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Targeting FMS-like tyrosine kinase 3 (FLT3) in acute myeloid leukemia: Novel molecular approaches and therapeutic challenges
J. Rataj, L. Gorecki, D. Muthna, A. Sorf, V. Krystof, P. Klener, M. Ceckova, M. Rezacova, J. Korabecny
Jazyk angličtina Země Francie
Typ dokumentu časopisecké články, přehledy
- MeSH
- akutní myeloidní leukemie * farmakoterapie genetika MeSH
- chemorezistence účinky léků MeSH
- cílená molekulární terapie * MeSH
- inhibitory proteinkinas * terapeutické užití farmakologie MeSH
- lidé MeSH
- mutace MeSH
- protinádorové látky terapeutické užití farmakologie MeSH
- signální transdukce účinky léků MeSH
- tyrosinkinasa 3 podobná fms * antagonisté a inhibitory genetika metabolismus MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
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.
Citace poskytuje Crossref.org
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- $a Rataj, Jan $u Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Kralove, Charles University, Akademika Heyrovskeho 1203, Hradec Kralove 500 05, Czech Republic
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- $a 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.
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- $a Gorecki, Lukas $u Department of Toxicology and Military Pharmacy, Military Faculty of Medicine, University of Defence, Trebesska 1575, Hradec Kralove 500 01, Czech Republic; Biomedical Research Centre, University Hospital Hradec Kralove, Sokolska 581, Hradec Kralove 500 05, Czech Republic
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- $a Krystof, Vladimir $u Department of Experimental Biology, Faculty of Science, Palacký University, Slechtitelu 27, Olomouc 779 00, Czech Republic
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- $a Ceckova, Martina $u Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Kralove, Charles University, Akademika Heyrovskeho 1203, Hradec Kralove 500 05, Czech Republic. Electronic address: novotnam@faf.cuni.cz
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- $a Rezacova, Martina $u Department of Medical Biochemistry, Faculty of Medicine in Hradec Kralove, Charles University, Simkova 870, Hradec Kralove 500 03, Czech Republic. Electronic address: RezacovaM@lfhk.cuni.cz
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- $a Korabecny, Jan $u Biomedical Research Centre, University Hospital Hradec Kralove, Sokolska 581, Hradec Kralove 500 05, Czech Republic. Electronic address: jan.korabecny@fnhk.cz
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