FOX01-rictor AXIS induces AKT phosporylation during CLL cell
adaptation to BCR inhibitors: Implications for combinatorial
therapy.

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FOX01-rictor AXIS induces AKT phosporylation during CLL cell adaptation to BCR inhibitors: ...

Přehled o publikaci

a 2023

FOX01-rictor AXIS induces AKT phosporylation during CLL cell adaptation to BCR inhibitors: Implications for combinatorial therapy.

ONDRIŠOVÁ, Laura, Václav ŠEDA, Eva HOFERKOVÁ, G. CHIODIN, Kryštof HLAVÁČ et. al.

Basic information

Original name

FOX01-rictor AXIS induces AKT phosporylation during CLL cell adaptation to BCR inhibitors: Implications for combinatorial therapy.

Authors

ONDRIŠOVÁ, Laura, Václav ŠEDA, Eva HOFERKOVÁ, G. CHIODIN, Kryštof HLAVÁČ, Lenka KOŠŤÁLOVÁ, Gabriela MLADONICKÁ PAVLASOVÁ, Daniel FILIP, Pedro FARIA ZENI, Jan OPPELT, Anna PANOVSKÁ, Karla PLEVOVÁ, Šárka POSPÍŠILOVÁ, M. SIMKOVIC, F. VRBACKÝ, Daniel LYSÁK, SM. FERNANDES, MS. DAVIDS, A. MAIQUES-DIAZ, S. CHARALAMPOPOULOU, JI. MARTIN-SUBERO, JR. BROWN, Michael DOUBEK, F. FORCONI, Jiří MAYER and Marek MRÁZ

Edition

ICML, Švýcarsko, Lugano, 2023

Other information

Language

English

Type of outcome

Konferenční abstrakta

Country of publisher

Switzerland

Confidentiality degree

is not subject to a state or trade secret

References:

URL

Organization

Středoevropský technologický institut – Repository – Repository

Keywords in English

BCR inhibitors; CLL; PI3K‐Akt activation

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

V originále

Although genetic mechanisms of resistance to BCR inhibitors in CLL are well‐known, it remains elusive whether non genetic adaptation mechanisms might exist. We focused on the possible role of Akt pathway as PI3K‐Akt activation is the only known factor that rescues the apoptosis induced by BCR deletionin mature Bcells in mouse models. We performed transcriptome profiling (Illumina) and analyzed samples obtained from CLL patients before andduring ibrutinib or idelalisib therapy (1–12weeks of therapy, n=70 patients with 194samples) and performed gene editing in MEC1 cells to reveal the functional role of FoxO1/Rictor.

Cite

@proceedings{60349,
   author = {Ondrišová, Laura and Šeda, Václav and Hoferková, Eva and Chiodin, G. and Hlaváč, Kryštof and Košťálová, Lenka and Mladonická Pavlasová, Gabriela and Filip, Daniel and Faria Zeni, Pedro and Oppelt, Jan and Panovská, Anna and Plevová, Karla and Pospíšilová, Šárka and Simkovic, M. and Vrbacký, F. and Lysák, Daniel and Fernandes, SM. and Davids, MS. and MaiquesandDiaz, A. and Charalampopoulou, S. and MartinandSubero, JI. and Brown, JR. and Doubek, Michael and Forconi, F. and Mayer, Jiří and Mráz, Marek},
   booktitle = {ICML, Švýcarsko, Lugano},
   keywords = {BCR inhibitors; CLL; PI3K‐Akt activation},
   language = {eng},
   title = {FOX01-rictor AXIS induces AKT phosporylation during CLL cell adaptation to BCR inhibitors: Implications for combinatorial therapy.},
   url = {https://www.icml.ch/icml/home.html},
   year = {2023}
}

TY  - CONF
ID  - 60349
AU  - Ondrišová, Laura - Šeda, Václav - Hoferková, Eva - Chiodin, G. - Hlaváč, Kryštof - Košťálová, Lenka - Mladonická Pavlasová, Gabriela - Filip, Daniel - Faria Zeni, Pedro - Oppelt, Jan - Panovská, Anna - Plevová, Karla - Pospíšilová, Šárka - Simkovic, M. - Vrbacký, F. - Lysák, Daniel - Fernandes, SM. - Davids, MS. - Maiques-Diaz, A. - Charalampopoulou, S. - Martin-Subero, JI. - Brown, JR. - Doubek, Michael - Forconi, F. - Mayer, Jiří - Mráz, Marek
PY  - 2023
TI  - FOX01-rictor AXIS induces AKT phosporylation during CLL cell adaptation to BCR inhibitors: Implications for combinatorial therapy.
KW  - BCR inhibitors
KW  - CLL
KW  - PI3K‐Akt activation
UR  - https://www.icml.ch/icml/home.html
N2  - Although genetic mechanisms of resistance to BCR inhibitors in CLL are well‐known, it remains elusive whether non genetic adaptation mechanisms might exist. We focused on the possible role of Akt pathway as PI3K‐Akt activation is the only known factor that rescues the apoptosis induced by BCR deletionin mature Bcells in mouse models. We performed transcriptome profiling (Illumina) and analyzed samples obtained from CLL patients before andduring ibrutinib or idelalisib therapy (1–12weeks of therapy, n=70 patients with 194samples) and performed gene editing in MEC1 cells to reveal the functional role of FoxO1/Rictor.
ER  -