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Table 1 Mutations associated with CML-BP

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]
  1. Ph, Philadelphia; NUP98, nucleoporin 98 kDa; HOXA9, homeobox A9; AML, acute myeloid leukemia; EVI1, ecotropic viral integration site 1; GATA-2, GATA binding protein 2; RUNX1, runt-related transcription factor 1; CDKN2A/B, cyclin-dependent kinase inhibitor 2A/B; IKZF1, IKAROS family zinc finger 1; ASXL1, additional sex combs like transcription regulator 1; TET2, tet methylcytosine dioxygenase 2; WT1, wilms tumor 1; NRAS, neuroblastoma RAS viral oncogene homolog; KRAS, Kirsten rat sarcoma viral oncogene homolog; NR, not reported.