ArticleAnimal models and experimental medicine2024
c-myb is involved in CML progression and is a therapeutic target in the zebrafish CML model.
Article in Animal models and experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Targeting SIRT6 epigenetically restrains neutrophil hyperplasia and enhances chemotherapeutic efficacy.Acta pharmaceutica Sinica. B · 2026Article
- Improving the Diagnosis and Follow-Up of Chronic Myeloid Leukemia Using Conventional and Molecular Techniques.Journal of clinical laboratory analysis · 2025Article
- Aurora B facilitates cholangiocarcinoma progression by stabilizing c-Myc.Animal models and experimental medicine · 2024Article
- c-myb is involved in CML progression and is a therapeutic target in the zebrafish CML model.Animal models and experimental medicine · 2024Article
- Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDespite the success of tyrosine kinase inhibitors in chronic myeloid leukemia (CML) therapy, CML still faces the challenges of drug resistance and progression to blast crisis. Twenty-five percent of patients have imatinib resistance and treatment difficulties due to heterogeneity after progression, but little is known about the mechanism. A key transcription factor in hematopoiesis, MYB, has been reported to increase abnormally in several types of aggressive blood disorders including CML.
methodsThis study used a zebrafish model to explore the relationship between BCR/ABL1 and c-myb in CML progression. A CML zebrafish model was crossed with a c-myb hyperactivity transgenic line.
resultsIt was found that both exogenous BCR/ABL1 and c-myb could up-regulate the expression of neutrophil-related genes. More seriously, neutrophil accumulation was observed when BCR/ABL1 was combined with c-myb overexpression. Further studies showed that c-myb may be one of the downstream targets of BCR/ABL1 and the effect of BCR/ABL1 on neutrophils was c-myb dependent. Taking advantage of this inheritable in vivo model, it was shown that a combination of imatinib and flavopiridol, a cyclin-dependent kinase inhibitor targeting MYB, could more effectively alleviate the aggressive phenotype of the double transgene line.
conclusionIn summary, this study suggests that c-myb acts downstream of BCR/ABL1 and is involved in CML progression and is therefore a risk factor and a valuable target for the treatment of CML progression. The model used in the study could be helpful in high-throughput drug screening in CML transformation.
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