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Review
. 2025 Jan 31;9(2):e70083.
doi: 10.1002/hem3.70083. eCollection 2025 Feb.

Diagnosis and treatment of AML in the context of WHO and ICC 2022 classifications: Divergent nomenclature converges on common therapies

Uwe Platzbecker  1 , Richard A Larson  2 , Sandeep Gurbuxani  3
Affiliations
Review

Diagnosis and treatment of AML in the context of WHO and ICC 2022 classifications: Divergent nomenclature converges on common therapies

Uwe Platzbecker et al. Hemasphere. .

Abstract

As a consequence of rapidly developing genetic technologies and advances in the understanding of the pathogenesis of acute myeloid leukemia (AML), the classification of AML has moved gradually from a morphologic and cytochemical-based system to one that is genetically defined. Recent molecular and genetic developments have been integrated into the diagnostic criteria for AML in the fifth edition of the World Health Organization (WHO) Classification of Haematolymphoid Tumours and the 2022 International Consensus Classification (ICC) of Myeloid Neoplasms and Acute Leukemias, expanding the list of genetically defined entities. In this review article, we use a case-based format describing the diagnostic workup, risk stratification, and possible treatment options to highlight the impact of the 2022 WHO and ICC classifications on clinical practice. We show that despite much commentary and anguish, there is a significant overlap between the two classifications. We further highlight the fact that even for entities with divergent nomenclature, such as TP53-mutated AML, the actual genetic lesion leads to convergent therapy.

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Conflict of interest statement

Uwe Platzbecker has acted as a consultant or advisor to AbbVie, Takeda, Celgene/BMS, Curis, Jazz Pharmaceuticals, Novartis, and Servier; has received clinical research support to his institution from Astellas, Celgene, Cellectis, Daiichi‐Sankyo, FortySeven/Gilead, Novartis, and Rafael Pharmaceuticals; and has received royalties from UpToDate. Richard A. Larson has acted as a consultant or advisor to AbbVie, Amgen, Ariad/Takeda, Astellas, Celgene/BMS, Curis, CVS/Caremark, Epizyme, Immunogen, Jazz Pharmaceuticals, Kling Biotherapeutics, MedPace, MorphoSys, Novartis, and Servier; has received clinical research support to his institution from Astellas, Celgene, Cellectis, Daiichi‐Sankyo, FortySeven/Gilead, Novartis, and Rafael Pharmaceuticals; and has received royalties from UpToDate. Sandeep Gurbuxani has served as a consultant to AbbVie; has received honoraria from Jazz Pharmaceuticals; and collects royalties from UpToDate.

Figures

Figure 1
Figure 1
Case study one: histopathological images. (A) Peripheral blood smear; (B) bone marrow biopsy; (C) bone marrow aspirate; (D) immunohistochemistry staining for NPM1 (red). Intracytoplasmic NPM1 is due to mutation.
Figure 2
Figure 2
Case study two: histopathological images. (A) Peripheral blood smear; (B) bone marrow biopsy; (C) bone marrow aspirate; (D) immunohistochemistry staining for TP53 (brown).
Figure 3
Figure 3
Case study three: histopathology and cytogenetics. (A) Bone marrow biopsy; (B) cytogenetics showing complex karyotype.
Figure 4
Figure 4
Case study four: histopathology and cytogenetics. (A, B) Bone marrow aspirate smears; (C) karyotype analysis showing t(8;21) as well as trisomy 8 and loss of Y.
See this image and copyright information in PMC

References

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