Dr Loghavi on Key Updates to the WHO Diagnostic Criteria for AML

“There’s now been an effort in harmonizing the 2 [WHO classifications for AML] into 1 classification that is going to be the WHO 6th edition.”

Sanam Loghavi, MD, an associate professor in the Department of Hematopathology, as well as co-director and medical director of the Department of Translational Molecular Pathology, all in the Division of Pathology-Lab Medicine, at The University of Texas MD Anderson Cancer Center, discussed the details of recent updates to the World Health Organization (WHO) diagnostic criteria for patients with acute myeloid leukemia (AML) and touched on the rationale behind the updates and the current problems in AML clinical practice that they seek to address.

Loghavi began by explaining the dynamics and different efforts that surround diagnostic criteria for AML. She specifically pointed out previous diagnostic criteria that are driving the updates, underscoring the WHO 5th edition diagnostic criteria for AML and the International Consensus Classification (ICC) diagnostic criteria for AML. Loghavi noted that both criteria were published at similar times, sharing many common characteristics but also possessing areas of divergence. The differences found between each criteria gave rise to confusion in everyday practice for clinicians when trying to diagnose AML, she said.

Loghavi outlined how updates to diagnostic criteria are efforts to harmonize each classification into one unified classification that will ultimately be the 6th edition of WHO diagnostic criteria for AML. In addition to harmonizing each classification, an equally important aspect of updating diagnostic criteria is the incorporation of novel data, technologies, and treatment strategies, she mentioned. One area of diagnostic criteria that require updates due to new FDA approvals that Loghavi underscored are menin inhibitors. She noted that with menin inhibitors are approved for select patients with relapsed/refractory AML, and determining eligibility for menin inhibition is important, along with understanding the underlying genetic profile of the disease.