Targeting FMS-like tyrosine kinase 3 (FLT3) in acute myeloid leukemia: Novel molecular approaches and therapeutic challenges

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11160%2F25%3A10492930" target="_blank" >RIV/00216208:11160/25:10492930 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/61989592:15310/25:73627217

Výsledek na webu

<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=GH3tAd0qEX" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=GH3tAd0qEX</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.biopha.2024.117788" target="_blank" >10.1016/j.biopha.2024.117788</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Targeting FMS-like tyrosine kinase 3 (FLT3) in acute myeloid leukemia: Novel molecular approaches and therapeutic challenges

Popis výsledku v původním jazyce

Acute myeloid leukemia (AML), a heterogeneous hematologic malignancy, has generally a poor prognosis despite the recent advancements in diagnostics and treatment. Genetic instability, particularly mutations in the FMS-like tyrosine kinase 3 (FLT3) gene, is associated with severe outcomes. Approximately 30 % of AML patients harbor FLT3 mutations, which have been linked to higher relapse and reduced survival rates. Traditional AML treatments employ cytarabine and anthracyclines drugs. Furthermore, the development of FLT3 inhibitors has significantly improved therapy for FLT3-mutated AML patients. For example, the introduction of midostaurin, the first FLT3 inhibitor, improved patient outcomes. However, resistant AML cell clones continue to pose a challenge to the success of AML treatment. This review discusses FLT3 kinase, mutations, and role in AML pathogenesis. It explores the molecular mechanisms of FLT3 activation, signaling pathways, and the structure and function of the FLT3 receptor. Current and emerging therapeutic approaches are presented, while highlighting the latest FLT3 inhibitors in clinical use, and strategies to overcome drug resistance. Future directions, including personalized therapies and novel drug designs, are examined to provide updated insights into FLT3-targeted treatments. This comprehensive review aims to guide clinicians and researchers in the development of innovative therapies to improve AML patient outcomes.

Název v anglickém jazyce

Targeting FMS-like tyrosine kinase 3 (FLT3) in acute myeloid leukemia: Novel molecular approaches and therapeutic challenges

Popis výsledku anglicky

Acute myeloid leukemia (AML), a heterogeneous hematologic malignancy, has generally a poor prognosis despite the recent advancements in diagnostics and treatment. Genetic instability, particularly mutations in the FMS-like tyrosine kinase 3 (FLT3) gene, is associated with severe outcomes. Approximately 30 % of AML patients harbor FLT3 mutations, which have been linked to higher relapse and reduced survival rates. Traditional AML treatments employ cytarabine and anthracyclines drugs. Furthermore, the development of FLT3 inhibitors has significantly improved therapy for FLT3-mutated AML patients. For example, the introduction of midostaurin, the first FLT3 inhibitor, improved patient outcomes. However, resistant AML cell clones continue to pose a challenge to the success of AML treatment. This review discusses FLT3 kinase, mutations, and role in AML pathogenesis. It explores the molecular mechanisms of FLT3 activation, signaling pathways, and the structure and function of the FLT3 receptor. Current and emerging therapeutic approaches are presented, while highlighting the latest FLT3 inhibitors in clinical use, and strategies to overcome drug resistance. Future directions, including personalized therapies and novel drug designs, are examined to provide updated insights into FLT3-targeted treatments. This comprehensive review aims to guide clinicians and researchers in the development of innovative therapies to improve AML patient outcomes.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30205 - Hematology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

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

Biomedicine &amp; Pharmacotherapy

ISSN

0753-3322

e-ISSN

1950-6007

Svazek periodika

182

Číslo periodika v rámci svazku

January

Stát vydavatele periodika

FR - Francouzská republika

Počet stran výsledku

18

Strana od-do

117788

Kód UT WoS článku

999

EID výsledku v databázi Scopus

2-s2.0-85213267299