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. 2012 Aug 1;120(11):2297–2306. doi: 10.1182/blood-2012-02-414425

Table 2.

Frequencies and distribution of genetic abnormalities by CD25 expression in the subgroup with E1900 patients with mutational analysis

Mutations CD25NEG (n = 321), no. (%) CD25POS (n = 75), no. (%) P
DNMT3A 55 (18) 33 (44) < .001
DNMT3A R882 36 (12) 27 (36) < .001
DNMT3A other 21 (7) 6 (8) .801
IDH1 or IDH2 51 (16) 5 (7) .043
TET2 28 (9) 5 (7) .695
FLT3-ITD 63 (20) 57 (76) < .001
FLT3-TKD mutated 23 (7) 4 (5) .79
NPM1 83 (26) 35 (46) .001
PHF6 7 (2) 2 (3) .688
KIT 22 (7) 1 (1) .096
CEBPa 32 (10) 2 (3) .040
WT1 21 (7) 9 (12) .149
KRAS 6 (2) 2 (3) .654
NRAS 37 (12) 3 (4) .055
TP53 6 (2) 2 (3) .654
PTEN 4 (2) 2 (3) .326
RUNX1 13 (4) 7 (9) .090
CBF 42 (13) 1 (1) .002
del(5q) 11 (3) 1 (1) .476
EVI1pos* 7 (2) 1 (1) 1.000
MLL-PTD 11 (3) 8 (11) .016
Split MLL* 25 (8) 0 (0) .007
del(7q) of monosomy 7† 8 (3) 3 (1) 1.000
Trisomy 8† 13 (4) 6 (8) .227
Complex karyotype 29 (9) 2 (3) .091

CBF indicates core-binding-factor leukemias (carrying transcripts AML1/ETO or CBFβ/MYH11) that were detected by OCR and FISH; ITD, internal tandem duplication; PTD, partial tandem duplication; TKD, tyrosine kinase domain.

EVI1 and chromosome translocation resulting into a split of the MLL gene (split MLL) were assessed by FISH.

del(7q)/monosomy 7 and trisomy 8 were assessed by standard cytogenetics or FISH.

Complex karyotypes were defined as ≥ 3 clonal cytogenetic aberrations.