ReviewInternational journal of hematology2006
Biology, clinical relevance, and molecularly targeted therapy in acute leukemia with FLT3 mutation.
Review in International journal of hematology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 67 citations in OpenAlex.
- Allogeneic hematopoietic stem cell transplantation at the first remission for younger adults with FLT3-internal tandem duplication AML: The JALSG AML209-FLT3-SCT study.Cancer science · 2020Trial
- Metabolic Signature ofJournal of personalized medicine · 2025Review
- Clinical data and MRI features-based nomogram for differentiation of central nervous system infection and central nervous system involvement in hematological malignancy.Annals of hematology · 2024Article
- Overcoming relapse: prophylactic or pre-emptive use of azacitidine or FLT3 inhibitors after allogeneic transplantation for AML or MDS.International journal of hematology · 2023Review
- Clinical Efficacies of FLT3 Inhibitors in Patients with Acute Myeloid Leukemia.International journal of molecular sciences · 2022Review
- Advances in the pharmacological management of acute myeloid leukemia in adults.Expert opinion on pharmacotherapy · 2022Article
- FLT3 inhibitors for acute myeloid leukemia: successes, defeats, and emerging paradigms.RSC medicinal chemistry · 2022Review
- Clinical implications of combination therapy with quizartinib and craniospinal irradiation for refractory acute myeloid leukemia positive for FMS-like tyrosine kinase 3-internal tandem duplication with central nervous system involvement.Clinical case reports · 2022Article
- FLT3-ITD allelic ratio and HLF expression predict FLT3 inhibitor efficacy in adult AML.Scientific reports · 2021Article
- Frequency of FLT3 Internal Tandem Duplications in Adult Syrian Patients with Acute Myeloid Leukemia and Normal Karyotype.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- Current progress, challenges and future prospects of indazoles as protein kinase inhibitors for the treatment of cancer.RSC advances · 2021Review
- 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
- ＜Editors' Choice＞ How to improve outcomes of elderly patients with acute myeloid leukemia: era of excitement.Nagoya journal of medical science · 2020Review
- FLT3 mutations in acute myeloid leukemia: Therapeutic paradigm beyond inhibitor development.Cancer science · 2020Review
- Silencing of COPB2 inhibits the proliferation of gastric cancer cells and induces apoptosis via suppression of the RTK signaling pathway.International journal of oncology · 2019Article
- Kinases and Cancer.Cancers · 2018Article
- Targeting cancer stem cell-specific markers and/or associated signaling pathways for overcoming cancer drug resistance.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Co-expression of wild-type FLT3 attenuates the inhibitory effect of FLT3 inhibitor on FLT3 mutated leukemia cells.Oncotarget · 2016Article
- Correlation between peripheral blood and bone marrow regarding FLT3-ITD and NPM1 mutational status in patients with acute myeloid leukemia.Haematologica · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression and activating mutations of receptor tyrosine kinases (RTKs) are known to be involved in the pathophysiology of several kinds of cancer cells. FMS-like receptor tyrosine kinase 3 (FLT3), together with KIT, FMS, and platelet-derived growth factor receptor, is a class III RTK. FLT3 mutations were first reported as internal tandem duplication (FLT3/ITD) of the juxtamembrane domain-coding sequence; subsequently, a missense point mutation at the D835 residue and point mutations, deletions, and insertions in the codons surrounding D835 within a FLT3 tyrosine kinase domain (FLT3/KDMs) have been found. FLT3 mutations are the most frequent genetic alterations so far reported in acute myeloid leukemia and are involved in the signaling pathway of autonomous proliferation and differentiation block in leukemia cells. Several large-scale studies have confirmed that FLT3/ITD is strongly associated with leukocytosis and a poor prognosis. Therefore, routine screening for FLT3 mutations is recommended to stratify patients into distinct risk groups. However, because high-dose chemotherapy and stem cell transplantation cannot overcome the adverse effects of FLT3 mutations, the development of FLT3 kinase inhibitors is expected to produce a more efficacious therapeutic strategy for leukemia therapy.
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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.