AI Article Synopsis
- Acute myeloid leukemia (AML) involves the halted development of blood cell precursors, with limited differentiation therapies available outside acute promyelocytic leukemia.
- A study evaluated seven benzimidazole anthelmintics, finding that most increased expression of monocyte markers in AML cells, with parbendazole (PBZ) being particularly effective at inducing differentiation, gene expression changes, and cell death.
- In tests with a mouse model of AML, PBZ treatment significantly reduced disease progression and improved survival, suggesting potential for better differentiation therapies in AML patients.
Article 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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10808455 | PMC |
| http://dx.doi.org/10.1038/s42003-024-05811-8 | DOI Listing |
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