ReviewHaematologica2021
Potential targeting of FLT3 acute myeloid leukemia.
Review in Haematologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05383014 (Assessment of Association Between FLT3-ITD Gene Mutation and CD135 Expression and Their Correlation With Hematological,Immunophenotypic and Biochemical Characteristics in Acute Myeloid Leukemia.), which is not on this map. Cited by 42 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.
Assessment of Association Between FLT3-ITD Gene Mutation and CD135 Expression and Their Correlation With Hematological,Immunophenotypic and Biochemical Characteristics in Acute Myeloid Leukemia.
Who cites it
42 citing papers in PubMed, 74 citations in OpenAlex.
- PHI-101: a novel FLT3 inhibitor with potent activity against the F691L gatekeeper resistance mutation.Leukemia · 2026Article
- Relapse following FLT3 inhibitor cessation in FLT3-ITD-positive AML: lessons from two clinical cases.Annals of hematology · 2026Article
- Precision oncology to overcome resistance in R/R AML in children and adults requires combinations of cytotoxic, targeted, and immunological treatments.Journal of internal medicine · 2025Review
- Lnk deficiency attenuates the immunosuppressive capacity of MDSCs via ferroptosis to suppress tumor development.Cell death & disease · 2025Article
- Targeting acute myeloid leukemia through antibody engineering: innovations in immunotherapy and combination regimens.Clinical and experimental medicine · 2025Review
- Concurrent inhibition of p300/CBP and FLT3 enhances cytotoxicity and overcomes resistance in acute myeloid leukemia.Acta pharmacologica Sinica · 2025Article
- Observational
- Precision Medicine in Myeloid Neoplasia: Challenges and Opportunities.Journal of personalized medicine · 2025Review
- Histamine dihydrochloride and low-dose interleukin-2 in an emerging landscape of relapse prevention in acute myeloid leukemia.Therapeutic advances in hematology · 2025Review
- The unexpected and unresolved roles of PDGFRA and PDGFRB in T-cell acute lymphoblastic leukemia.Haematologica · 2024Article
- Tracking Response and Resistance in Acute Myeloid Leukemia through Single-Cell DNA Sequencing Helps Uncover New Therapeutic Targets.International journal of molecular sciences · 2024Article
- Enhancing Therapeutic Efficacy of FLT3 Inhibitors with Combination Therapy for Treatment of Acute Myeloid Leukemia.International journal of molecular sciences · 2024Review
- Phase I Study of GS-3583, an FMS-like Tyrosine Kinase 3 Agonist Fc Fusion Protein, in Patients with Advanced Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- A phase 1 study of the irreversible FLT3 inhibitor FF-10101 in relapsed or refractory acute myeloid leukemia.Blood advances · 2024Article
- A year in pharmacology: new drugs approved by the US Food and Drug Administration in 2023.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Current knowledge about FLT3 gene mutations, exploring the isoforms, and protein importance in AML.Molecular biology reports · 2024Review
- Article
- The Clinical Utility ofCurrent oncology (Toronto, Ont.) · 2023Article
- A combinatorial therapeutic approach to enhance FLT3-ITD AML treatment.Cell reports. Medicine · 2023Article
- Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant FLT3 receptor signaling is common in acute myeloid leukemia (AML) and has important implications for the biology and clinical management of the disease. Patients with FLT3-mutated AML frequently present with critical illness, are more likely to relapse after treatment, and have worse clinical outcomes than their FLT3 wild type counterparts. The clinical management of FLT3-mutated AML has been transformed by the development of FLT3 inhibitors, which are now in use in the frontline and relapsed/refractory settings. However, many questions regarding the optimal approach to the treatment of these patients remain. In this paper, we will review the rationale for targeting the FLT3 receptor in AML, the impact of FLT3 mutation on patient prognosis, the current standard of care approaches to FLT3-mutated AML management, and the diverse array of FLT3 inhibitors in use and under investigation. We will also explore new opportunities and strategies for targeting the FLT3 receptor. These include targeting the receptor in patients with non-canonical FLT3 mutations or wild type FLT3, pairing FLT3 inhibitors with other novel therapies, using minimal residual disease (MRD) testing to guide the targeting of FLT3, and novel immunotherapeutic approaches.
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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.