Table 1 |
||||
|
The main morphological, clinical, cytogenetic and molecular genetic characteristics, and treatment options, in the major myeloid malignancies |
||||
|
Characteristics/treatment options |
CML |
CMML |
APL |
AML |
|
|
||||
|
Morphological characteristics |
Proliferation of mature granulocytes and precursors |
Proliferation of monocytes, also dysplasia in other cell lineages |
Accumulation of promyelocytes |
Accumulation of immature myeloid cells |
|
Clinical characteristics |
Mild symptoms (malaise, low fever), often asymptomatic; slow progression of disease |
Bone marrow failure; often general symptoms: weight loss, night sweats |
Often severe bone marrow failure (anemia, infection, bleeding) often coagulopathy; aggressive disease |
Often severe bone marrow failure (anemia, infection, bleeding); aggressive disease |
|
Cytogenetic characteristics |
Reciprocal translocation between chromosomes 9 and 22 t(9;22) |
Several described; could also be normal (60% to 70%) |
Balances reciprocal translocation between chromosomes 15 and 17 t(15;17) |
Several described; could also be normal (45%) |
|
Molecular genetic characteristics |
Probably important in disease development and resistance to TKIs |
Several described; RAS family (N-RAS/K-RAS) seems of special interest |
None recognized |
Several discovered (Table 2), important in risk stratification |
|
Main treatment options |
First- and second-generation TKIs, allo-SCT |
Chemotherapeutics, 5-azacitidine, allo-SCT |
ATRA, arsenic trioxide, chemotherapeutics, allo-SCT |
Chemotherapeutics, allo-SCT |
|
|
||||
|
allo-SCT, allogenic stem cell transplantation; AML, acute myeloid leukemia; APL, acute promyelocytic leukemia; ATRA, all-trans retinoic acid; CML, chronic myeloid leukemia; CMML, chronic myelomonocytic leukemia; TKI, tyrosine kinase inhibitor. |
||||
|
Hjelle et al. Genome Med 2010 2:41 doi:10.1186/gm162 |
||||