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

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14740%2F23%3A00131268" target="_blank" >RIV/00216224:14740/23:00131268 - isvavai.cz</a>

Výsledek na webu

<a href="https://www.icml.ch/icml/home.html" target="_blank" >https://www.icml.ch/icml/home.html</a>

DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

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

Popis výsledku anglicky

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.

Druh

O - Ostatní výsledky

CEP obor

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OECD FORD obor

30204 - Oncology

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)

Rok uplatnění

2023

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů