ArticleBlood2012
KIT with D816 mutations cooperates with CBFB-MYH11 for leukemogenesis in mice.
Article in Blood, 2012. 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, 46 citations in OpenAlex.
- Combination of dasatinib with chemotherapy in previously untreated core binding factor acute myeloid leukemia: CALGB 10801.Blood advances · 2020Trial
- Mutation Patterns Define Clinical Heterogeneity in Acute Myeloid Leukemia.Journal of Cancer · 2026Article
- Comparing the efficacy and safety of venetoclax combined with hypomethylating agents versus intensive chemotherapy as induction therapy in newly diagnosed core binding factor acute myeloid leukemia patients.Blood cancer journal · 2025Article
- N-MYC regulates cell survival via eIF4G1 in inv(16) acute myeloid leukemia.Science advances · 2024Article
- Core-binding factor abnormalities involving chromosome 16 in acute myeloid leukaemia: prognostic and therapeutic implications.BMJ case reports · 2023Article
- Neoantigen-specific TCR-T cell-based immunotherapy for acute myeloid leukemia.Experimental hematology & oncology · 2022Review
- Phosphorylation of SHP2 at Tyr62 Enables Acquired Resistance to SHP2 Allosteric Inhibitors in FLT3-ITD-Driven AML.Cancer research · 2022Article
- Murine Models of Acute Myeloid Leukemia.Frontiers in oncology · 2022Review
- Review
- [Prognostic value of KIT and other clonal genetic mutations in core-binding factor acute myeloid leukemia].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2021Article
- Targeted inhibition of cooperative mutation- and therapy-induced AKT activation in AML effectively enhances response to chemotherapy.Leukemia · 2021Article
- Emerging therapies for inv(16) AML.Blood · 2021Review
- CBFB-MYH11 fusion neoantigen enables T cell recognition and killing of acute myeloid leukemia.The Journal of clinical investigation · 2020Article
- Mutant CEBPA directly drives the expression of the targetable tumor-promoting factor CD73 in AML.Science advances · 2019Article
- Regulation of Kit Expression in Early Mouse Embryos and ES Cells.Stem cells (Dayton, Ohio) · 2019Article
- IL1RL1 is dynamically expressed on Cbfb-MYH11Scientific reports · 2019Article
- The Impact of the Cellular Origin in Acute Myeloid Leukemia: Learning From Mouse Models.HemaSphere · 2019Review
- Pediatric Acute Myeloid Leukemia (AML): From Genes to Models Toward Targeted Therapeutic Intervention.Frontiers in pediatrics · 2019Review
- Preleukemia and Leukemia-Initiating Cell Activity in inv(16) Acute Myeloid Leukemia.Frontiers in oncology · 2018Review
- Targeting binding partners of the CBFβ-SMMHC fusion protein for the treatment of inversion 16 acute myeloid leukemia.Oncotarget · 2016Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
KIT mutations are the most common secondary mutations in inv(16) acute myeloid leukemia (AML) patients and are associated with poor prognosis. It is therefore important to verify that KIT mutations cooperate with CBFB-MYH11, the fusion gene generated by inv(16), for leukemogenesis. Here, we transduced wild-type and conditional Cbfb-MYH11 knockin (KI) mouse bone marrow (BM) cells with KIT D816V/Y mutations. KIT transduction caused massive BM Lin(-) cell death and fewer colonies in culture that were less severe in the KI cells. D816Y KIT but not wild-type KIT enhanced proliferation in Lin(-) cells and led to more mixed lineage colonies from transduced KI BM cells. Importantly, 60% and 80% of mice transplanted with KI BM cells expressing D816V or D816Y KIT, respectively, died from leukemia within 9 months, whereas no control mice died. Results from limiting dilution transplantations indicate higher frequencies of leukemia-initiating cells in the leukemia expressing mutated KIT. Signaling pathway analysis revealed that p44/42 MAPK and Stat3, but not AKT and Stat5, were strongly phosphorylated in the leukemia cells. Finally, leukemia cells carrying KIT D816 mutations were sensitive to the kinase inhibitor PKC412. Our data provide clear evidence for cooperation between mutated KIT and CBFB-MYH11 during leukemogenesis.
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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.