Pharmaceutical inhibition of BCL6 ameliorates resistance to imatinib in chronic myeloid leukemia
Chronic myeloid leukaemia
Pharmaceutical Sciences
DOI:
10.1016/j.heliyon.2024.e36640
Publication Date:
2024-08-23T09:54:45Z
AUTHORS (4)
ABSTRACT
The tyrosine kinase inhibitors (TKIs) have improved overall survival of CML (chronic myeloid leukemia) patients and allow them to experience normal life expectancy. However, relapse drug resistance remain the main challenges in clinical treatment CML. B-cell lymphoma 6 (BCL6) is essential regulation multiple function such as immune response lymphomagenesis lymph node germinal cells. Recent studies shown that BCL6 required for maintenance leukemia stem cells CML, but expression Bcl-6 Imatinib underlying mechanism are still unclear. Here, we found expressed at high levels primary bone marrow samples TKI-resistance cell lines. with higher were generally sensitive inhibitors, BI-3812. Treatment inhibitor TKIs suggested enhanced anti-leukemia activity. In summary, our findings suggest a therapeutic target
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