ORLANDO, Fla. — A new analysis of three decades of clinical trial data confirms that Black patients with acute myeloid leukemia (AML) have worse survival outcomes than White patients. However, researchers found no link between heightened genomic risk and worse outcomes in Black vs White patients.
So, what explains the difference?
“There could be social factors that we're not accounting for,” lead study author Shella Saint Fleur-Lominy, MD, PhD, University of Maryland School of Medicine and Greenebaum Comprehensive Cancer Center, Baltimore, said in an interview.
Or “there could be other mutations that we don't know about. We only looked at a very limited number of mutations because of the limitations of the dataset,” said Saint Fleur-Lominy, who presented the results of the analysis here at the American Society of Hematology (ASH) 2025 Annual Meeting.
Researchers have varying theories about what could explain the differences in AML mortality between Black and White patients, including access to treatment, access to novel treatment, or differences in genetic abnormalities associated with the disease, she explained. “But we don't fully understand all the factors that are contributing to the disparity in outcomes,” she added.
During a media briefing at the meeting, Saint Fleur-Lominy added that the current study findings are based on a patient population that was able to participate in large, cooperative clinical trials. “So, we think that is less likely related to social factors,” she said. Instead, mutations “that we’re not testing for” could be responsible.
ECOG-ACRIN Trials
For the study, researchers examined patients across 10 ECOG-ACRIN phase 2 or 3 interventional clinical trials from 1984 to 2019: 3469 White, 184 Black, and 156 other ethnicities. Black patients were younger at diagnosis, with a median age of 47.9 years vs 53.5 years in White patients (P < .001).
Complete cytogenetic results were available for 117 Black and 2162 White patients.
No difference was observed between Black and White patients in the prevalence of complex karyotype (CK), CK with -5/del(5q), -7/del(7q), or -17/del(17p), and AML-MRC including +8 and del(20q). In addition, in patients with molecular data, there was no sign of racial differences in prevalence of FLT3-ITD, CEBPA, TP53, or NPM1. However, NPM1 mutations were linked to worse overall survival in Black vs White patients (19.1 vs 8.9 months, respectively; P = .0095).
European LeukemiaNet 2017 risk stratification by favorable, intermediate, and adverse similarly predicted overall survival in Black patients (57.8 vs 14.2 vs 5.8 months; P = .018) and White patients (60.1 vs 15.2 vs 7.1 months; P < .0004). However, it only predicted disease-free survival in White patients (P < .0001) and not Black patients (P = .48).
Overall, Black race was an independent prognostic factor for inferior overall survival (hazard ratio [HR], 1.21; P = .0383) and disease-free survival (HR, 1.31; P = .017).
Complete remission and treatment tolerability rates were similar. Among those who underwent stem cell transplants (about 20% in both Black and White patients), White patients were more likely to receive allogeneic transplants vs Black patients (48.5% vs 37.1%; P < .01).
A More Aggressive Disease?
Hematologist-oncologist Bhavana “Tina” Bhatnagar, DO, director of hematology and medical oncology at the West Virginia University Cancer Institute at Wheeling Hospital, who was familiar with the study findings but didn’t take part in the research, noted that worse survival in AML in Black patients is sometimes linked to more aggressive disease. But the study found that adverse cytogenetic risk was the same in Black vs White patients.
She also highlighted the finding that Black patients were more likely to have the NPM1 mutation, present in about 30% of people, she said. “When you see an NPM1, you get a little encouraged by it” because it's usually linked to better response to care.
However, a 2025 report published in Blood Advances noted that “growing evidence suggests that NPM1 mutations do not seem to confer as favorable a prognostic impact on Black patients as on White patients treated with intensive chemotherapy; therefore, the most effective regimen for Black patients with NPM1-mutated AML is unknown.”
What’s next? More research is needed to better understand the racial disparities in outcomes, Saint Fleur-Lominy said, adding it is possible that there could still be an interplay between cytogenetics and other factors.
As for take-home messages for clinicians, Saint Fleur-Lominy said it is important to advise patients — particularly Black patients — about the limitations of prognostic studies in AML. “We may still be missing things,” she said, and patients “should understand that we don't really have the full picture.”
Bhatnagar agreed: “The way we prognosticate is based on a predominantly White population.”
What might be considered good or bad in the overall AML population might not apply to Black patients, she added. Black patients may require more aggressive treatment.
There was no specific funding for the study. Saint Fleur-Lominy has disclosed a relationship with AstraZeneca. Some other authors have reported various disclosures. Bhatnagar had no disclosures.
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