摘要
Internal tandem duplication of FMs-like tyrosine kinase 3(FLT3-ITD)is one of the most common genetic alterations in human acute myeloid leukemia(AML)and confers a poor prognosis for the disease.1 Though several FLT3 inhibitors have been approved in AML,their clinical benefits are still unsatisfactory due to primary refractory and drug resistance.Therefore,it may be crucial to develop novel therapeutics forFLT3-ITD+AML.
基金
This project was supported by grants from Theme-based Research Scheme of the Research Grants Council(Hongkong)(No.T12-707/20-N,A.Y.H.Leung.)
National Natural Science Foundation of China(No.32000569,B.L.He)
GuangDong Basic and Applied Basic Research Foundation,China(No.2019A1515110281,B.L.He).
