Impact of race on mutational profile and survival in acute myeloid leukemia: a single-institution experience (2014-2024).

Authors

Utsav Joshi, Fatima Tuz Zahra, Pujan Patel, Najla Al Ali, Zachary Thompson, Nagehan Pakasticali, Jinming Song, Vishakha Agrawal, Rory Shallis, Zhuoer Xie, Seongseok Yun, Andrew Kuykendall, Eric Padron, Alison Walker, David Sallman, Rami Komrokji, Jeffrey Lancet, Mohammad Hussaini, Onyee Chan

Published in

Annals of hematology. Jul 02, 2026. Epub Jul 02, 2026.

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.

PMID:
42393270
Bibliographic data and abstract were imported from PubMed on 03 Jul 2026.

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