Gain-of-function somatic mutations of SET binding protein 1(SETBP1)result in the accumulation of SETBP protein and are detected in 17%of secondary acute myeloid leukemia(AML)patients.1 In fact,high expression of SETBP...Gain-of-function somatic mutations of SET binding protein 1(SETBP1)result in the accumulation of SETBP protein and are detected in 17%of secondary acute myeloid leukemia(AML)patients.1 In fact,high expression of SETBP1 also drives adverse outcomes in human AML.However,the roles of SETBP1 during developmental hematopoiesis and AML progression are still not fully understood.Here we first sought to investigate the functions of SETBP1 in developmental hematopoiesis.展开更多
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 i...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.展开更多
基金supported by grants from the National Natural Science Foundation of China (No.32000569)the Basic and Applied Basic Research Foundation of Guangdong Province,China (No.2019A1515110281).
文摘Gain-of-function somatic mutations of SET binding protein 1(SETBP1)result in the accumulation of SETBP protein and are detected in 17%of secondary acute myeloid leukemia(AML)patients.1 In fact,high expression of SETBP1 also drives adverse outcomes in human AML.However,the roles of SETBP1 during developmental hematopoiesis and AML progression are still not fully understood.Here we first sought to investigate the functions of SETBP1 in developmental hematopoiesis.
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).
文摘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.
