ReviewEuropean journal of haematology2025
Advances and Challenges in Quizartinib-Based FLT3 Inhibition for Acute Myeloid Leukemia: Mechanisms of Resistance and Prospective Combination Therapies.
Review in European journal of haematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- A New Paradigm for Pediatric AML: Improving the Pipeline for Treatments Targeting Cytogenetic and Molecular Alterations.Cancers · 2026Review
- Modern Concepts in Precision Targeting of Acute Myeloid Leukemia Based on Principles of Molecular Oncology.Cancers · 2026Review
- Integration of Bioinformatics and Machine Learning Strategies Identifies Ferroptosis and Immune Infiltration Signatures in Peri-Implantitis.International journal of molecular sciences · 2025Article
- Network-based analysis and experimental validation of identified natural compounds from Yinchen Wuling San for acute myeloid leukemia.Frontiers in pharmacology · 2025Article
- The interaction between common genetic mutations in AML and the immune landscape: mechanisms and implications for immune response.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FLT3 mutations are among the most common genetic alterations in acute myeloid leukemia (AML) and are associated with poor prognosis. Significant advancements have been made in developing FLT3 inhibitors (FLT3Is), such as quizartinib, which have improved treatment outcomes in both newly diagnosed and relapsed/refractory AML. Resistance to FLT3Is remains a major clinical challenge, driven by diverse mechanisms including FLT3 point mutations, cellular escape pathways, and the influence of the bone marrow microenvironment. Sustained STAT5 phosphorylation, AXL upregulation, and CXCR4 signaling have been identified as key factors in FLT3I resistance. Additionally, metabolic adaptations have been shown to support the survival of FLT3I-resistant cells. Ongoing clinical trials are investigating various combination regimens, including quizartinib with chemotherapy, Bcl-2 inhibitors, hypomethylating agents, and immune-modulatory drugs, with promising preliminary results. The European LeukemiaNet 2022 guidelines recommend incorporating FLT3Is into treatment regimens; however, questions remain regarding the best timing for the administration of each FLT3I. Additional studies are required to determine the optimal FLT3I-based combinations, reduce resistance emergence, and improve outcomes. This review highlights the current state of FLT3I therapy, ongoing challenges with resistance, and future directions in optimizing treatment for FLT3-mutated AML, focusing on quizartinib.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.