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: ...

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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.

Základní údaje

Originální název

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

Autoři

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 a Marek MRÁZ

Vydání

ICML, Švýcarsko, Lugano, 2023

Další údaje

Jazyk

angličtina

Typ výsledku

Konferenční abstrakta

Stát vydavatele

Švýcarsko

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Organizace

Středoevropský technologický institut – Masarykova univerzita – Repozitář

Klíčová slova anglicky

BCR inhibitors; CLL; PI3K‐Akt activation

Návaznosti

LX22NPO5102, projekt VaV. MUNI/A/1224/2022, interní kód Repo. 802644, interní kód Repo.

Změněno: 25. 3. 2024 03:21, RNDr. Daniel Jakubík

Anotace

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.

Citovat

@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  -