Associated Papers
Clonal architecture of FLT3-ITD and acquired 13q uniparental disomy define prognostic heterogeneity and therapeutic vulnerabilities in acute myeloid leukemia.
Lai A et al.
Neoplasia (new York, N.y.), 2025
Unveiling splicing disruptions due to common somatic variants in acute myeloid leukemia.
Morote-Faubel M et al.
Human Genomics, 2025
Leveraging genomic diagnostics for prognostics and therapeutics in pediatric acute leukemia.
Newman H et al.
Hemasphere, 2025
Non-canonical FLT3 alterations reveal novel germline FLT3 variants leading to somatic gene rescue mutations.
Gordon J et al.
Blood Cancer Journal, 2024
Multi-target measurable residual disease assessed by error-corrected sequencing in patients with acute myeloid leukemia: An ALFA study.
Hirsch P et al.
Blood Cancer Journal, 2024
Current knowledge about FLT3 gene mutations, exploring the isoforms, and protein importance in AML.
Macečková D et al.
Molecular Biology Reports, 2024
Landscape of FLT3 Variations Associated with Structural and Functional Impact on Acute Myeloid Leukemia: A Computational Study.
Mirza Z et al.
International Journal of Molecular Sciences, 2024
Allosteric SHP2 inhibition increases apoptotic dependency on BCL2 and synergizes with venetoclax in FLT3- and KIT-mutant AML.
Popescu B et al.
Cell Reports. Medicine, 2023
A Review of FLT3 Kinase Inhibitors in AML.
Negotei C et al.
Journal of Clinical Medicine, 2023
Mutation spectrum of FLT3 and significance of non-canonical FLT3 mutations in haematological malignancy.
Ge SS et al.
British Journal of Haematology, 2023
The international consensus classification of eosinophilic disorders and systemic mastocytosis.
Wang SA et al.
American Journal of Hematology, 2023
Updates on eosinophilic disorders.
Tzankov A et al.
Virchows Archiv : an International Journal of Pathology, 2023
Transcriptome-based molecular subtypes and differentiation hierarchies improve the classification framework of acute myeloid leukemia.
Cheng WY et al.
Proceedings of the National Academy of Sciences of the United States of America, 2022
Compartment-specific mutational landscape of clonal hematopoiesis.
Hartmann L et al.
Leukemia, 2022
Genome-wide analyses of 200,453 individuals yield new insights into the causes and consequences of clonal hematopoiesis.
Kar SP et al.
Nature Genetics, 2022
Preclinical and Pilot Study of Type I FLT3 Tyrosine Kinase Inhibitor, Crenolanib, with Sorafenib in Acute Myeloid Leukemia and FLT3-Internal Tandem Duplication.
Inaba H et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2022
Detection of oncogenic and clinically actionable mutations in cancer genomes critically depends on variant calling tools.
Garcia-Prieto CA et al.
Bioinformatics (oxford, England), 2022
Genomic Abnormalities as Biomarkers and Therapeutic Targets in Acute Myeloid Leukemia.
Ribeiro S et al.
Cancers, 2021
Myeloid/lymphoid neoplasms with FLT3 rearrangement.
Tang G et al.
Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc, 2021
Patterns of Resistance Differ in Patients with Acute Myeloid Leukemia Treated with Type I versus Type II FLT3 inhibitors.
Alotaibi AS et al.
Blood Cancer Discovery, 2021
Myeloid/lymphoid neoplasms with eosinophilia and FLT3 rearrangement.
Shao H et al.
Leukemia Research, 2020
Gilteritinib is a clinically active FLT3 inhibitor with broad activity against FLT3 kinase domain mutations.
Tarver TC et al.
Blood Advances, 2020
First Report of Sorafenib in Patients With Acute Myeloid Leukemia Harboring Non-Canonical FLT3 Mutations.
Daver N et al.
Frontiers in Oncology, 2020
FLT3 Mutations in Acute Myeloid Leukemia: Key Concepts and Emerging Controversies.
Kennedy VE et al.
Frontiers in Oncology, 2020
Gene mutation profile and risk stratification in AML1‑ETO‑positive acute myeloid leukemia based on next‑generation sequencing.
Yu G et al.
Oncology Reports, 2019
Clinical resistance to crenolanib in acute myeloid leukemia due to diverse molecular mechanisms.
Zhang H et al.
Nature Communications, 2019
Parallel targeted next generation sequencing of childhood and adult acute myeloid leukemia patients reveals uniform genomic profile of the disease.
Marjanovic I et al.
Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine, 2016
Acute promyelocytic leukemia harbouring rare FLT3-TKD and WT1 mutations: A case report.
Liu TT et al.
Oncology Letters, 2015
Characterizing and Overriding the Structural Mechanism of the Quizartinib-Resistant FLT3 "Gatekeeper" F691L Mutation with PLX3397.
Smith CC et al.
Cancer Discovery, 2015
AMG 925 is a dual FLT3/CDK4 inhibitor with the potential to overcome FLT3 inhibitor resistance in acute myeloid leukemia.
Li C et al.
Molecular Cancer Therapeutics, 2015
Response of ETV6-FLT3-positive myeloid/lymphoid neoplasm with eosinophilia to inhibitors of FMS-like tyrosine kinase 3.
Walz C et al.
Blood, 2011
FLT3 tyrosine kinase domain mutations are biologically distinct from and have a significantly more favorable prognosis than FLT3 internal tandem duplications in patients with acute myeloid leukemia.
Mead AJ et al.
Blood, 2007
A novel FLT3 activation loop mutation N841K in acute myeloblastic leukemia.
Matsuno N et al.
Leukemia, 2005
Mutations within the Activation Loop Domain of FLT3 in Two Pediatric Patients with Refractory Infant Acute Myeloid Leukemia.
Muhlbauer N et al.
Case Reports in Oncology, 0