ReviewBiomarker insights2015
Class III Receptor Tyrosine Kinases in Acute Leukemia - Biological Functions and Modern Laboratory Analysis.
Review in Biomarker insights, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 42 citations in OpenAlex.
- FLT3-ITD signals for CEBPA and p53 proteolysis by the ubiquitin-proteosome pathway.Research square · 2026Article
- FLT3-ITD signals for CEBPA and p53 proteolysis by the ubiquitin-proteosome pathway.bioRxiv : the preprint server for biology · 2026Article
- Novel molecular mechanisms of FLT3 deregulation: from the acute myeloid leukemia experience to therapeutic insights in acute lymphoblastic leukemia.Molecular cancer · 2025Review
- Innovative Approaches in Cancer Treatment: Emphasizing the Role of Nanomaterials in Tyrosine Kinase Inhibition.Pharmaceutics · 2025Review
- SERS and Machine Learning-Enabled Liquid Biopsy: A Promising Tool for Early Detection and Recurrence Prediction in Acute Leukemia.ACS omega · 2025Article
- FLT3 targeting in the modern era: from clonal selection to combination therapies.International journal of hematology · 2024Review
- Novel biomolecules in targeted cancer therapy: a new approach towards precision medicine.Medical oncology (Northwood, London, England) · 2023Review
- An Updated Overview of the Role of CYP450 during Xenobiotic Metabolization in Regulating the Acute Myeloid Leukemia Microenvironment.International journal of molecular sciences · 2023Review
- CPX-351 and allogeneic stem cell transplant for a therapy-related acute myeloid leukemia that developed after treatment of acute promyelocytic leukemia: a case report and review of the literature.Frontiers in oncology · 2023Article
- Preclinical Evaluation of the Multiple Tyrosine Kinases Inhibitor Anlotinib in Leukemia Stem Cells.Pharmaceuticals (Basel, Switzerland) · 2022Article
- "FLipping" the Story: FLT3-Mutated Acute Myeloid Leukemia and the Evolving Role of FLT3 Inhibitors.Cancers · 2022Review
- Mutated KIT Tyrosine Kinase as a Novel Molecular Target in Acute Myeloid Leukemia.International journal of molecular sciences · 2022Review
- Exonic variants in multiple myeloma patients associated with relapsed/ refractory and response to bortezomib regimens.Saudi journal of biological sciences · 2022Article
- A Comprehensive Updated Review on Magnetic Nanoparticles in Diagnostics.Nanomaterials (Basel, Switzerland) · 2021Review
- Evolution of Functional Diversity in the Holozoan Tyrosine Kinome.Molecular biology and evolution · 2021Article
- Targeting multiple signaling pathways: the new approach to acute myeloid leukemia therapy.Signal transduction and targeted therapy · 2020Review
- 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
- Application of magnetic nanoparticles in nucleic acid detection.Journal of nanobiotechnology · 2020Review
- Theoretical Studies Aimed at Finding FLT3 Inhibitors and a Promising Compound and Molecular Pattern with Dual Aurora B/FLT3 Activity.Molecules (Basel, Switzerland) · 2020Article
- Clinical use of FLT3 inhibitors in acute myeloid leukemia.OncoTargets and therapy · 2018Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is a complex disease caused by deregulation of multiple signaling pathways. Mutations in class III receptor tyrosine kinases (RTKs) have been implicated in alteration of cell signals concerning the growth and differentiation of leukemic cells. Point mutations, insertions, or deletions of RTKs as well as chromosomal translocations induce constitutive activation of the receptor, leading to uncontrolled proliferation of undifferentiated myeloid blasts. Aberrations can occur in all domains of RTKs causing either the ligand-independent activation or mimicking the activated conformation. The World Health Organization recommended including RTK mutations in the AML classification since their detection in routine laboratory diagnostics is a major factor for prognostic stratification of patients. Polymerase chain reaction (PCR)-based methods are well-validated for the detection of fms-related tyrosine kinase 3 (FLT3) mutations and can easily be applied for other RTKs. However, when methodological limitations are reached, accessory techniques can be applied. For a higher resolution and more quantitative approach compared to agarose gel electrophoresis, PCR fragments can be separated by capillary electrophoresis. Furthermore, high-resolution melting and denaturing high-pressure liquid chromatography are reliable presequencing screening methods that reduce the sample amount for Sanger sequencing. Because traditional DNA sequencing is time-consuming, next-generation sequencing (NGS) is an innovative modern possibility to analyze a high amount of samples simultaneously in a short period of time. At present, standardized procedures for NGS are not established, but when this barrier is resolved, it will provide a new platform for rapid and reliable laboratory diagnostic of RTK mutations in patients with AML. In this article, the biological and physiological role of RTK mutations in AML as well as possible laboratory methods for their detection will be reviewed.
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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.