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. Author manuscript; available in PMC: 2014 Jan 2.
Published in final edited form as: Leukemia. 2010 Oct 29;25(1):10.1038/leu.2010.247. doi: 10.1038/leu.2010.247

Table 1.

Characteristics of 10 primary AML samples showing PHF6 inactivation

ID Sex Age (yr) FAB Cytogenetics PHF6 lesion
Cooperative gene mutations
Type of alteration Predicted protein IDH1 IDH2 TET2 ASXL1 FLT3 NPM1 CEBPA WT1 KRAS NRAS
1 M 60 M0 normal Missense H329L WT WT WT WT TKD WT WT WT WT WT
2 M 45 M1 normal Nonsense R274X WT WT WT WT WT WT WT WT WT WT
3 M 72 2nd tri(8) Frameshift R335fs WT WT WT A637fs WT WT WT NA NA NA
4 M 66 M2 tri(8) Nonsense R342X WT R140Q WT WT WT WT WT NA NA NA
5 M 65 2nd normal Missense H302Y WT WT WT WT WT WT WT NA NA NA
6 M 41 M2 tri(8) Frameshift C20fs WT WT WT WT ITD WT WT NA NA NA
7 M 74 2nd del(5q),-7,-20 Missense A40G WT WT WT WT ITD WT H195fs NA NA NA
8 M NA M0 NA Frameshift P200fs WT WT WT E1192X WT WT WT WT WT WT
9 F NA M0* NA Frameshift N171fs WT WT WT WT WT WT WT WT WT G12V
10 M NA M0 NA Nonsense R319X WT R172K WT E558X WT WT P39H WT WT WT

2nd, secondary AML; TKD, tyrosine kinase domain mutation; ITD, internal tandem duplication

*

Biphenotypic T-myeloid leukemia