Venetoclax in combination with ponatinib for the treatment of asciminib-resistant chronic myeloid leukemia

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F25%3A10500914" target="_blank" >RIV/00216208:11110/25:10500914 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11130/25:10500914 RIV/00064203:_____/25:10500914

Výsledek na webu

<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=jTTYD9hIwR" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=jTTYD9hIwR</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/s41375-025-02732-1" target="_blank" >10.1038/s41375-025-02732-1</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Venetoclax in combination with ponatinib for the treatment of asciminib-resistant chronic myeloid leukemia

Popis výsledku v původním jazyce

Asciminib, an allosteric inhibitor specifically targeting the myristoyl pocket of BCR::ABL1, has expanded therapeutic options for heavily pretreated patients with chronic myeloid leukemia (CML), and for those with the BCR::ABL1 T315I mutation. Several clinical studies evaluating asciminib in frontline CML therapy are currently ongoing (e.g., ASCI4FIRST, ASCI4START, ASCEND), with promising preliminary results indicating superior efficacy, improved tolerability, and a lower rate of treatment discontinuation due to toxicity compared to ATP-competitive inhibitorsHowever, clinical trials of asciminib in both advanced-line and first-line CML treatment also report the emergence of resistance, often due to acquired or persisting mutations in BCR::ABL1. The full spectrum of these mutations remains unidentified, underscoring the need for further investigation and the exploration of backup therapeutic strategies, including combination therapies.

Název v anglickém jazyce

Venetoclax in combination with ponatinib for the treatment of asciminib-resistant chronic myeloid leukemia

Popis výsledku anglicky

Asciminib, an allosteric inhibitor specifically targeting the myristoyl pocket of BCR::ABL1, has expanded therapeutic options for heavily pretreated patients with chronic myeloid leukemia (CML), and for those with the BCR::ABL1 T315I mutation. Several clinical studies evaluating asciminib in frontline CML therapy are currently ongoing (e.g., ASCI4FIRST, ASCI4START, ASCEND), with promising preliminary results indicating superior efficacy, improved tolerability, and a lower rate of treatment discontinuation due to toxicity compared to ATP-competitive inhibitorsHowever, clinical trials of asciminib in both advanced-line and first-line CML treatment also report the emergence of resistance, often due to acquired or persisting mutations in BCR::ABL1. The full spectrum of these mutations remains unidentified, underscoring the need for further investigation and the exploration of backup therapeutic strategies, including combination therapies.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30205 - Hematology

Projekt

<a href="/cs/project/NW24-03-00056" target="_blank" >NW24-03-00056: Molekulární podklad pro terapii s BH3 mimetiky k překonání refrakterních/relabujících Ph+ leukémií</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2025

Kód důvěrnosti údajů

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

Název periodika

Leukemia

ISSN

0887-6924

e-ISSN

1476-5551

Svazek periodika

39

Číslo periodika v rámci svazku

10

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

4

Strana od-do

2555-2558

Kód UT WoS článku

001559387600001

EID výsledku v databázi Scopus

2-s2.0-105014147538