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BIOMARKER:

FLT3 mutation

i
Entrez ID:
Related tests:
4d
Discovery of pyridine-based derivatives as FLT3 inhibitors for the treatment of acute myeloid leukemia. (PubMed, Eur J Med Chem)
With the acceptable oral bioavailability of 19.2 % in SD rats, 12y prolonged the survival rate of NSG mice dose-dependently in MOLM-13 inoculated xenograft model without obvious toxicity. Overall, this study might provide a new insight for the development of novel FLT3 inhibitors.
Journal
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FLT3 (Fms-related tyrosine kinase 3) • KDR (Kinase insert domain receptor)
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FLT3 mutation
5d
FLT3 mutation-related immune checkpoint molecule absent in melanoma 2 (AIM2) contributes to immune infiltration in pediatric and adult acute myeloid leukemia: evidence from bioinformatics analysis. (PubMed, Transl Cancer Res)
AMI2 may be involved in the activation of suppressive immune cell populations, such as macrophages, neutrophils, and monocytes. AIM2 could serve as a promising immunotherapeutic target for combination therapy with FLT3 inhibitors in AML.
Journal • IO biomarker
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FLT3 (Fms-related tyrosine kinase 3) • AIM2 (Absent In Melanoma 2)
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FLT3 mutation
6d
A GIMEMA survey on therapeutic use and response rates of FLT3 inhibitors in acute myeloid leukemia: Insights from Italian real-world practice. (PubMed, EJHaem)
The 3/7 + midostaurin treatment resulted in a 63% of complete remission (CR) rates and gilteritinib in a 44% of CR rates. The discontinuation rate of gilteritinib for intolerance or toxicity was low (accounting for 4% of treated cases).
Journal • Real-world evidence • Real-world
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3 mutation
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Xospata (gilteritinib) • Rydapt (midostaurin)
6d
Trial primary completion date • Combination therapy
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3-ITD mutation • FLT3 mutation • FLT3-TKD mutation
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Xospata (gilteritinib) • Rydapt (midostaurin)
7d
Salvage Therapy with Second-Generation Inhibitors for FLT3 Mutated Acute Myeloid Leukemia: A Real-World Study by the CETLAM and PETHEMA Groups. (PubMed, Cancers (Basel))
Gilter/quizar monotherapy are effective and tolerable options for patients with R/R FLT3mut AML in a real-world setting. Response and toxicity rates are similar to those reported in the phase 3 trials, despite the more heterogeneous nature of the study population.
Journal • Real-world evidence • Real-world
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3-ITD mutation • FLT3 mutation
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Xospata (gilteritinib) • Rydapt (midostaurin) • Vanflyta (quizartinib)
12d
Preclinical development of tuspetinib for the treatment of acute myeloid leukemia. (PubMed, Cancer Res Commun)
Oral TUS markedly extended survival in subcutaneously and orthotopically inoculated xenograft models of FLT3 mutant human AML, was well tolerated, and delivered enhanced activity when combined with venetoclax or 5-azacytidine...Cells selected for stable acquired resistance to TUS exhibited increased BAX and hypersensitivity to venetoclax (1900-fold), navitoclax and MCL1 inhibitors. MV-4-11 FLT3-ITD clones expressing NRASG12D revealed that high-level expression of NRASG12D generated modest resistance to TUS and greater resistance to venetoclax (VEN), yet the TUS/VEN combination exhibited synergy in NRASG12D AML model. Favorable preclinical safety and pharmacology properties, the efficacy of the TUS/VEN combination in a murine model, and the synthetic lethal vulnerability to VEN that accompanies TUS resistance provide the basis for exploration of the TUS/VEN combination in patients with relapsed or refractory AML.
Preclinical • Journal
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FLT3 (Fms-related tyrosine kinase 3) • SYK (Spleen tyrosine kinase) • EIF4EBP1 (Eukaryotic translation initiation factor 4E binding protein 1) • RPS6KA3 (Ribosomal Protein S6 Kinase A3)
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FLT3 mutation • MCL1 expression • NRAS G12
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Venclexta (venetoclax) • azacitidine • navitoclax (ABT 263) • tuspetinib (HM43239)
14d
The Dual PIM/FLT3 Inhibitor MEN1703 Combines Synergistically With Gilteritinib in FLT3-ITD-Mutant Acute Myeloid Leukaemia. (PubMed, J Cell Mol Med)
We also show that MEN1703 downregulates stromal cytokines that promote cytokine-mediated resistance of AML blast cells to FLT3 inhibition. These results demonstrate the importance of the combination approach to overcome microenvironment-mediated resistance to FLT3 inhibitors.
Journal
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3-ITD mutation • FLT3 mutation • MCL1 overexpression
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Xospata (gilteritinib) • MEN1703
15d
Study of FF-10101-01 in Patients With Relapsed or Refractory Acute Myeloid Leukemia (clinicaltrials.gov)
P1, N=97, Completed, Fujifilm Pharmaceuticals U.S.A., Inc. | Phase classification: P1/2 --> P1
Phase classification
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3 mutation
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FF-10101
23d
FLT3 inhibitors and hematopoietic cell transplantation prolong survival in patients with FLT3-ITD-positive AML. (PubMed, Ann Hematol)
These results demonstrate the clinical impact of FLT3 inhibitors on survival outcomes in patients with FLT3-ITD-positive AML, particularly when combined with HCT. FLT3 inhibitors can improve the prognosis of AML with FLT3 mutations, especially in patients who undergo HCT.
Journal
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FLT3 (Fms-related tyrosine kinase 3)
|
FLT3 mutation
28d
Central nervous system relapse after allogeneic HCT in FLT3-mutated AML. (PubMed, Ann Hematol)
This was not abrogated by pre-emptive or salvage therapy with FLT3i in first relapse. Targeted therapies prior to transplant, use of intrathecal chemoprophylaxis or closer monitoring may be considered in patients with FLT3-mutated AML with active disease prior to HCT in order to prevent CNS relapse.
Journal
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3 mutation
1m
Discovery of IRAK1/4/pan-FLT3 Kinase Inhibitors as Treatments for Acute Myeloid Leukemia. (PubMed, ACS Med Chem Lett)
Optimization of this series has produced compound 31 which displays potent and selective inhibition of IRAK1, IRAK4, FLT3, and all mutant forms of FLT3, as well as good in vitro ADME and pharmacokinetic properties. In a mouse xenograft model of AML, 31 produces survival prolongation equal to that of Gilteritinib, the leading marketed FLT3 inhibitor currently used to treat AML.
Journal
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FLT3 (Fms-related tyrosine kinase 3) • IRAK1 (Interleukin 1 Receptor Associated Kinase 1) • IRAK4 (Interleukin 1 Receptor Associated Kinase 4)
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FLT3 mutation
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Xospata (gilteritinib)
1m
A Combinatorial Functional Precision Medicine Platform for Rapid Therapeutic Response Prediction in AML. (PubMed, Cancer Med)
Overall, this study demonstrates the feasibility of applying QPOP as a functional combinatorial precision medicine platform to predict therapeutic sensitivities in AML and provides the basis for prospective clinical trials evaluating ex vivo-guided combination therapy.
Journal
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FLT3 (Fms-related tyrosine kinase 3) • FOXM1 (Forkhead Box M1)
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FLT3 mutation
1m
TIPIC syndrome in a patient following sorafenib treatment for acute myeloid leukemia: a rare case report. (PubMed, Front Oncol)
Treatment involved a one-week course of oral steroid therapy with dexamethasone and non-steroidal anti-inflammatory drugs, which led to complete clinical recovery. TIPIC syndrome involves transient nonspecific perivascular inflammation of the carotid adventitia; however, the precise underlying cause remains unclear. In this study, we report a rare case and explore the potential pathophysiological mechanisms through a review of the existing literature.
Journal
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3 mutation
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sorafenib • dexamethasone
1m
Approaching a therapeutic inflection point for FLT3-mutated AML. (PubMed, Blood)
Finally, recent data also suggest FLT3 inhibitors could transform outcomes in patients unsuitable for intensive therapy. If confirmed, this has important implications for fit patients and could revolutionize the treatment paradigm.
Journal
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3 mutation
1m
The Immunomodulatory Effect of Different FLT3 Inhibitors on Dendritic Cells. (PubMed, Cancers (Basel))
Our results suggest different immunosuppressive effects of these three FLT3i and may, therefore, provide an additional rationale for optimal maintenance therapy after alloHSCT of FLT3-positive AML patients to prevent infectious complications and GvHD mediated by DCs.
Journal • Immunomodulating
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FLT3 (Fms-related tyrosine kinase 3) • IL6 (Interleukin 6) • TNFA (Tumor Necrosis Factor-Alpha) • CD86 (CD86 Molecule)
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FLT3 mutation • FLT3 positive
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Xospata (gilteritinib) • Rydapt (midostaurin) • Vanflyta (quizartinib)
1m
Homoharringtonine Added to Venetoclax and Azacitidine Improves Outcome and Mitigates Genetic Impact in Relapsed/Refractory AML: A Multi-center Cohort Study. (PubMed, Clin Cancer Res)
Our findings suggest the addition of HHT to VA might enhance response and mitigate the negative impact of certain genetic patterns in RR-AML while being well tolerated.
Journal
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KRAS (KRAS proto-oncogene GTPase) • FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1) • DNMT3A (DNA methyltransferase 1) • TET2 (Tet Methylcytosine Dioxygenase 2)
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KRAS mutation • FLT3-ITD mutation • FLT3 mutation • DNMT3A mutation • TET2 mutation
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Venclexta (venetoclax) • azacitidine • Synribo (omacetaxine mepesuccinate)
1m
In vivo models of subclonal oncogenesis and dependency in hematopoietic malignancy. (PubMed, Cancer Cell)
We next use a generalizable, reversible approach to demonstrate that mutation reversion results in rapid leukemic regression with distinct differentiation patterns depending upon co-occurring mutations. These studies provide a path to experimentally model sequential mutagenesis, investigate mechanisms of transformation and probe oncogenic dependency in disease evolution.
Preclinical • Journal
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FLT3 (Fms-related tyrosine kinase 3) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NPM1 (Nucleophosmin 1) • DNMT3A (DNA methyltransferase 1)
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FLT3 mutation • NPM1 mutation • DNMT3A mutation
1m
Safety and Efficacy Study of CI-135 CAR-T Cells in Subjects with Relapsed or Refractory Acute Myeloid Leukemia (clinicaltrials.gov)
P1, N=0, Withdrawn, Beijing Boren Hospital | Trial completion date: Dec 2025 --> Dec 2023 | Recruiting --> Withdrawn | Trial primary completion date: Dec 2024 --> Dec 2023
Trial completion date • Trial withdrawal • Trial primary completion date • CAR T-Cell Therapy
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3 mutation • FLT3 expression
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cyclophosphamide • CI-135 CAR-T
1m
New P4 trial
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3 mutation
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Venclexta (venetoclax) • cytarabine
2ms
Tretinoin and Arsenic Trioxide in Treating Patients With Untreated Acute Promyelocytic Leukemia (clinicaltrials.gov)
P3, N=158, Active, not recruiting, Children's Oncology Group | Trial completion date: Sep 2024 --> Sep 2025
Trial completion date
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FLT3 (Fms-related tyrosine kinase 3) • RARA (Retinoic Acid Receptor Alpha) • PML (Promyelocytic Leukemia)
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FLT3 mutation • FLT3 wild-type
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cytarabine • idarubicin hydrochloride • mitoxantrone • Vesanoid (tretinoin) • arsenic trioxide • Hemady (dexamethasone tablets) • Starasid (cytarabine ocfosfate)
2ms
Measurable residual mutated IDH1 before allogeneic transplant for acute myeloid leukemia. (PubMed, Bone Marrow Transplant)
For patients with IDH1 mutated AML co-mutated with NPM1 and/or FLT3-ITD, only detection of persistent mutated NPM1 and/or FLT3-ITD was associated with significantly higher rates of relapse (p = 0.01). These data, from the largest study to date, do not support the detection of IDH1 mutation in CR1 blood prior to alloHCT as evidence of AML MRD for increased post-transplant relapse risk.
Journal
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FLT3 (Fms-related tyrosine kinase 3) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • NPM1 (Nucleophosmin 1)
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FLT3-ITD mutation • IDH1 mutation • FLT3 mutation • NPM1 mutation
2ms
A phase 1/2 study of gilteritinib in combination with chemotherapy in newly diagnosed patients with AML in Asia. (PubMed, Int J Hematol)
In this interim analysis, gilteritinib 120 mg/day in combination with chemotherapy was well tolerated, with similar CRc rates to previous studies.
P1/2 data • Journal • Combination therapy
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3 mutation
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cytarabine • Xospata (gilteritinib) • idarubicin hydrochloride
2ms
Measurable Residual Mutated NPM1 before Allogeneic Transplant for Acute Myeloid Leukemia (ASH 2024)
NPM1 MRD positive patients receiving nonmyeloablative conditioning or reduced-intensity conditioning (RIC) without melphalan (mel) had increased risk of relapse or death compared to patients receiving myeloablative conditioning or RIC with mel, regardless of FLT3-ITD co-mutational status (3yrs : relapse 87% vs 55%, P=0.006; OS 15% vs 42%, P=0.013). Conclusions : In patients with NPM1 mutated AML from the Pre-MEASURE study, we show that detection of residual NPM1 variants in pre-transplant blood during CR1 using a highly sensitive DNA-based assay is associated in a dose-dependent manner with a significantly increased risk of relapse and death after allo-HCT, which can be mitigated in part by conditioning regimen. In patients co-mutated for both FLT3-ITD and NPM1 at diagnosis, NPM1 should be prioritized as a target for NGS-MRD if only one test is available.
FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1)
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FLT3-ITD mutation • FLT3 mutation • NPM1 mutation
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FLT3 ITD MRD Assay • NPM1 Mutation Assay
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melphalan
2ms
T/NK Cell-Associated Transcriptomic Profile Informs Response to FLT3 Inhibitors in Acute Myeloid Leukemia (ASH 2024)
We then profiled a wet-lab cohort of 37 FLT3-mut AML patients treated either with Midostaurin plus chemotherapy (M) or Gilteritinib (G) at Bologna Hematology Institute by using the PanCancer IO 360 Panel (NanoString Technologies, San Diego, CA). S.R. & A.C. equally contributed
FLT3 (Fms-related tyrosine kinase 3) • CD8 (cluster of differentiation 8) • CD4 (CD4 Molecule) • GLI2 (GLI Family Zinc Finger 2)
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FLT3 mutation
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nCounter® PanCancer IO 360™ Panel
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Xospata (gilteritinib) • Rydapt (midostaurin)
2ms
Analysis of Morphologic Classification System for Acute Promyelocytic Leukemia and Its Correlation with Laboratory Tests and FLT3-ITD Mutation (PubMed, Zhongguo Shi Yan Xue Ye Xue Za Zhi)
The newly established morphologic classification system in this study can objectively characterize different types of APL blast cells, which helps to better assess the intra- and inter-individual heterogeneity of APL blast cells, and further use in accurately analyzing the correlation of morphological phenotypes with biological properties of APL.
Journal
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3-ITD mutation • FLT3 mutation
2ms
Characteristics and Prognosis of "Acute Promyelocytic Leukemia-like" Nucleophosmin-1-Mutated Acute Myeloid Leukemia in a Retrospective Patient Cohort. (PubMed, Biomedicines)
Our findings contribute to a comprehensive characterization of NPM1-mutated AML, enhancing diagnostic accuracy and aiding in the detailed classification of the disease. This information may potentially guide targeted therapies or differentiation-based treatment strategies.
Retrospective data • Journal
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FLT3 (Fms-related tyrosine kinase 3) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NPM1 (Nucleophosmin 1) • DNMT3A (DNA methyltransferase 1) • TET2 (Tet Methylcytosine Dioxygenase 2) • CD34 (CD34 molecule)
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FLT3 mutation • NPM1 mutation • DNMT3A mutation • TET2 mutation
2ms
Midostaurin shapes macroclonal and microclonal evolution of FLT3-mutated acute myeloid leukemia. (PubMed, Blood Adv)
Considering both treatment groups, if only 24% of FLT3-ITD microclones detected at diagnosis were retained at relapse, 43% of them became macroclones. Together, these results identify parameters influencing the fitness of FLT3-ITD clones and highlight the importance of using sensitive techniques for FLT3--ITD screening in clinical practice.
Clinical • Journal
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FLT3 (Fms-related tyrosine kinase 3)
|
FLT3 mutation
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Rydapt (midostaurin)
2ms
Journal
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3-ITD mutation • FLT3 mutation
2ms
Autophagy and inflammasome activation are associated with poor response to FLT3 inhibitors in patients with FLT3-ITD acute myeloid leukemia. (PubMed, Sci Rep)
Inflammasome activation was also shown to strongly increase the likelihood of a poor ex vivo response to the FLT3 inhibitors quizartinib and sorafenib. These findings reveal a distinct molecular pattern within FLT3-ITD AML samples that underscores the necessity for further exploration into how approaching these supportive parallel yet altered pathways could improve therapeutic strategies.
Journal
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3 mutation
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sorafenib • Vanflyta (quizartinib)
2ms
In silico and in vitro study of FLT3 inhibitors and their application in acute myeloid leukemia. (PubMed, Mol Med Rep)
The present study aimed to gain insights into the molecular interactions and affinity forces of four TKI drugs (sorafenib, midostaurin, gilteritinib and quizartinib) with the wild‑type (WT)‑FLT3 and ITD‑mutated (ITD‑FLT3) structural models of FLT3, in its inactive aspartic acid‑phenylalanine‑glycine motif (DFG‑out) and active aspartic acid‑phenylalanine‑glycine motif (DFG‑in) conformations. Thus, the current study presented novel information about molecular interactions between the FLT3 receptors (WT or ITD‑mutated) and some of their inhibitors. It also paves the way for the search for novel inhibitory molecules with potential use against AML.
Preclinical • Journal
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FLT3 (Fms-related tyrosine kinase 3)
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FLT3 mutation • FLT3 wild-type
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sorafenib • Xospata (gilteritinib) • Rydapt (midostaurin) • Vanflyta (quizartinib)
2ms
AML typical mutations (CEBPA, FLT3, and NPM1) identify a high-risk CMML independent of CPSS-Mol classification. (PubMed, Blood Adv)
The genetic profile of these mutCFN CMML patients closely resembled that of AML, with higher-risk clinical characteristics. Our findings lead us to suggest including the assessment of these mutations in CMML prognostic models and treating these patients with AML-type therapies, including intensive chemotherapy and allogeneic stem cell transplantation, whenever feasible, and consider certain targeted therapies approved for use in AML.
Journal
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FLT3 (Fms-related tyrosine kinase 3) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NPM1 (Nucleophosmin 1) • CEBPA (CCAAT Enhancer Binding Protein Alpha)
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IDH1 mutation • IDH2 mutation • FLT3 mutation • NPM1 mutation • CEBPA mutation
3ms
Midostaurin added to 10-day decitabine, for patients unfit for intensive chemotherapy with AML and higher risk MDS, irrespective of FLT3 mutational status, does not improve outcome. (PubMed, Ann Hematol)
In the decitabine plus midostaurin arm 24% reached CR/CRi, the median OS was 4.8 months and 1-yrs OS was 31% which compared with 34% CR/CRi, median OS of 7.4 months and 1-yrs OS of 37% for the decitabine alone group (NS). Thus, while the addition of midostaurin appears safe, it does not enhance therapeutic efficacy of decitabine in unfit AML patients.
Clinical • Journal
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FLT3 (Fms-related tyrosine kinase 3)
|
FLT3 mutation
|
Rydapt (midostaurin) • decitabine
3ms
Enrollment open
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FLT3 (Fms-related tyrosine kinase 3)
|
FLT3 mutation • CBL mutation
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Venclexta (venetoclax) • Xospata (gilteritinib)
3ms
Pathogenesis and treatment of acute myeloid leukemia with FLT3 mutations (PubMed, Rinsho Ketsueki)
In Japan, alongside monotherapy with gilteritinib or quizartinib for relapsed/refractory patients, combination of quizartinib with intensive chemotherapy was approved in 2023 for untreated FLT3-ITD mutation-positive AML. Thus, FLT3 mutations are utilized not only as a prognostic factor in AML but also as a target for treatment and for response assessment. Furthermore, the development of new treatment strategies involving FLT3 inhibitors is highly anticipated to improve clinical outcomes for patients with FLT3 mutation-positive AML.
Journal
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FLT3 (Fms-related tyrosine kinase 3)
|
FLT3-ITD mutation • FLT3 mutation
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Xospata (gilteritinib) • Vanflyta (quizartinib)
3ms
Recent progress in AML with recurrent genetic abnormalities. (PubMed, Int J Hematol)
However, resistance to targeted therapies is also a challenge. This Progress in Hematology features current trends and challenges in favorable-risk AML and FLT3 mutations that are frequently identified in these patients.
Journal
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FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1) • CEBPA (CCAAT Enhancer Binding Protein Alpha)
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FLT3 mutation • NPM1 mutation • CEBPA mutation
3ms
Cholesterol inhibition enhances antitumor response of gilteritinib in lung cancer cells. (PubMed, Cell Death Dis)
In a xenograft model, the combination of gilteritinib and 25HC showed significantly better efficacy than either monotherapy in suppressing lung cancer growth, without obvious general toxicity. Thus, our findings identify an increase in cholesterol induced by gilteritinib as a mechanism for LCC survival, and highlight the potential of combining gilteritinib with cholesterol-lowering drugs to treat lung cancer.
Journal
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FLT3 (Fms-related tyrosine kinase 3)
|
FLT3 mutation
|
Xospata (gilteritinib)
3ms
Retrospective data • Journal
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FLT3 (Fms-related tyrosine kinase 3) • NRAS (Neuroblastoma RAS viral oncogene homolog) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2)
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NRAS mutation • FLT3 mutation
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Venclexta (venetoclax)
3ms
Tracking Response and Resistance in Acute Myeloid Leukemia through Single-Cell DNA Sequencing Helps Uncover New Therapeutic Targets. (PubMed, Int J Mol Sci)
For Pt #1, disease resistance was associated with clonal expansion of minor clones, and 2nd line TKI therapy with gilteritinib provided a proliferative advantage to the clones carrying NRAS and KIT mutations, thereby responsible for relapse. In Pt #2, clonal architecture was less complex, and 1st line TKI therapy with midostaurin was able to eradicate the leukemic clones. Our results corroborate previous findings about clonal selection driven by TKIs, highlighting the importance of a deeper characterization of individual clonal architectures for choosing the best treatment plan for personalized approaches aimed at optimizing outcomes.
Journal
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FLT3 (Fms-related tyrosine kinase 3) • NRAS (Neuroblastoma RAS viral oncogene homolog) • KIT (KIT proto-oncogene, receptor tyrosine kinase)
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NRAS mutation • FLT3 mutation • KIT mutation
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Xospata (gilteritinib) • Rydapt (midostaurin)
3ms
Early Prediction and Streamline of Nucleophosmin Mutation Status in Acute Myeloid Leukemia Using Cup-Like Nuclear Morphology. (PubMed, Medicina (Kaunas))
Our investigation confirmed that the morphological identification of CLB at diagnosis represents a reliable and easily reproducible tool for the early prediction of NPM1 mutations, enabling a streamlined genetic work-up for its confirmation. This may facilitate considering the early administration of individualized therapies by clinicians for specific patients.
Retrospective data • Journal
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FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1)
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FLT3 mutation • NPM1 mutation
3ms
High expression of ARHGEF5 predicts unfavorable prognosis in acute myeloid leukemia. (PubMed, Discov Oncol)
Pathway enrichment analyses using GO and KEGG, along with protein-protein interaction network and single sample gene set enrichment analyses, revealed key pathways and immune cell associations linked to ARHGEF5. These findings suggest that ARHGEF5 overexpression could serve as a biomarker for unfavorable outcomes in AML, providing insights into the underlying mechanisms of AML onset and progression.
Journal
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FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1)
|
FLT3 mutation • NPM1 mutation • RAS wild-type
3ms
Journal
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FLT3 (Fms-related tyrosine kinase 3)
|
FLT3 mutation
|
sorafenib
3ms
Quizartinib: a new hope in acute myeloid leukemia, an applied comprehensive review. (PubMed, Future Oncol)
It has shown promise in clinical studies since 2013 due to its excellent oral absorption and potent activity on FLT3. This review explores Quizartinib's mechanism of action, efficacy in monotherapy or combination with chemotherapy, drug interactions, adverse events, resistance mechanisms and future research directions.
Review • Journal
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FLT3 (Fms-related tyrosine kinase 3)
|
FLT3-ITD mutation • FLT3 mutation
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Vanflyta (quizartinib)