ReviewCurrent hematologic malignancy reports2017
The Future of Targeting FLT3 Activation in AML.
Review in Current hematologic malignancy reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
26 citing papers in PubMed, 1 synthesis or guideline pooled it.
- FLT3 Tyrosine Kinase Inhibitors for the Treatment of Fit and Unfit Patients with FLT3-Mutated AML: A Systematic Review.International journal of molecular sciences · 2021Pooled it
- Olverembatinib (HQP1351): a third-generation tyrosine kinase inhibitor in the treatment of hematologic and solid malignancies-a comprehensive review of clinical outcomes.Discover oncology · 2026Review
- A Two-way Mendelian randomisation study of inflammatory factors and the risk of meningioma.Translational neuroscience · 2026Article
- Functional combination of resveratrol and midostaurin induces cytotoxicity to overcome acquired midostaurin resistance in FLT3-ITD expressing acute myeloid leukemia cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Overcoming the sorafenib resistance mechanism in FLT3-mutated acute myeloid leukemia: molecular basis and new targets.Frontiers in oncology · 2025Review
- Therapeutic Targeting of FLT3 in Acute Myeloid Leukemia: Current Status and Novel Approaches.OncoTargets and therapy · 2022Review
- 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
- Exploiting Clonal Evolution to Improve the Diagnosis and Treatment Efficacy Prediction in Pediatric AML.Cancers · 2021Review
- Engineering and crystal structure of a monomeric FLT3 ligand variant.Acta crystallographica. Section F, Structural biology communications · 2021Article
- The current landscape of single-cell transcriptomics for cancer immunotherapy.The Journal of experimental medicine · 2021Review
- Cell Metabolism and DNA Repair Pathways: Implications for Cancer Therapy.Frontiers in cell and developmental biology · 2021Review
- Discovery of Potent EGFR Inhibitors WithFrontiers in pharmacology · 2021Article
- Therapeutic targeting of FLT3 and associated drug resistance in acute myeloid leukemia.Journal of hematology & oncology · 2020Review
- Chlorpromazine eliminates acute myeloid leukemia cells by perturbing subcellular localization of FLT3-ITD and KIT-D816V.Nature communications · 2020Article
- Knowledge-primed neural networks enable biologically interpretable deep learning on single-cell sequencing data.Genome biology · 2020Article
- Review
- Article
- Prognosis and outcome of patients with acute myeloid leukemia based onOncology letters · 2019Article
- Targeting Glutamine Metabolism and Redox State for Leukemia Therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Single-Cell RNA-Seq Reveals AML Hierarchies Relevant to Disease Progression and Immunity.Cell · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Internal tandem duplications (ITD) and tyrosine-kinase domain (TKD) mutations of the FMS-like tyrosine-kinase 3 (FLT3) can be found in up to one third of patients with acute myeloid leukemia (AML) and confer a poor prognosis. First discovered 20 years ago, these mutations were identified as viable therapeutic targets, and FLT3 tyrosine-kinase inhibitors (TKIs) have been in development for the last decade with steadily increasing potency. However, FLT3-mutated AML often acquires resistance to the growing armamentarium of FLT3 inhibitors through a variety of mechanisms. In this review, we discuss the distinct clinical phenotype of FLT3-mutated AML, historically and currently available therapeutics, mechanisms of resistance, ongoing trials, and future outlook at treatment strategies.
Indexed as
Identifiers
28421420What OpenQuestion holds
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.