MXD1 regulates the imatinib resistance of chronic myeloid leukemia cells by repressing BCR-ABL1 expression

Chronic myeloid leukemia (CML) is a common myeloproliferative neoplasm characterized by the chromosomal translocation t(9;22) (q34;q11) [1]. This translocation causes the generation of a fusion oncogene, namely, the BCR-ABL1 encoding fusion protein with constitutive tyrosine kinase activity, which gives rise to the uncontrolled growth of myeloid cells in the bone marrow through a series of downstream pathways [2,3]. One of the first-line treatments for CML is imatinib, a tyrosine kinase inhibitor (TKI) that competitively binds to the ATP-binding site of Bcr-Abl and blocks the downstream signal pathway [4,5].

Source: Leukemia Research - October 25, 2018 Category: Hematology Authors: Chen Huan, Lou Jin, Wang Heng, An Na, Pan Yuming, Du Xin, Zhang Qiaoxia Source Type: research