The role of FLT3 in haematopoietic malignancies
Abstract
Normal haematopoietic cells use complex systems to control proliferation, differentiation and cell death. The control of proliferation is, in part, accomplished through the ligand-induced stimulation of receptor tyrosine kinases, which signal to downstream effectors through the RAS pathway. Recently, mutations in the FMS-like tyrosine kinase 3 (FLT3) gene, which encodes a receptor tyrosine kinase, have been found to be the most common genetic lesion in acute myeloid leukaemia (AML), occurring in approximately 25% of cases. Exploring the mechanism by which these FLT3 mutations cause uncontrolled proliferation might lead to a better understanding of how cells become cancerous and provide insights for the development of new drugs.
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FLT-3 ITD results in constitutive activation in these malignancies.
“Mutations in the FLT-3 gene, such as the most common internal tandem duplication (ITD), result in its constitutive activation in these malignancies.”
From Proteolysis targeting chimeras (PROTACs) are emerging therapeutics for hematologic malignancies (2020) · cites this paper as [128]
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- Authors
- Stirewalt, D. L., & Radich, J. P.
- Affiliations
- University of Washington (US)
- Corresponding author
- Stirewalt, Derek L.
- Venue
- Nature Reviews Cancer
- Published
- 2003-09
- Volume
- 3
- Issue
- 9
- Pages
- 650-665
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- OpenAlex
- W1971028883
- Cited by
- 865
- References
- 123
- Citations by year
- 2026: 18 · 2025: 24 · 2024: 20 · 2023: 40 · 2022: 32 · 2021: 32 · 2020: 38 · 2019: 37 · 2018: 34 · 2017: 33 · 2016: 30 · 2015: 41 · 2014: 44 · 2013: 42 · 2012: 48
- FWCI
- 6.28
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Keywords
- FLT3, FMS-like tyrosine kinase 3, FLT3 mutation, acute myeloid leukemia, hematologic malignancies, receptor tyrosine kinase, Ras signaling, cell proliferation, malignant transformation, targeted therapy
- MeSH terms
- Acute Disease, Cell Division, Cell Transformation, Neoplastic, Humans, Immune System, Leukemia, Myeloid, Ligands, Membrane Proteins, Mutation, Proto-Oncogene Proteins, Receptors, Cell Surface, Signal Transduction, Hematologic Neoplasms, Receptor Protein-Tyrosine Kinases, fms-Like Tyrosine Kinase 3
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