ReviewLeukemia & lymphoma2014
FLT3 tyrosine kinase inhibitors in acute myeloid leukemia: clinical implications and limitations.
Review in Leukemia & lymphoma, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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.
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Who cites it
59 citing papers in PubMed, 98 citations in OpenAlex.
- Pharmacogenomic, pharmacokinetic, and safety analysis of CYP3A4/CYP3A5 polymorphisms of midostaurin in patients with acute myeloid leukemia.European journal of clinical pharmacology · 2025Trial
- Phase I/II trial of the combination of midostaurin (PKC412) and 5-azacytidine for patients with acute myeloid leukemia and myelodysplastic syndrome.American journal of hematology · 2015Trial
- Trial
- Current Research in Polypharmacology for Cancer Treatment Using Dual-Target Histone Deacetylase Inhibitors.International journal of molecular sciences · 2026Review
- Rational design and comparative docking and simulation of modified FLT3 inhibitors: a study on enhanced binding stability and inhibition potency.Journal of molecular modeling · 2026Article
- Targeting rapid TKI-induced AXL upregulation overcomes adaptive ERK reactivation and exerts antileukemic effects in FLT3/ITD acute myeloid leukemia.Molecular oncology · 2025Article
- Inhibition of NOTCH4 sensitizes FLT3/ITD acute myeloid leukemia cells to FLT3 tyrosine kinase inhibition.Leukemia · 2024Article
- Indole-based FLT3 inhibitors and related scaffolds as potential therapeutic agents for acute myeloid leukemia.BMC chemistry · 2023Review
- FLT3 inhibitors for acute myeloid leukemia: successes, defeats, and emerging paradigms.RSC medicinal chemistry · 2022Review
- Article
- FLT3 Inhibitors as Maintenance Therapy after Allogeneic Stem-Cell Transplantation.Blood and lymphatic cancer : targets and therapy · 2022Review
- Synergistic Lethality Effects of Apatinib and Homoharringtonine in Acute Myeloid Leukemia.Journal of oncology · 2022Article
- Targeted Therapies in Cancer: To Be or Not to Be, Selective.Biomedicines · 2021Review
- The Ups and Downs of STAT Inhibition in Acute Myeloid Leukemia.Biomedicines · 2021Review
- The Structural Effect of FLT3 Mutations at 835th Position and Their Interaction with Acute Myeloid Leukemia Inhibitors: In Silico Approach.International journal of molecular sciences · 2021Article
- Clinical implication and prognostic significance of FLT3-ITD and ASXL1 mutations in Egyptian AML patients: A single-center study.Cancer biomarkers : section A of Disease markers · 2021Article
- Inhibition of class I PI3K enhances chaperone-mediated autophagy.The Journal of cell biology · 2020Article
- Pro-myogenic small molecules revealed by a chemical screen on primary muscle stem cells.Skeletal muscle · 2020Article
- ULK1 inhibition as a targeted therapeutic strategy for FLT3-ITD-mutated acute myeloid leukemia.Journal of experimental & clinical cancer research : CR · 2020Article
- Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Internal tandem duplications of the FMS-like tyrosine kinase 3 (FLT3) gene are one of the most frequent gene mutations in acute myeloid leukemia (AML) and are associated with poor clinical outcome. The remission rate is high with intensive chemotherapy, but most patients eventually relapse. During the last decade, FLT3 mutations have emerged as an attractive target for a molecularly specific treatment strategy. Targeting FLT3 receptor tyrosine kinases in AML has shown encouraging results in the treatment of FLT3 mutated AML, but in most patients responses are incomplete and not sustained. Newer, more specific compounds seem to have a higher potency and selectivity against FLT3. During therapy with FLT3 tyrosine kinase inhibitors (TKIs) the induction of acquired resistance has emerged as a clinical problem. Therefore, optimization of the targeted therapy and potential treatment options to overcome resistance is currently the focus of clinical research. In this review we discuss the use and limitations of TKIs as a therapeutic strategy for the treatment of FLT3 mutated AML, including mechanisms of resistance to TKIs as well as possible novel strategies to improve FLT3 inhibitor therapy.
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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.