Exploring the mechanisms of Venetoclax resistence via drug screening and genome-wide CRISPR screening.
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14740%2F23%3A00132771" target="_blank" >RIV/00216224:14740/23:00132771 - isvavai.cz</a>
Výsledek na webu
<a href="https://ashpublications.org/blood/article/142/Supplement%201/5759/505860/Exploring-the-Mechanisms-of-Venetoclax-Resistance" target="_blank" >https://ashpublications.org/blood/article/142/Supplement%201/5759/505860/Exploring-the-Mechanisms-of-Venetoclax-Resistance</a>
DOI - Digital Object Identifier
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Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Exploring the mechanisms of Venetoclax resistence via drug screening and genome-wide CRISPR screening.
Popis výsledku v původním jazyce
Combining Venetoclax, a selective BCL-2 inhibitor, with hypomethylating agents has revolutionized frontline acute myeloid leukemia (AML) treatment. Despite its success, the occurrence of resistance remains a significant concern, limiting the range of available treatment alternatives. Little is known about the mechanism by which the cells escape the treatment. Recent studies have observed MCL1 upregulation in AML cells to promote resistance, and the rationale to use an MCL1 inhibitor became attractive. Although MCL1 inhibitors work exceptionally well in vitro their clinical trials were unsuccessful due to their toxicity. Here, we aim to identify other genes responsible for acquiring resistance and tackle the problem through screening for clinically approved drugs to rapidly benefit the patients with our study.
Název v anglickém jazyce
Exploring the mechanisms of Venetoclax resistence via drug screening and genome-wide CRISPR screening.
Popis výsledku anglicky
Combining Venetoclax, a selective BCL-2 inhibitor, with hypomethylating agents has revolutionized frontline acute myeloid leukemia (AML) treatment. Despite its success, the occurrence of resistance remains a significant concern, limiting the range of available treatment alternatives. Little is known about the mechanism by which the cells escape the treatment. Recent studies have observed MCL1 upregulation in AML cells to promote resistance, and the rationale to use an MCL1 inhibitor became attractive. Although MCL1 inhibitors work exceptionally well in vitro their clinical trials were unsuccessful due to their toxicity. Here, we aim to identify other genes responsible for acquiring resistance and tackle the problem through screening for clinically approved drugs to rapidly benefit the patients with our study.
Klasifikace
Druh
O - Ostatní výsledky
CEP obor
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OECD FORD obor
30204 - Oncology
Návaznosti výsledku
Projekt
<a href="/cs/project/LX22NPO5102" target="_blank" >LX22NPO5102: Národní ústav pro výzkum rakoviny</a><br>
Návaznosti
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Ostatní
Rok uplatnění
2023
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů