ReviewLeukemia2012
Targeting the FMS-like tyrosine kinase 3 in acute myeloid leukemia.
Review in Leukemia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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
73 citing papers in PubMed, 133 citations in OpenAlex.
- Targeting PRL phosphatases in hematological malignancies.Expert opinion on therapeutic targets · 2024Review
- PRL2 Phosphatase Promotes Oncogenic KIT Signaling in Leukemia Cells through Modulating CBL Phosphorylation.Molecular cancer research : MCR · 2024Article
- Optimization of Tyrosine Kinase Inhibitor-Loaded Gold Nanoparticles for Stimuli-Triggered Antileukemic Drug Release.Journal of functional biomaterials · 2023Article
- Severe Gastrointestinal Toxicity Following the Use of Gilteritinib: A Case Series and Analysis of Postmarketing Surveillance Data.Healthcare (Basel, Switzerland) · 2023Article
- ITDetect: a method to detect internal tandem duplication of FMS-like tyrosine kinase (FLT3) from next-generation sequencing data with high sensitivity and clinical application.BMC bioinformatics · 2023Article
- Article
- Development of Gilteritinib-Based Chimeric Small Molecules that Potently Induce Degradation of FLT3-ITD Protein.ACS medicinal chemistry letters · 2022Article
- Nanocarriers: A Reliable Tool for the Delivery of Anticancer Drugs.Pharmaceutics · 2022Review
- Role of Biomarkers in FLT3 AML.Cancers · 2022Review
- Review
- Patterns of Resistance Differ in Patients with Acute Myeloid Leukemia Treated with Type I versus Type II FLT3 inhibitors.Blood cancer discovery · 2021Article
- Correction to: Outcomes with sequential FLT3-inhibitor-based therapies in patients with AML.Journal of hematology & oncology · 2021Article
- Discovery of 5-methyl-Journal of enzyme inhibition and medicinal chemistry · 2020Article
- Outcomes with sequential FLT3-inhibitor-based therapies in patients with AML.Journal of hematology & oncology · 2020Article
- Conformational restriction of a type II FMS inhibitor leading to discovery of 5-methyl-Journal of enzyme inhibition and medicinal chemistry · 2019Article
- Rationale for a Combination Therapy Consisting of MCL1- and MEK-Inhibitors in Acute Myeloid Leukemia.Cancers · 2019Article
- Aberrant DNA Methylation in Acute Myeloid Leukemia and Its Clinical Implications.International journal of molecular sciences · 2019Review
- 8-chloro-adenosine activity in FLT3-ITD acute myeloid leukemia.Journal of cellular physiology · 2019Article
- Mutant p53 enhances leukemia-initiating cell self-renewal to promote leukemia development.Leukemia · 2019Article
- FLT3, a prognostic biomarker for acute myeloid leukemia (AML): Quantitative monitoring with a simple anti-FLT3 interaction and flow cytometric method.Journal of clinical laboratory analysis · 2019Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is a highly heterogenous disease with multiple signaling pathways contributing to its pathogenesis. A key driver of AML is the FMS-like tyrosine kinase receptor-3 (FLT3). Activating mutations in FLT3, primarily the FLT3-internal tandem duplication (FLT3-ITD), are associated with decreased progression-free and overall survival. Identification of the importance of FLT3-ITD and the FLT3 pathway in the prognosis of patients with AML has stimulated efforts to develop therapeutic inhibitors of FLT3. Although these inhibitors have shown promising antileukemic activity, they have had limited efficacy to date as single agents and may require use in combination with cytotoxic chemotherapies. Here, we review clinical and preclinical results for the clinically mature FLT3 inhibitors currently in development. We conclude that multitargeted FLT3 inhibitors may have more utility earlier in the course of disease, when in vitro evidence suggests that AML cells are less dependent on FLT3 signaling, perhaps because of upregulation of multiple other signaling pathways. More potent agents may have greater utility in relapsed and heavily pretreated patients, in whom high levels of circulating FLT3 ligand may necessitate use of an agent with a very favorable pharmacokinetic/pharmacodynamic profile. Novel combination regimens are also discussed.
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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.