ArticleAnnals of hematology2026
Impact of race on mutational profile and survival in acute myeloid leukemia: a single-institution experience (2014-2024).
Article in Annals of hematology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
19 authors.
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Abstract
Acute myeloid leukemia (AML) is a biologically heterogeneous hematologic malignancy, and racial disparities in outcomes remain incompletely characterized. This retrospective study analyzed 677 patients diagnosed with AML at Moffitt Cancer Center (2014-2024) to evaluate the impact of race on genomic profiles and clinical outcomes. The cohort comprised 18.6% Black, 19.1% Hispanic, and 62.3% White patients. While ELN 2022 risk groups and most driver mutations were similarly distributed, Black patients exhibited a higher frequency of KRAS mutations (p < 0.05). With a median follow-up of 3.3 years, median overall survival (OS) was 2.2 years for White, 1.5 years for Black, and 2.4 years for Hispanic patients (p = 0.045). Notably, no survival differences existed within favorable or adverse ELN risk categories; however, Black patients with intermediate-risk disease experienced significantly inferior OS compared to White (p = 0.02) and Hispanic patients (p = 0.003). Among those receiving intensive induction, Black patients had significantly worse OS (p ≤ 0.001), while Hispanic patients treated with lower-intensity regimens demonstrated inferior OS compared to White patients (p = 0.01). In multivariable analysis, race was not an independent predictor of OS. Survival was independently driven by prior myeloid malignancy, ELN risk, allogeneic HCT, and mutations in TP53 and IDH2. Regarding race-specific molecular drivers, TP53 and IDH2 mutations were associated with OS in White patients, TP53 in Black patients, and IDH1 in Hispanic patients. These findings suggest that while racial disparities exist in specific clinical subgroups, they are primarily driven by distinct molecular profiles, cytogenetic heterogeneity, and patient-specific clinical factors rather than race alone.
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