ArticleCommunications biology2024
Parbendazole as a promising drug for inducing differentiation of acute myeloid leukemia cells with various subtypes.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Targeting WNK1 Releases Differentiation Block in Acute Myeloid Leukemia.bioRxiv : the preprint server for biology · 2026Article
- Statins induce monocytic differentiation in acute myeloid leukemia cells through the KLF4/DPYSL2A axis.FEBS open bio · 2025Article
- A deep learning framework forNational science review · 2025Article
- STK405759 targets microtubules, modulates STAT1, and enhances ruxolitinib efficacy in myeloproliferative neoplasms.American journal of cancer research · 2025Article
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Authors and funding
15 authors at 2 institutions in 1 country.
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Abstract
Acute myeloid leukemia (AML) is a malignancy characterized by differentiation arrest of hematopoietic precursor cells. Differentiation therapy is effective for patients with acute promyelocytic leukemia; however, only a few effective differentiation therapies have been established for patients with other AML subtypes. In this study, seven benzimidazole anthelmintics were examined to determine the effects of differentiation on AML cells. The expression of monocyte markers (CD11b and CD14) was elevated after treatment with most benzimidazole anthelmintics. Among these drugs, parbendazole (PBZ) induced AML cell differentiation at low concentration. PBZ induced the monocyte marker expression, KLF4/DPYSL2A gene expression, and apoptosis for 21 AML cell lines with various subtypes and a primary AML sample. Finally, an in vivo analysis using an AML patient-derived xenograft mouse model showed a significant decrease in the chimerism level and prolonged survival in PBZ-treated mice. These findings could lead to a more effective differentiation therapy for AML.
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Registered trials
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