ReviewBiomedicines2020
Mechanisms Underlying Resistance to FLT3 Inhibitors in Acute Myeloid Leukemia.
Review in Biomedicines, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 85 citations in OpenAlex.
- Mislocalisation of FLT3-ITD receptor contributes to MV4-11 leukaemia cell resistance to antibody-drug conjugate.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Adaptor-mediated rewiring of FLT3 signaling engages p38 MAPK to sustain gilteritinib resistance in acute myeloid leukemia.Leukemia · 2026Article
- Chromosomal Heterogeneity and Enrichment of Mitotic Regulatory Programs Reveal a Therapeutic Vulnerability in Cytarabine-Resistant FLT3-ITD AML.Current issues in molecular biology · 2026Article
- Recent advances of dual PROTACs for potential therapeutic applications.Molecular diversity · 2026Review
- Targeting FLT3 in Acute Myeloid Leukemia: Structural Insights and Key Challenges.ACS bio & med chem Au · 2026Review
- Quizartinib Resistance Mutations and Treatment Outcomes in Relapsed or Refractory FLT3-ITD-Positive AML.Cancer science · 2026Article
- Review
- SGI-7079 as a novel type I FLT3 inhibitor overcomes resistance to gilteritinib and quizartinib mediated by ITD and TKD mutations in acute myeloid leukemia.NPJ precision oncology · 2026Article
- Novel treatment strategies in acute myeloid leukemia.Blood research · 2026Review
- TRIM22-mediated ubiquitin-dependent degradation of FLT3-ITD overcomes TKI resistance in acute myeloid leukemia.Life medicine · 2026Article
- Dual FLT3/MAPK14 Proteolysis-Targeting Chimera (PROTAC) Induces Potent Acute Myeloid Leukemia Cell Death.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Computer-aided drug design in acute myeloid leukemia: a comprehensive review of advances, challenges, and future prospect.Journal of computer-aided molecular design · 2026Review
- TIP-20, a novel feline McDonough sarcoma-like tyrosine kinase 3 inhibitor with potent antileukemia activity.The Journal of international medical research · 2026Article
- Recent Advances in FLT3-Based Dual Inhibitors: A Promising Strategy for the Treatment of Acute Myeloid Leukemia.Current medicinal chemistry · 2026Review
- Article
- Novel molecular mechanisms of FLT3 deregulation: from the acute myeloid leukemia experience to therapeutic insights in acute lymphoblastic leukemia.Molecular cancer · 2025Review
- Counter-Therapeutic Strategies for Resistance of FLT3 Inhibitors in Acute Myeloid Leukemia.Cells · 2025Review
- Heme oxygenase 1 confers gilteritinib resistance in FLT3-ITD acute myeloid leukemia in a STAT6-dependent manner.Cancer cell international · 2025Article
- Inhibition of NLRP3 enhances pro-apoptotic effects of FLT3 inhibition in AML.Cell communication and signaling : CCS · 2025Article
- Discovery of novel and highly potent small molecule inhibitors targeting FLT3-ITD for the treatment of acute myeloid leukemia using structure-based virtual screening and biological evaluation.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FLT3-ITD and FLT3-TKD mutations were observed in approximately 20 and 10% of acute myeloid leukemia (AML) cases, respectively. FLT3 inhibitors such as midostaurin, gilteritinib and quizartinib show excellent response rates in patients with FLT3-mutated AML, but its duration of response may not be sufficient yet. The majority of cases gain secondary resistance either by on-target and off-target abnormalities. On-target mutations (i.e., FLT3-TKD) such as D835Y keep the TK domain in its active form, abrogating pharmacodynamics of type II FLT3 inhibitors (e.g., midostaurin and quizartinib). Second generation type I inhibitors such as gilteritinib are consistently active against FLT3-TKD as well as FLT3-ITD. However, a "gatekeeper" mutation F691L shows universal resistance to all currently available FLT3 inhibitors. Off-target abnormalities are consisted with a variety of somatic mutations such as
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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.