Table 1. Characteristics of the three different phases of chronic myeloid leukemia (CML): chronic phase (CP), accelerated phase (AP), and blast crisis (BC).
| Alterations | CP | AP | BC |
|---|---|---|---|
| Oncogene | BCR-ABL1 | BCR-ABL1 | BCR-ABL1 |
| Blast count | <10% | 10–19% in the peripheral blood and/or bone marrow |
>20% |
| Cell of origin | Hematopoietic stem cell |
Hematopoietic stem or progenitor cell | |
|
Additional chromosomal alterations |
Second Ph, trisomy 8, isochromosome 17q, trisomy 19, complex karyotype, or abnormalities of 3q26.228 |
Trisomy 8, isochromosome 17, duplication of the Ph chromosome or chromosome 19, 21, or 17, loss of chromosome Y or monosomy 729 |
|
| Epigenetic factors | ASXL1, DNMT3A, RUNX1, and TET230 | ||
| Tumor suppressors | RB1, TP53, and CDKN2A29 | ||
| Other kinase involvement | Fyn kinase, CaMKIIγ31,32 | ||
| DNA damage response | Relatively low | Impaired33 |
Abbreviations: ASXL1, ASXL transcriptional regulator 1; CaMKIIγ, calcium/calmodulin dependent protein kinase II gamma; CDKN2A, cyclin dependent kinase inhibitor 2A; DNMT3A, DNA methyltransferase 3 alpha; Ph, Philadelphia chromosome; RB1, RB transcriptional corepressor 1; RUNX1, RUNX family transcription factor 1; TET2, Tet methylcytosine dioxygenase 2; TP53, tumor protein P53.