摘要
Dear editor,Chronic myeloid leukemia(CML)is a malignant myeloproliferative disorder arising from hematopoietic stem cells and accounts for 15%of newly diagnosed cases of leukemia in adults.Central to the pathogenesis of CML is the presence of the BCR-ABL fusion gene resulting from the chromosome translocation t(9;22)(q34;q11)[1].The chimeric oncoprotein encoded by BCR-ABL exhibits aberrant tyrosine kinase activity and drives oncogenic processes by dysregulating or reprogramming multiple downstream signaling pathways involved in cell proliferation,differentiation,and survival[2].Recently,emerging evidences have demonstrated that fusion genes can not only encode oncoprotein but also generate circular RNAs(circRNAs)involved in tumor progression[3].
基金
This work is supported by grants from the National Natural Science Foundation of China(81900156),the China Post-doctoral Science Foundation(2018M640927)
the Post-Doctor Research Project,West China Hospital,Sichuan University(2018HXBH022).