Přehled o publikaci
2023
FOXO1-RICTOR AXIS induces adaptive increase in AKT activity during BCR inhibitor therapy in CLL: Implications for combination therapy.
ONDRIŠOVÁ, Laura; Václav ŠEDA; Giorgia CHIODIN; Kryštof HLAVÁČ; Lenka KOŠŤÁLOVÁ et al.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
Language
English
Type of outcome
Konferenční abstrakta
Country of publisher
Germany
Confidentiality degree
is not subject to a state or trade secret
References:
Marked to be transferred to RIV
No
Organization
Středoevropský technologický institut – Repository – Repository
ISSN
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: 25/3/2024 03:21, RNDr. Daniel Jakubík
Abstract
In the original language
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.