Pharmaceutical inhibition of BCL6 ameliorates resistance to imatinib in chronic myeloid leukemia

作者全名："Xiao, Yingying; Deng, Fang; Luo, Yun; Wang, Teng"

作者地址："[Xiao, Yingying; Luo, Yun; Wang, Teng] Chongqing Med Univ, Affiliated Hosp 2, Dept Hematol, Chongqing, Peoples R China; [Deng, Fang] Chongqing Med Univ, Affiliated Hosp 2, Dept Gynecol & Obstet, Chongqing, Peoples R China"

通信作者："Luo, Y; Wang, T (通讯作者)，Chongqing Med Univ, Affiliated Hosp 2, Dept Hematol, Chongqing, Peoples R China."

来源：HELIYON

ESI学科分类：　

WOS号：WOS:001300635700001

JCR分区：Q2

影响因子：4

年份：2024

卷号：10

期号：16

开始页：　

结束页：　

文献类型：Article

关键词：Chronic myeloid leukemia; Resistance; Imatinib; BI-3812; Bcl6 inhibitor

摘要："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 and drug resistance remain the main challenges in the clinical treatment of CML. The B-cell lymphoma 6 (BCL6) is essential to regulation of multiple function such as immune response and lymphomagenesis in lymph node germinal cells. Recent studies have shown that BCL6 is required for the maintenance of leukemia stem cells in CML, but the expression of Bcl-6 in response to Imatinib and the underlying mechanism are still unclear. Here, we found that BCL6 is expressed at high levels in primary CML bone marrow samples and CML TKI-resistance cell lines. CML cells with higher levels of BCL6 were generally sensitive to treatment with BCL6 inhibitors, BI-3812. Treatment of CML cells with BCL6 inhibitor and TKIs suggested enhanced anti-leukemia activity. In summary, our findings suggest BCL6 as a therapeutic target for the treatment of CML."

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