Observational studyCancer gene therapy2020
The mutational spectrum of FLT3 gene in acute lymphoblastic leukemia is different from acute myeloid leukemia.
Observational study in Cancer gene therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 25 citations in OpenAlex.
- Review
- The clinical relevance of RAS pathway gene mutations in childhood B-cell acute lymphoblastic leukemia.Annals of hematology · 2026Article
- Article
- FLT3: A 35-Year Voyage from Discovery to the Next Generation of Targeted Therapy in AML.Cancers · 2025Review
- Novel molecular mechanisms of FLT3 deregulation: from the acute myeloid leukemia experience to therapeutic insights in acute lymphoblastic leukemia.Molecular cancer · 2025Review
- Effective Utilization of a Customized Targeted Hybrid Capture RNA Sequencing in the Routine Molecular Categorization of Adolescent and Adult B-Lineage Acute Lymphoblastic Leukemia: A Real-World Experience.Molecular diagnosis & therapy · 2025Article
- Prognostic Factors, FLT-3 Mutations, and Treatment Outcomes with Pediatric-Inspired Protocols in Adolescent and Young Adults and Adult Patients with Acute Lymphoblastic Leukemia.Acta haematologica · 2025Article
- DistinctInternational journal of molecular sciences · 2024Article
- Deep Learning Techniques to Characterize theBiomedicines · 2024Article
- Prevalence ofFrontiers in pediatrics · 2024Article
- In vivo activity of the dual SYK/FLT3 inhibitor TAK-659 against pediatric acute lymphoblastic leukemia xenografts.Pediatric blood & cancer · 2023Article
- Targeting Proliferation Signals and the Cell Cycle Machinery in Acute Leukemias: Novel Molecules on the Horizon.Molecules (Basel, Switzerland) · 2023Review
- PAX5 and TDT-Negative B-Acute Lymphoblastic Leukemia with Unusual Genetic Mutations: A Case Report.Avicenna journal of medicine · 2022Article
- Point Mutations in theFrontiers in oncology · 2022Article
- Developments and challenges of FLT3 inhibitors in acute myeloid leukemia.Frontiers in oncology · 2022Review
- Tyrosine kinases in KMT2A/MLL-rearranged acute leukemias as potential therapeutic targets to overcome cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2022Article
- 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
- Review
- CD19/CD22 chimeric antigen receptor T-cell therapy for refractory acute B-cell lymphoblastic leukemia with FLT3-ITD mutations.Bone marrow transplantation · 2020Article
- ProfilingFrontiers in pediatrics · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in FMS-like tyrosine kinase 3 (FLT3) gene occur frequently in acute myeloid leukemia (AML) and are rare in acute lymphoblastic leukemia (ALL). We aimed to analyze the incidence and characteristics of FLT3 mutations in ALL. Amplicon-targeted next-generation sequencing of 58 genes was performed on 1571 patients (AML, n = 829; ALL, n = 742). FLT3 mutations were identified in 5.12% (38/742) of ALL patients. Four types of FLT3 mutations were disclosed, including internal tandem duplication (ITD), tyrosine kinase domain (TKD), juxtamembrane insertion and deletion (JM-INDEL), and juxtamembrane point mutation (JM-PM), which were respectively identified in 1.21, 1.89, 0.67, and 1.89% of patients. The incidence of FLT3-JM-PM (1.89 vs 0.48%, P = 0.009) and the proportion of TKD non-D835 mutations that accounted for the total TKD mutations (57.14 vs 18.18%, P = 0.013) were significantly higher in ALL when compared with AML. FLT3-JM-INDEL were mainly found in B-ALL. In addition, FLT3-JM-INDEL and FLT3-JM-PM were first reported in patients with B-ALL. Patients with FLT3 mutations besides of ITD and/or TKD had a potential response to tyrosine kinase inhibitors. We showed that the mutation spectrum of FLT3 gene in ALL is distinct from AML that will facilitated an in-depth understand of the pathogenesis and provide a guidance for treatment.
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.