Reclassification of Acute Myeloid Leukemia According to the 2016 WHO Classification

Ann Lab Med. 2019 May;39(3):311-316. doi: 10.3343/alm.2019.39.3.311.

Abstract

We reviewed our leukemia database to reclassify 610 patients previously diagnosed as having acute myeloid leukemia (AML) according to the updated 2016 WHO classification. Nine patients were categorized as having myelodysplastic syndrome and myeloid neoplasms with germline predisposition. AML with recurrent genetic abnormalities accounted for 57.4% (345/601) of the patients under the 2016 WHO classification. AML with mutated NPM1 was the most common form (16.5%), with the majority associated with monocytic differentiation (63.6%). AML with double CEBPA mutations accounted for 8.3% of these cases, and the majority were previously diagnosed as AML with/without maturation (78.0%). These newly classified mutations were mutually exclusive without overlapping with other forms of AML with recurrent genetic abnormalities. AML with mutated NPM1 and AML with myelodysplasia-related changes comprised the oldest patients, whereas AML with RUNX1-RUNX1T1 included the youngest patients. The leukocyte count was highest in AML with mutated NPM1, and the percentage of peripheral blood blasts was the highest in AML with double CEBPA mutations. Our results indicate that implementation of the 2016 WHO classification of AML would not pose major difficulties in clinical practice. Hematopathologists should review and prepare genetic tests for the new classification, according to their clinical laboratory conditions.

Keywords: 2016 WHO classification; Acute myeloid leukemia; CEBPA; NPM1.

Publication types

  • Review

MeSH terms

  • CCAAT-Enhancer-Binding Proteins / genetics
  • Chromosome Aberrations
  • Core Binding Factor Alpha 2 Subunit / genetics
  • Humans
  • Leukemia, Myeloid, Acute / classification*
  • Leukemia, Myeloid, Acute / genetics
  • Leukemia, Myeloid, Acute / pathology
  • Mutation
  • Nuclear Proteins / genetics
  • Nucleophosmin
  • Oncogene Proteins, Fusion / genetics
  • RNA, Long Noncoding
  • World Health Organization

Substances

  • CCAAT-Enhancer-Binding Proteins
  • CEBPA protein, human
  • Core Binding Factor Alpha 2 Subunit
  • NPM1 protein, human
  • Nuclear Proteins
  • Oncogene Proteins, Fusion
  • RNA, Long Noncoding
  • RUNX1 protein, human
  • RUNX1-IT1 long non-coding RNA, human
  • Nucleophosmin