Here’s a stark reality: Black patients with acute myeloid leukemia (AML) face significantly lower survival rates compared to their White counterparts, and the reasons behind this disparity remain shrouded in mystery. But here’s where it gets controversial: while clinical data confirms this alarming trend, researchers have yet to pinpoint a clear biological or genetic explanation. Could it be social factors, undiscovered mutations, or something else entirely? This question is at the heart of a groundbreaking study presented at the American Society of Hematology (ASH) 2025 Annual Meeting, leaving both experts and patients eager for answers.
Lead researcher Shella Saint Fleur-Lominy, MD, PhD, from the University of Maryland School of Medicine, highlights the complexity of the issue. “We’ve ruled out heightened genomic risk as a primary factor,” she explains. “But there could be social determinants or unknown mutations at play that we’re not accounting for.” And this is the part most people miss: the study’s dataset, while extensive, only scratches the surface of potential contributing factors. For instance, the analysis focused on a limited number of mutations due to data constraints, leaving room for unseen genetic variations.
The study examined data from 10 ECOG-ACRIN phase 2 or 3 clinical trials spanning 1984 to 2019, involving 3,469 White, 184 Black, and 156 patients of other ethnicities. Black patients were diagnosed at a younger median age (47.9 years) compared to White patients (53.5 years). Cytogenetic and molecular analyses revealed no significant racial differences in the prevalence of complex karyotypes (CK), AML-MRC, or mutations like FLT3-ITD, CEBPA, TP53, and NPM1. However, NPM1 mutations—typically associated with better outcomes—were linked to worse overall survival in Black patients (19.1 months vs. 8.9 months in White patients).
Here’s the kicker: European LeukemiaNet’s 2017 risk stratification accurately predicted overall survival in both Black and White patients but failed to predict disease-free survival in Black patients. This suggests that while risk categories may align across races, the underlying biology or response to treatment could differ significantly. Saint Fleur-Lominy emphasizes, “We don’t fully understand all the factors driving these disparities, but it’s clear that race is an independent prognostic factor for poorer outcomes in Black patients.”
Hematologist-oncologist Bhavana ‘Tina’ Bhatnagar, DO, points out that while adverse cytogenetic risk was similar across races, Black patients were more likely to carry the NPM1 mutation. “This mutation is usually a good sign, as it often responds well to treatment,” she notes. However, a 2025 report in Blood Advances challenges this assumption, suggesting that NPM1 mutations may not confer the same prognostic benefit in Black patients treated with intensive chemotherapy. Is this a case of one-size-fits-all treatment failing a specific population?
The study also raises questions about treatment access and equity. While complete remission and treatment tolerability rates were similar, White patients were more likely to receive allogeneic stem cell transplants (48.5%) compared to Black patients (37.1%). Could this disparity in advanced treatment options contribute to the survival gap?
So, what’s next? Saint Fleur-Lominy calls for more comprehensive research to unravel the interplay between cytogenetics, social factors, and treatment responses. For clinicians, the takeaway is clear: prognostic studies in AML, largely based on White populations, may not fully apply to Black patients. “We need to acknowledge the limitations of our current understanding and advocate for more inclusive research,” she urges.
Here’s a thought-provoking question for you: If treatment protocols are primarily designed based on data from White patients, are we inadvertently disadvantaging Black patients? Share your thoughts in the comments—let’s spark a conversation that could drive change in AML care.
