From: Individualizing kinase-targeted cancer therapy: the paradigm of chronic myeloid leukemia
Mutation | Percentage prevalence | Reference |
---|---|---|
Double Ph chromosome | 38% | [6] |
Isochromosome 17q | 30% (myeloid) | [7] |
Trisomy 8 | 53% (myeloid) | [7] |
Trisomy 19 | 23% (myleoid) | [7] |
p53 mutations | 20-30% (myeloid) | [8] |
p16 mutations | 50% (lymphoid) | [9] |
NUP98-HOXA9 translocations | NR | [10] |
AML-EVI1 translocations | NR | [11] |
GATA-2 mutations | 18% (lymphoid) | [12] |
RUNX1 mutations | 38% (myeloid) | [13] |
CDKN2A/B mutations | 50% (lymphoid) | [14] |
IKZF1 mutations | 55% (lymphoid) | [14] |
ASXL1 mutations | 20.5% (myeloid) | [16] |
TET2 mutations | 7.7% (myeloid) | [16] |
WT1 mutations | 15.4% (myeloid) | [16] |
NRAS/KRAS mutations | 5.1/ 5.1% (myeloid) | [16] |