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Atypical chronic myeloid leukemia (aCML) (myelodysplastic \u201c[<jats:italic>MDS<\/jats:italic>]\/<jats:italic>MPN with neutrophilia<\/jats:italic>\u201d per World Health Organization [WHO]) is a MDS\/MPN overlap disorder featuring dysplastic neutrophilia and circulating myeloid precursors. Both manifest with frequent hepatosplenomegaly and less commonly, bleeding, with high rates of leukemic transformation and death. The 2022 revised WHO classification conserved CNL diagnostic criteria of leukocytosis \u226525\u2009\u00d7\u200910<jats:sup>9<\/jats:sup>\/L, neutrophils \u226580% with &lt;10% circulating precursors, absence of dysplasia, and presence of an activating <jats:italic>CSF3R<\/jats:italic> mutation. ICC criteria are harmonized with those of other myeloid entities, with a key distinction being lower leukocytosis threshold (\u226513\u2009\u00d7\u200910<jats:sup>9<\/jats:sup>\/L) for cases <jats:italic>CSF3R\u2010<\/jats:italic>mutated. Criteria for aCML include leukocytosis \u226513\u2009\u00d7\u200910<jats:sup>9<\/jats:sup>\/L, dysgranulopoiesis, circulating myeloid precursors \u226510%, and at least one cytopenia for MDS\u2010thresholds (ICC). In both classifications <jats:italic>ASXL1<\/jats:italic> and <jats:italic>SETBP1<\/jats:italic> (ICC), or <jats:italic>SETBP1<\/jats:italic>\u2009\u00b1\u2009<jats:italic>ETNK1<\/jats:italic> (WHO) mutations can be used to support the diagnosis. Both diseases show hypercellular bone marrow due to a granulocytic proliferation, aCML distinguished by dysplasia in granulocytes\u2009\u00b1\u2009other lineages. Absence of monocytosis, rare\/no basophilia, or eosinophilia, &lt;20% blasts, and exclusion of other MPN, MDS\/MPN, and tyrosine kinase fusions, are mandated. Cytogenetic abnormalities are identified in ~1\/3 of CNL and ~15\u201340% of aCML patients. The molecular signature of CNL is a driver mutation in colony\u2010stimulating factor 3 receptor\u2014classically T618I, documented in &gt;80% of cases. Atypical CML harbors a complex genomic backdrop with high rates of recurrent somatic mutations in <jats:italic>ASXL1<\/jats:italic>, <jats:italic>SETBP1<\/jats:italic>, <jats:italic>TET2<\/jats:italic>, <jats:italic>SRSF2<\/jats:italic>, <jats:italic>EZH2<\/jats:italic>, and less frequently in <jats:italic>ETNK1<\/jats:italic>. Leukemic transformation rates are ~10\u201325% and 30\u201340% for CNL and aCML, respectively. Overall survival is poor: 15\u201331\u2009months in CNL and 12\u201320\u2009months in aCML. The Mayo Clinic CNL risk model for survival stratifies patients according to platelets &lt;160\u2009\u00d7\u200910<jats:sup>9<\/jats:sup>\/L (2 points), leukocytes &gt;60\u2009\u00d7\u200910<jats:sup>9<\/jats:sup>\/L (1 point), and <jats:italic>ASXL1<\/jats:italic> mutation (1 point); distinguishing low\u2010 (0\u20131 points) versus high\u2010risk (2\u20134 points) categories. The Mayo Clinic aCML risk model attributes 1 point each for: age &gt;67\u2009years, hemoglobin &lt;10\u2009g\/dL, and <jats:italic>TET2<\/jats:italic> mutation, delineating low\u2010 (0\u20131 risk factor) and high\u2010risk (\u22652 risk factors) subgroups. Management is risk\u2010driven and symptom\u2010directed, with no current standard of care. Most commonly used agents include hydroxyurea, interferon, Janus kinase inhibitors, and hypomethylating agents, though none are disease\u2010modifying. Hematopoietic stem cell transplant is the only potentially curative modality and should be considered in eligible patients. Recent genetic profiling has disclosed <jats:italic>CBL<\/jats:italic>, <jats:italic>CEBPA<\/jats:italic>, <jats:italic>EZH2<\/jats:italic>, <jats:italic>NRAS<\/jats:italic>, <jats:italic>TET2<\/jats:italic>, and <jats:italic>U2AF1<\/jats:italic> to represent high\u2010risk mutations in both entities. Actionable mutations (<jats:italic>NRAS\/KRAS<\/jats:italic>, <jats:italic>ETNK1<\/jats:italic>) have also been identified, supporting novel agents targeting involved pathways. Preclinical and clinical studies evaluating new drugs (e.g., fedratinib, phase 2) and combinations are detailed.<\/jats:p>","DOI":"10.1002\/ajh.27321","type":"journal-article","created":{"date-parts":[[2024,4,22]],"date-time":"2024-04-22T06:53:35Z","timestamp":1713768815000},"page":"1360-1387","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Chronic neutrophilic leukemia and atypical chronic myeloid leukemia: 2024 update on diagnosis, genetics, risk stratification, and management"],"prefix":"10.1002","volume":"99","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1499-6171","authenticated-orcid":false,"given":"Natasha","family":"Szuber","sequence":"first","affiliation":[{"name":"Department of Hematology Maisonneuve\u2010Rosemont Hospital  Montreal Quebec 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