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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.