ReviewInternational journal of hematology2013
FLT3 inhibitors for acute myeloid leukemia: a review of their efficacy and mechanisms of resistance.
Review in International journal of hematology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 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
83 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.
- Clinical Benefits and Safety of FMS-Like Tyrosine Kinase 3 Inhibitors in Various Treatment Stages of Acute Myeloid Leukemia: A Systematic Review, Meta-Analysis, and Network Meta-Analysis.Frontiers in oncology · 2021Pooled it
- Dual FLT3/MAPK14 Proteolysis-Targeting Chimera (PROTAC) Induces Potent Acute Myeloid Leukemia Cell Death.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Heme oxygenase 1 confers gilteritinib resistance in FLT3-ITD acute myeloid leukemia in a STAT6-dependent manner.Cancer cell international · 2025Article
- PROTACs: Walking through hematological malignancies.Frontiers in pharmacology · 2023Review
- Recent Advances in PROTACs for Drug Targeted Protein Research.International journal of molecular sciences · 2022Review
- FLT3 inhibitors for acute myeloid leukemia: successes, defeats, and emerging paradigms.RSC medicinal chemistry · 2022Review
- Article
- PCW-A1001, AI-assistedFrontiers in molecular biosciences · 2022Article
- Gilteritinib-induced upregulation of S100A9 is mediated through BCL6 in acute myeloid leukemia.Blood advances · 2021Article
- Gilteritinib Inhibits Glutamine Uptake and Utilization inMolecular cancer therapeutics · 2021Article
- Identification of Protein Biomarker Signatures for Acute Myeloid Leukemia (AML) Using Both Nontargeted and Targeted Approaches.Proteomes · 2021Article
- 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
- High-throughput proteomic profiling reveals mechanisms of action of AMG925, a dual FLT3-CDK4/6 kinase inhibitor targeting AML and AML stem/progenitor cells.Annals of hematology · 2021Article
- OTS167 blocks FLT3 translation and synergizes with FLT3 inhibitors in FLT3 mutant acute myeloid leukemia.Blood cancer journal · 2021Article
- LT-171-861, a novel FLT3 inhibitor, shows excellent preclinical efficacy for the treatment of FLT3 mutant acute myeloid leukemia.Theranostics · 2021Article
- Article
- Sunitinib in Patients with Metastatic Colorectal Cancer (mCRC) with FLT-3 Amplification: Results from the Targeted Agent and Profiling Utilization Registry (TAPUR) Study.Targeted oncology · 2020Article
- Proteolysis targeting chimeras (PROTACs) are emerging therapeutics for hematologic malignancies.Journal of hematology & oncology · 2020Review
- Cutting Edge Molecular Therapy for Acute Myeloid Leukemia.International journal of molecular sciences · 2020Review
- Review
23 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Since the Food and Drug Administration approval of imatinib for treatment of chronic myeloid leukemia in 2001, tyrosine kinase inhibitors (TKIs) have become a mainstay in the care of many malignancies. In acute myeloid leukemia (AML), activating mutations in the FMS-like tyrosine kinase 3 (FLT3) gene result in survival and proliferation of leukemic blasts and are associated with adverse prognosis. Therefore, the FLT3 receptor is an appealing target for inhibition. Multiple small molecule TKIs are currently in development for FLT3-mutated AML, and agents are beginning to show promising efficacy. In other malignancies, the development of resistance to TKIs during the course of therapy has proven to be a challenge, and thus far, in clinical trials of FLT3 TKIs, resistance to inhibition represents a significant barrier to successful FLT3 inhibition. Understanding the mechanisms of resistance and overcoming these obstacles to target inhibition will be central to the success of these agents.
Indexed as
Identifiers
What 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.