific surface markers of which CD26 is perhaps the best described with high positive correlation with the occurrence of BCR-ABL1. Our aim was to compare gene expression (GE) profiles of CD26+ LSC, CD26- HSC and CD38+ progenitor cells (PC) from CML patients and identify potential novel CML LSC markers or disrupted pathways. In summary, we identified consistent changes of gene expression in CD26+ LSC as well as CD38+ progenitor populations, with only 3% gene overlap showing specificity of these patterns for selected populations.These results were successfully verified using highthroughput real-time PCR. The involvement of identified candidate genes and pathways, which could provide important insights into the CML stem cell biology, are currently evaluated.

Druh

O - Ostatní výsledky

CEP obor

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OECD FORD obor

30205 - Hematology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2019

Kód důvěrnosti údajů

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