Cover option for Nature based on Figure 2a.

Figure 2: Graphical representation of clonal evolution from the primary tumour to relapse in UPN 933124, and patterns of tumour evolution observed in eight primary tumour and relapse pairs. a, The founding clone in the primary tumour in UPN 933124 contained somatic mutations in DNMT3A,NPM1, PTPRT, SMC3 and FLT3 that are all recurrent in AML and probably relevant for pathogenesis; one subclone within the founding clone evolved to become the dominant clone at relapse by acquiring additional mutations, including recurrent mutations in ETV6 and MYO18B, and a WNK1-WAC fusion gene. HSC, haematopoietic stem cell. b, Examples of the two major patterns of tumour evolution in AML. Model 1 shows the dominant clone in the primary tumour evolving into the relapse clone by gaining relapse-specific mutations; this pattern was identified in three primary tumour and relapse pairs (UPN 804168, UPN 573988 and UPN 400220). Model 2 shows a minor clone carrying the vast majority of the primary tumour mutations survived and expanded at relapse. This pattern was observed in five primary tumour and relapse pairs (UPN 933124, UPN 452198, UPN 758168, UPN 426980 and UPN 869586).