Diagnostic criteria for atypical chronic myeloid leukemia (aCML)
| Leukocytosis ≥ 13 × 109/L, due to increased numbers of neutrophils and their precursors (promyelocytes, myelocytes and metamyelocytes), the latter constituting ≥ 10% of the leukocytes |
| Cytopenia (thresholds same as for MDS) |
| Blasts < 20% of the cells in blood and bone marrow |
| Dysgranulopoiesis, including the presence of abnormal hyposegmented and/or hypersegmented neutrophils ± abnormal chromatin clumping |
| No or minimal absolute monocytosis; monocytes constitute < 10% of the peripheral blood leukocytes |
| No eosinophilia; eosinophils constitute < 10% of the peripheral blood leukocytes |
| Hypercellular bone marrow with granulocytic proliferation and granulocytic dysplasia, with or without dysplasia in the erythroid and megakaryocytic lineages |
| No BCR::ABL1 or genetic abnormalities of myeloid/lymphoid neoplasms with eosinophilia and tyrosine kinase gene fusions. The absence of MPN-associated driver mutations and the presence of SETBP1 mutations in association with ASXL1 provide additional support for a diagnosis of aCML |
| Leukocytosis ≥ 13 × 109/L, due to increased numbers of neutrophils and their precursors (promyelocytes, myelocytes and metamyelocytes), the latter constituting ≥ 10% of the leukocytes |
| Cytopenia (thresholds same as for MDS) |
| Blasts < 20% of the cells in blood and bone marrow |
| Dysgranulopoiesis, including the presence of abnormal hyposegmented and/or hypersegmented neutrophils ± abnormal chromatin clumping |
| No or minimal absolute monocytosis; monocytes constitute < 10% of the peripheral blood leukocytes |
| No eosinophilia; eosinophils constitute < 10% of the peripheral blood leukocytes |
| Hypercellular bone marrow with granulocytic proliferation and granulocytic dysplasia, with or without dysplasia in the erythroid and megakaryocytic lineages |
| No BCR::ABL1 or genetic abnormalities of myeloid/lymphoid neoplasms with eosinophilia and tyrosine kinase gene fusions. The absence of MPN-associated driver mutations and the presence of SETBP1 mutations in association with ASXL1 provide additional support for a diagnosis of aCML |