B-cell acute lymphoblastic leukemia(B-ALL)is a malignant tumor originating from B-lineage lymphoid precursor cells.The incidence of B-ALL is about 80%in childhood acute leukemia and 20%in adults.In recent years,with s...B-cell acute lymphoblastic leukemia(B-ALL)is a malignant tumor originating from B-lineage lymphoid precursor cells.The incidence of B-ALL is about 80%in childhood acute leukemia and 20%in adults.In recent years,with standardized treatment guided by risk stratification,the long-term disease-free survival rate of children is about 80%,while that of adults is less than 40%.However,the specific pathogenesis of the newly identified B-ALL and the targeted therapy strategies have not been vigorously investigated.In this review,we highlight the recent breakthroughs in mechanistic studies and novel therapeutic options in DUX4-and MEF2D-subtype B-ALLs.展开更多
基金This work was supported by research grants 81970132,81770142,81800144,and 31800642 from National Natural Science Foundation of Chinaa research grant 20JC1410600 from Shanghai Science and Technology Committee+1 种基金Shanghai Guangci Translational Medical Research Development Foundationa research grant 20152504 from“Shanghai Municipal Education Commission-Gaofeng Clinical Medicine Grant Support”,“The Program for Professor of Special Appointment(Eastern Scholar)at Shanghai Institute of Higher Learning”,Samuel Waxman Cancer Research Foundation。
文摘B-cell acute lymphoblastic leukemia(B-ALL)is a malignant tumor originating from B-lineage lymphoid precursor cells.The incidence of B-ALL is about 80%in childhood acute leukemia and 20%in adults.In recent years,with standardized treatment guided by risk stratification,the long-term disease-free survival rate of children is about 80%,while that of adults is less than 40%.However,the specific pathogenesis of the newly identified B-ALL and the targeted therapy strategies have not been vigorously investigated.In this review,we highlight the recent breakthroughs in mechanistic studies and novel therapeutic options in DUX4-and MEF2D-subtype B-ALLs.
