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. 2017 Jan 3;31(3):534–542. doi: 10.1038/leu.2016.364

Table 1. Exome sequencing: mutational defects in MDS and sAML versus de novo AML.

MDS
sAML
De novo AML
Gene Mutations (%) Gene Mutations (%) Gene Mutations (%)
TET2a 33 TET2a 20 FLT3b 28
→SF3B1a 32 SF3B1a 11 NPM1b 27
ASXL1a 23 ASXL1a 32 DNMT3A 26
→SRSF2a 17 SRSF2a 20 IDH1/2 10
→ZRSR2a 8 ZRSR2a 8 RUNX1b 9
EZH2 a 5 EZH2a 9 TET2 9
BCORa 4 BCORa 8 NRAS/KRASb 8
→U2AF1a 8 U2AF1a 16 TP53 8
STAG2a 8 STAG2a 14 CEBPAb 6
RUNX1 10 RUNX1b 31 WT1b 6
DNMT3A 13 NF1b 6 PTPN11b 5
IDH2/IDH1 5 NRAS/KRASb 31 KITb 4
TP53 6 TP53 15 U2AF1 4
FLT3 5 IDH1/2 20 KRASb 4
CBL 5 FLT3b 19 SMC1A 4
JAK2 5 DNMT3A 19 SMC3 4
BCOR 3 PTPN11b 5 PHF6 3
NRAS or KRAS 7 CEBPAb 3 STAG2 2
MPL 3 NPM1b 5 RAD21 2
NF1 3 SMC3 2 FAM5C 2
ATM 3 CBL 5 EZH2 1

→, mutant spliceosome gene; sAML, secondary AML (MDS→AML). MDS data;9 sAML data;30 de novo AML data.26

a

Notable difference of incidence during MDS and sAML versus de novo AML.

b

Driver (Pan AML) mutations.