Novel AF1q/MLLT11 favorably affects imatinib resistance and cell survival in chronic myeloid leukemia.

ABSTRACT: Tyrosine kinase inhibitor treatment of chronic myeloid leukemia (CML) has demonstrated beneficial effects. However, resistance to tyrosine kinase inhibitors and disease relapse are still a challenge for CML therapy. In this study, we analyzed bone marrow samples from 149 CML patients and 15 control donors, and investigated the affect of AF1q on CML cell survival and engraftment in vitro and in vivo. We found that AF1q/MLLT11 expression was significantly upregulated in CML patients, especially in CD34⁺ CML cells. Elevated AF1q expression was associated with disease progression. Knockdown of AF1q enhanced imatinib sensitivity, induced apoptosis, and suppressed growth in CML cells. Moreover, AF1q deficiency sensitized CD34⁺ CML cells to imatinib. In contrast, upregulatio

SUBMITTER: Li W 

PROVIDER: S-EPMC6113287 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature