ArticleOncotarget2016
An essential pathway links FLT3-ITD, HCK and CDK6 in acute myeloid leukemia.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 40 citations in OpenAlex.
- A Type II CDK6 Degrader Enables Cellular Targeting beyond the Limits of Type II Inhibition.Journal of the American Chemical Society · 2026Article
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- RNAPaceDB: a dedicated database to dissect RNA velocity across diverse cell types.Nucleic acids research · 2026Article
- NUP98 oncofusions in myeloid malignancies: An update on molecular mechanisms and therapeutic opportunities.HemaSphere · 2024Review
- Priming lymphocyte responsiveness and differential T cell signaling in pediatric IBD patients withbioRxiv : the preprint server for biology · 2024Article
- Narazaciclib, a novel multi-kinase inhibitor with potent activity against CSF1R, FLT3 and CDK6, shows strong anti-AML activity in defined preclinical models.Scientific reports · 2024Article
- HCK maintains the self-renewal of leukaemia stem cells via CDK6 in AML.Journal of experimental & clinical cancer research : CR · 2021Article
- The RUNX1/RUNX1T1 network: translating insights into therapeutic options.Experimental hematology · 2021Review
- Review
- CDK6 Inhibition: A Novel Approach in AML Management.International journal of molecular sciences · 2020Review
- Preclinical efficacy for a novel tyrosine kinase inhibitor, ArQule 531 against acute myeloid leukemia.Journal of hematology & oncology · 2020Article
- Nucleotide binding domain and leucine-rich repeat pyrin domain-containing protein 12: characterization of its binding to hematopoietic cell kinase.International journal of biological sciences · 2020Article
- Computer simulations of the signalling network in FLT3BMC bioinformatics · 2018Article
- The Src family kinase LCK cooperates with oncogenic FLT3/ITD in cellular transformation.Scientific reports · 2017Article
- Aminoisoquinoline benzamides, FLT3 and Src-family kinase inhibitors, potently inhibit proliferation of acute myeloid leukemia cell lines.Future medicinal chemistry · 2017Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CDK4/CDK6 and RB proteins drive the progression through the G1 phase of the cell cycle. In acute myeloid leukemia (AML), the activity of the CDK/Cyclin D complex is increased. The mechanism involved is unknown, as are the respective roles played by CDK4 or CDK6 in this process. Here, we report that AML cells carrying FLT3-ITD mutations are dependent on CDK6 for cell proliferation while CDK4 is not essential. We showed that FLT3-ITD signaling is responsible for CDK6 overexpression, through a pathway involving the SRC-family kinase HCK. Accordingly, FLT3-ITD failed to transform primary hematopoietic progenitor cells from Cdk6-/- mice. Our results demonstrate that CDK6 is the primary target of CDK4/CDK6 inhibitors in FLT3-ITD positive AML. Furthermore, we delineate an essential protein kinase pathway -FLT3/HCK/CDK6- in the context of AML with FLT3-ITD mutations.
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Registered trials
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.