ONDRIŠOVÁ, Laura, Václav ŠEDA, Giorgia CHIODIN, Kryštof HLAVÁČ, Lenka KOŠŤÁLOVÁ, Daniel FILIP, Pedro FARIA ZENI, Anna PANOVSKÁ, Karla PLEVOVÁ, Šárka POSPÍŠILOVÁ, Martin ŠIMKOVIČ, Filip VRBACKÝ, Daniel LYSÁK, Stacey M. FERNANDEZ, MS. DAVIDS, Alba MAIQUES-DIAZ, Stella CHARALAMPOPOULOU, Jose I. MARTIN-SUBERO, Jennifer R. BROWN, Michael DOUBEK, Francesco FORCONI, Jiří MAYER and Marek MRÁZ. FOXO1-RICTOR AXIS induces adaptive increase in AKT activity during BCR inhibitor therapy in CLL: Implications for combination therapy. In EHA 2023 in HemaSphere (2023). 2023. ISSN 2572-9241.
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Basic information
Original name FOXO1-RICTOR AXIS induces adaptive increase in AKT activity during BCR inhibitor therapy in CLL: Implications for combination therapy.
Authors ONDRIŠOVÁ, Laura, Václav ŠEDA, Giorgia CHIODIN, Kryštof HLAVÁČ, Lenka KOŠŤÁLOVÁ, Daniel FILIP, Pedro FARIA ZENI, Anna PANOVSKÁ, Karla PLEVOVÁ, Šárka POSPÍŠILOVÁ, Martin ŠIMKOVIČ, Filip VRBACKÝ, Daniel LYSÁK, Stacey M. FERNANDEZ, MS. DAVIDS, Alba MAIQUES-DIAZ, Stella CHARALAMPOPOULOU, Jose I. MARTIN-SUBERO, Jennifer R. BROWN, Michael DOUBEK, Francesco FORCONI, Jiří MAYER and Marek MRÁZ.
Edition EHA 2023 in HemaSphere (2023), 2023.
Other information
Original language English
Type of outcome Konferenční abstrakta
Country of publisher Germany
Confidentiality degree is not subject to a state or trade secret
WWW URL
Organization Středoevropský technologický institut – Repository – Repository
ISSN 2572-9241
Keywords in English BCR inhibitors; BTK inhibitors; CCL; BCR; FoxO1/Rictor
Links LX22NPO5102, research and development project. MUNI/A/1224/2022, interní kód Repo. 802644, interní kód Repo.
Changed by Changed by: RNDr. Daniel Jakubík, učo 139797. Changed: 25/3/2024 03:21.
Abstract
Genetic mechanisms of resistance to BCR inhibitors in CLL have been extensively described. However, it remainsunknown whether non-genetic adaptation mechanisms to BTK inhibitors might exist. We focused on the possible role of the Akt pathway in adapting to BCR inhibitors since, in mouse models, PI3K-Akt activation is the only known factor that rescues the apoptosis induced by BCR deletion in mature B cells. We aim to describe non-genetic mechanisms of adaptation to BCR inhibitor therapy. We performed transcriptome profiling (Illumina) and analyzed samples obtained from CLL patients before and during ibrutinib or idelalisib therapy and performed gene editing in MEC1 cells to reveal the functional role of FoxO1/Rictor.
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