a, CCFs of shared (left), MDS-specific (middle), AML
specific (right) mutations across all cell populations in patient P7024.
b, Single cell targeted sequencing of mutations across
different cell populations of patient P7024. Each column represents the
sequencing results of one single cell of the indicated cell population
(preMDS-SC, MDS-SC, MDS-blasts, preAML-SC, AML-SC, AML-blasts), and the number
of single cells tested in each population is shown in parentheses. The
occurrence of a mutation in a single cell is indicated with the same color as in
(a). c, Schematic model of clonal evolution in
different stem and blast cell populations in patient P7024. Mutations in
EZH2 were acquired early in the founding clone at the MDS
stage, and acquisition of additional mutations in NTRK3 and
DUSP22 contributed to the progression to sAML, while MDS
blasts were characterized by different co-mutations. In this patient sAML
developed from a rare subclone contained within MDS stem cells, and not through
further evolution of MDS blasts. d, CCFs of shared (left),
MDS-specific (middle), AML specific (right) mutations across all cell
populations in patient P7026. e, Single cell targeted sequencing of
mutations across different cell populations of patient P7026. f,
Schematic model of clonal evolution in different stem and blast cell populations
in patient P7026. Data again indicate that the dominant clone present in sAML
stem and blast cells developed from a clone within the MDS stem cells that was
nearly undetectable in MDS blast, indicating a crucial role of MDS stem cells in
sAML initiation. g, CCFs of shared (left), MDS-specific (middle),
AML-specific (right) mutations in different stem and blast populations at the
MDS and sAML stage of patient P7030. h, Single cell targeted
sequencing of mutations across different cell populations of patient P7030.
i, Schematic model of clonal evolution in different stem and
blast cell populations in patient P7030. Subclones of MDS stem cells with early
founding mutations (i.e. U2AF1) remained present during MDS
blast generation as well as AML progression, whereas other mutations, e.g.
PAX3, RNF213, NIN and
KDM6A, only occurred in MDS but not during progression to
sAML. Progression to sAML originated from a subclone of MDS stem cells with
NRAS mutation.