Fig. 3

Single-cell sequencing reveals differential clonal evolutionary and mutational patterns in leukemia. (a) Non-linear, parallel clonal evolution was found from clonal hematopoiesis to MDS or AML [41]. (b) The typical AML leukemia evolutionary pattern is summarized. Mutual exclusive driver mutations are frequently observed in different subclones, where subsequent branched or linear clonal architecture was found [43]. (c) The sequence of mutation gain was also depicted by single-cell studies in AML and ALL, where DITA (DNMT3A, TET2, ASXL1 and/or IDH1 or IDH2) is the most prevalent initiating mutation in AML [15], and linage-related mutation often occurs earlier than kinase-activating mutations in ALL [49]