ReviewProtein & cell2011
Differential signaling of Flt3 activating mutations in acute myeloid leukemia: a working model.
Review in Protein & cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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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, 37 citations in OpenAlex.
- Very short insertions in the FLT3 gene are of therapeutic significance in acute myeloid leukemia.Blood advances · 2023Article
- Evaluating the clinical significance ofHeliyon · 2022Article
- Which FLT3 Inhibitor for Treatment of AML?Current treatment options in oncology · 2022Review
- The IL-3, IL-5, and GM-CSF common receptor beta chain mediates oncogenic activity of FLT3-ITD-positive AML.Leukemia · 2022Article
- Frequency of FLT3 Internal Tandem Duplications in Adult Syrian Patients with Acute Myeloid Leukemia and Normal Karyotype.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- De novo adult acute myeloid leukemia with two new mutations in juxtatransmembrane domain of the FLT3 gene: a case report.Journal of medical case reports · 2021Article
- Modeling pediatric AML FLT3 mutations using CRISPR/Cas12a- mediated gene editing.Leukemia & lymphoma · 2020Article
- Therapeutic targeting of FLT3 and associated drug resistance in acute myeloid leukemia.Journal of hematology & oncology · 2020Review
- Novel Approaches to Target Mutant FLT3 Leukaemia.Cancers · 2020Review
- Wild-type FLT3 and FLT3 ITD exhibit similar ligand-induced internalization characteristics.Journal of cellular and molecular medicine · 2020Article
- Targeting Immunophenotypic Markers on Leukemic Stem Cells: How Lessons from Current Approaches and Advances in the Leukemia Stem Cell (LSC) Model Can Inform Better Strategies for Treating Acute Myeloid Leukemia (AML).Cold Spring Harbor perspectives in medicine · 2020Review
- ProfilingFrontiers in pediatrics · 2020Article
- Antigen Targets for the Development of Immunotherapies in Leukemia.International journal of molecular sciences · 2019Review
- Impact ofHaematologica · 2019Article
- Article
- Acute Myeloid Leukemia-Genetic Alterations and Their Clinical Prognosis.International journal of hematology-oncology and stem cell research · 2017Review
- Imipramine blue sensitively and selectively targets FLT3-ITD positive acute myeloid leukemia cells.Scientific reports · 2017Article
- FLT3-ITD and its current role in acute myeloid leukaemia.Medical oncology (Northwood, London, England) · 2017Review
- The Cytokine Flt3-Ligand in Normal and Malignant Hematopoiesis.International journal of molecular sciences · 2017Review
- Class III Receptor Tyrosine Kinases in Acute Leukemia - Biological Functions and Modern Laboratory Analysis.Biomarker insights · 2015Review
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
Receptor tyrosine kinases couple a wide variety of extracellular cues to cellular responses. The class III subfamily comprises the platelet-derived growth factor receptor, c-Kit, Flt3 and c-Fms, all of which relay cell proliferation signals upon ligand binding. Accordingly, mutations in these proteins that confer ligand-independent activation are found in a subset of cancers. These mutations cluster in the juxtamembrane (JM) and catalytic tyrosine kinase domain (TKD) regions. In the case of acute myeloid leukemia (AML), the juxtamembrane (named ITD for internal tandem duplication) and TKD Flt3 mutants differ in their spectra of clinical outcomes. Although the mechanism of aberrant activation has been largely elucidated by biochemical and structural analyses of mutant kinases, the differences in disease presentation cannot be attributed to a change in substrate specificity or signaling strength of the catalytic domain. This review discusses the latest literature and presents a working model of differential Flt3 signaling based on mis-localized juxtamembrane autophosphorylation, to account for the disease variation. This will have bearing on therapeutic approaches in a complex disease such as AML, for which no efficacious drug yet exists.
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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.