ArticleMolecular medicine reports2018
High expression of FLT3 is a risk factor in leukemia.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- QuANTUM-Wild: a Phase III, randomized trial of quizartinib in newly diagnosedFuture oncology (London, England) · 2026Trial
- Quizartinib for Newly DiagnosedJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2026Trial
- Mislocalisation of FLT3-ITD receptor contributes to MV4-11 leukaemia cell resistance to antibody-drug conjugate.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Immunotherapy in acute myeloid leukemia: The antibodies, TriKEs, and CARs on the arduous road to cure.Blood reviews · 2026Review
- CD135 (FLT3 receptor) expression as an indicator of prognosis in patients with de novo acute myeloid leukemia.Annals of hematology · 2026Article
- Novel molecular mechanisms of FLT3 deregulation: from the acute myeloid leukemia experience to therapeutic insights in acute lymphoblastic leukemia.Molecular cancer · 2025Review
- Gene expression profiling and pathway analysis in acute myeloid leukaemia-normal karyotype patients.PloS one · 2025Article
- Antisense oligonucleotides as a targeted therapeutic approach in model of acute myeloid leukemia.Molecular biology reports · 2024Article
- Atypical Multifocal Granular Cell Tumor with FLT3 Y842C Somatic Mutation: A case report and a review of the literature.La Tunisie medicale · 2024Review
- Cellular hierarchy insights reveal leukemic stem-like cells and early death risk in acute promyelocytic leukemia.Nature communications · 2024Article
- Distinct roles of hematopoietic cytokines in the regulation of leukemia stem cells in murine MLL-AF9 leukemia.Stem cell reports · 2024Article
- Infantile B-cell acute lymphoblastic leukaemia with the highest recorded count of white blood cells in the literature: case report and literature review.Annals of medicine and surgery (2012) · 2023Article
- Molecular and clinical significance of FLT3, NPM1, DNMT3A and TP53 mutations in acute myeloid leukemia patients.Molecular biology reports · 2023Article
- Article
- Infantile B-lymphoblastic leukemia: a case series and review of the literature.The Journal of international medical research · 2023Review
- Lineage tracking to reveal the fate of hematopoietic stem cells influenced by Flk2Experimental & molecular medicine · 2023Article
- Article
- A novel IgG-based FLT3xCD3 bispecific antibody for the treatment of AML and B-ALL.Journal for immunotherapy of cancer · 2022Article
- Longitudinal analyses of CLL in mice identify leukemia-related clonal changes including a Myc gain predicting poor outcome in patients.Leukemia · 2022Article
- Targets for chimeric antigen receptor T-cell therapy of acute myeloid leukemia.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several studies have shown that internal tandem duplication (ITD) of FMS-like tyrosine kinase 3 (FLT3) can result in the failure of leukemia treatment and contribute to a poor prognosis. However, the role of the overexpression of FLT3 in leukemia remains to be fully elucidated. By mining public database, the present study first identified that the expression of FLT3 in leukemia was markedly higher, compared with that in other types of tumor and cell lines, indicating that FLT3 is important in leukemia. In leukemia, FLT3 was found to be significantly upregulated in acute myeloid leukemia and acute lymphoblastic leukemia, and a high expression of FLT3 contributed to reduced survival rates. By analyzing Gene Expression Omnibus and The Cancer Genome Atlas data, it was found that genetic alterations and modification of DNA methylation increased the expression of FLT3 in leukemia. FLT3‑ITD and FLT3 tyrosine kinase domain point mutations increased the expression of FLT3 in four independent datasets. In addition, the status of FLT3 gene methylation was negatively correlated with the expression of FLT3, and haploinsufficiency of DNA methyltransferase 1 increased the expression of Flt3 in mouse leukemia cells. By analyzing the enrichment of differentially‑expressed genes in chemical and genetic perturbation datasets, it was found that genes, which were upregulated in the FLT3 high expression group had myeloid lymphoid leukemia‑ and nucleophosmin 1‑like signatures, indicating that the overexpression of FLT3 may use the same mechanism to promote leukemia. Collectively, the results of the present study showed that the overexpression of FLT3 is a potential risk factor in leukemia.
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