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    BIOMARKER:

    FLT3-ITD mutation

    i
    Other names: FLT3, Fms Related Tyrosine Kinase 3, Receptor-Type Tyrosine-Protein Kinase FLT3, Stem Cell Tyrosine Kinase 1, Fms-Like Tyrosine Kinase 3, CD135, FLK-2, STK1, Growth Factor Receptor Tyrosine Kinase Type III, Fetal Liver Kinase 2
    Entrez ID:
    2322
    Related biomarkers:
    Expression
    Mutation
    CNA
    Fusion
    Others
    Related tests:
    1d
    Mislocalisation of FLT3-ITD receptor contributes to MV4-11 leukaemia cell resistance to antibody-drug conjugate. (PubMed, J Enzyme Inhib Med Chem)
    To evaluate the impact of this trafficking difference, we synthesised an anti-FLT3 mAb-MMAE, linked via a Val-Cit-PAB linker at the Fc N-glycan, which exhibited lower cytotoxicity in MV4-11 than THP-1 cells, indicating that the impaired lysosomal trafficking of FLT3-ITD limits drug release and reduces ADC potency. These findings highlight that effective lysosomal targeting is essential for ADC activity and suggest that optimising linker design or restoring lysosome trafficking may enhance FLT3-targeted ADC in AML.
    Journal
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    FLT3 (Fms-related tyrosine kinase 3)
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    FLT3-ITD mutation • FLT3 mutation
    2d
    HAP2HCT: TCRαβ-depleted Progenitor Cell Graft With Additional Memory T-cell DLI, Plus Selected Use of Blinatumomab, in Naive T-cell Depleted Haploidentical Donor Hematopoietc Cell Transplantation for Hematologic Malignancies (clinicaltrials.gov)
    P2, N=69, Active, not recruiting, St. Jude Children's Research Hospital | N=140 --> 69 | Trial completion date: Aug 2025 --> Jun 2026
    Enrollment change • Trial completion date
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    FLT3 (Fms-related tyrosine kinase 3) • RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • ETV6 (ETS Variant Transcription Factor 6) • WT1 (WT1 Transcription Factor) • CREBBP (CREB binding protein) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • NSD1 (Nuclear Receptor Binding SET Domain Protein 1) • HOXA9 (Homeobox A9) • NUP214 (Nucleoporin 214) • CBFA2T3 (CBFA2/RUNX1 Partner Transcriptional Co-Repressor 3) • GLIS2 (GLIS Family Zinc Finger 2) • KAT6A (Lysine Acetyltransferase 6A) • KDM5A (Lysine Demethylase 5A) • DEK (DEK Proto-Oncogene) • AFDN (Afadin, Adherens Junction Formation Factor) • MLLT10 (MLLT10 Histone Lysine Methyltransferase DOT1L Cofactor)
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    FLT3-ITD mutation
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    cyclophosphamide • Blincyto (blinatumomab) • melphalan • fludarabine IV • mesna • thiotepa • Neupogen (filgrastim)
    4d
    Day + 30 detection of minimal residual FLT3-ITD by high-sensitivity PCR-NGS predicts relapse risk and guides post-transplant maintenance in AML. (PubMed, BMC Med)
    This is the first study to demonstrate that detection of minimal FLT3-ITD clones at the fixed time point of day + 30 post-HSCT can reliably stratify relapse risk in AML patients and provide a rationale for individualized post-transplant maintenance therapy.
    Journal • Next-generation sequencing
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    FLT3 (Fms-related tyrosine kinase 3)
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    FLT3-ITD mutation
    5d
    Comparison of maintenance with decitabine or chemotherapy in a real-world cohort of patients with acute myeloid leukemia. (PubMed, Front Pharmacol)
    All patients achieved complete remission (CR) after 1-2 courses of induction therapy, followed by consolidation with high-dose cytarabine (HiDAC). MT with either decitabine or chemotherapy can improve outcomes of AML patients in this real-world cohort. Decitabine maintenance exhibits better tolerability compared with chemotherapy and enhances survival in specific patient subgroups.
    Journal • Real-world evidence
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    FLT3 (Fms-related tyrosine kinase 3)
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    FLT3-ITD mutation
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    cytarabine • decitabine
    8d
    Homoharringtonine and Gilteritinib Synergistically Induce Apoptosis and Suppress Viability in FLT3-ITD-Positive AML Cells. (PubMed, Biomedicines)
    The combination enhanced the p53 expression. Our findings elucidate the mechanism underlying this synergistic interaction and underscore the potential of p53 status as a predictive biomarker for identifying patients most likely to benefit from HHT and gilteritinib combination therapy.
    Journal
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    FLT3 (Fms-related tyrosine kinase 3) • HSPA8 (Heat Shock Protein Family A (Hsp70) Member 8)
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    TP53 mutation • FLT3-ITD mutation • TP53 wild-type
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    Xospata (gilteritinib) • Synribo (omacetaxine mepesuccinate)
    8d
    FLT3-SYK inhibitor and Ixazomib combination impact HOXA and oxidative stress control by β-catenin, SQSTM1 and NRF2 in AML. (PubMed, NPJ Precis Oncol)
    Dual targeting of FLT3/SYK (TAK-659) and the proteasome (Ixazomib) showed strong synergy across genetically defined AML subsets, irrespective of FLT3 mutant status. These findings define a therapeutically targetable axis linking FLT3/SYK/β-catenin signaling to stress adaptation, provide a mechanistic basis for combinatorial targeting in high-risk AML. Trial registration: NCT04079738, Date of registration 03 September 2019.
    Journal
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    FLT3 (Fms-related tyrosine kinase 3) • TET2 (Tet Methylcytosine Dioxygenase 2) • CTNNB1 (Catenin (cadherin-associated protein), beta 1) • PTPRC (Protein Tyrosine Phosphatase Receptor Type C) • SQSTM1 (Sequestosome 1) • HOXA9 (Homeobox A9) • SYK (Spleen tyrosine kinase) • JUN (Jun proto-oncogene)
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    FLT3-ITD mutation • FLT3 mutation • TET2 mutation
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    Ninlaro (ixazomib) • mivavotinib (CB-659)
    11d
    Risk stratification of low-dose cytarabine and venetoclax in patients with AML ineligible for intensive chemotherapy. (PubMed, Blood Adv)
    Although the European LeukemiaNet (ELN) classifications (2017 and 2022) for AML have been used to stratify outcomes for patients receiving intensive chemotherapy, their application to patients receiving less intensive therapy, such as azacitidine plus venetoclax, has been less satisfactory. Overall, these data support the importance of molecular subclassification in defining treatment outcomes to venetoclax-based therapies. These trials were registered at www.clinicaltrials.gov as #NCT02287233 and #NCT03069352.
    Journal
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    KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • NRAS (Neuroblastoma RAS viral oncogene homolog) • NPM1 (Nucleophosmin 1)
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    TP53 mutation • KRAS mutation • NRAS mutation • FLT3-ITD mutation
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    Venclexta (venetoclax) • cytarabine • azacitidine
    12d
    FIT-AML: FLT3-ITD Targeted Therapy in Fit AML Patients (clinicaltrials.gov)
    P2/3, N=230, Not yet recruiting, European Organisation for Research and Treatment of Cancer - EORTC
    New P2/3 trial
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    FLT3 (Fms-related tyrosine kinase 3)
    |
    FLT3-ITD mutation
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    Venclexta (venetoclax) • cytarabine • Xospata (gilteritinib) • azacitidine • midostaurin
    14d
    Validation and Refinement of the European LeukemiaNet 2022 Genetic Risk Stratification of AML. (PubMed, JCO Glob Oncol)
    We conclude that ELN22 is prognostically valid in intensively treated younger patients with AML. Incorporation of WT1 mutation status, triple-mutated NPM1, and LSC burden may improve risk stratification, particularly within the heterogeneous intermediate-risk category.
    Retrospective data • Journal
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    FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1) • DNMT3A (DNA methyltransferase 1) • WT1 (WT1 Transcription Factor) • CEBPA (CCAAT Enhancer Binding Protein Alpha)
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    FLT3-ITD mutation • NPM1 mutation
    14d
    TIP-20, a novel feline McDonough sarcoma-like tyrosine kinase 3 inhibitor with potent antileukemia activity. (PubMed, J Int Med Res)
    Gene Set Enrichment Analysis indicated that TIP-20 enhanced or restored antigen presentation in MV4-11 cells.ConclusionsTIP-20 is a novel FLT3 inhibitor with potent antileukemic activity. These findings suggest that TIP-20 may provide a new therapeutic option for leukemia patients.
    Journal
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    FLT3 (Fms-related tyrosine kinase 3)
    |
    FLT3-ITD mutation • FLT3 mutation
    17d
    ISR007028: Administration of Gilteritinib to eliminate MRD in patients with AML and FLT3-ITD mutation. (2025-521875-30-00)
    P1/2, N=58, Not yet recruiting, Hellenic Society Of Hematology
    New P1/2 trial
    |
    FLT3 (Fms-related tyrosine kinase 3)
    |
    FLT3-ITD mutation
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    Xospata (gilteritinib)
    19d
    Outcomes of therapy-related non-core binding factor acute myeloid leukemia with venetoclax-based therapies. (PubMed, Hemasphere)
    On multivariate analysis in LIT + VEN-treated patients, HSCT and NPM1/IDH2 mutations were favorable, while TP53/RAS mutations were associated with inferior survival. VEN-based therapy improves outcomes in patients with T-AML, especially in those with VEN-sensitizing genomics and receiving an HSCT.
    Journal
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    TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NPM1 (Nucleophosmin 1)
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    TP53 mutation • FLT3-ITD mutation • IDH2 mutation • NPM1 mutation • RAS mutation
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    Venclexta (venetoclax)