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. 2025 Feb 11;9(3):533-544.
doi: 10.1182/bloodadvances.2024014127.

Evolving racial/ethnic disparities in AML survival in the novel therapy era

Xin Wang  1   2 , Phyllis A Gimotty  3 , Andrew H Matthews  1 , Ronac Mamtani  1 , Selina M Luger  1 , Elizabeth O Hexner  1 , Daria V Babushok  1 , Shannon R McCurdy  1 , Noelle V Frey  1 , Ximena Jordan Bruno  1 , Saar Gill  1 , Mary Ellen Martin  1 , Vikram R Paralkar  1 , Ivan Maillard  1 , David L Porter  1 , Alison W Loren  1 , Alexander E Perl  1 , Keith W Pratz  1 , Kelly D Getz  3   4 , Catherine Lai  1
Affiliations

Evolving racial/ethnic disparities in AML survival in the novel therapy era

Xin Wang et al. Blood Adv. .

Abstract

Little is known about the impact of recent advances in acute myeloid leukemia (AML) treatment on racial/ethnic disparities in survival outcomes. We performed a retrospective cohort study of patients with newly diagnosed AML using data from a nationwide electronic health record-derived deidentified database. Patients were categorized based on their diagnosis date relative to venetoclax approval, as pre-novel therapy era (Pre era; 2014-2018; n = 2998) or post-novel therapy era (Post era; 2019-2022; n = 2098). Patients in the Post era were older and had more comorbidities than Pre era. Non-Hispanic Black (NHB) and Hispanic patients were younger and more likely to have lower socioeconomic status than non-Hispanic White (NHW) patients, with no differences in the distributions of key disease features. After accounting for age and comorbidity, overall survival (OS) was higher in patients in Post era than Pre era (adjusted hazard ratio [aHR], 0.90; 95% confidence interval [CI], 0.83-0.96). In Pre era, NHB had a 22% higher hazard of death than NHW (aHR, 1.22; 95% CI, 1.04-1.43), whereas worse OS was not observed for NHB in Post era (aHR, 0.86; 95% CI, 0.69-1.08; predicted 2-year survival, 45.3% vs 39.9%). Utilization of novel therapeutics in frontline therapy did not differ by race/ethnicity. Among patients receiving venetoclax-based induction, particularly those without TP53, RAS, or FLT3-ITD mutations, results suggested higher OS for NHB than NHW patients (aHR, 0.67; 95% CI, 0.45-1.01). Additional studies are needed to elucidate factors contributing to these observed survival differences and to inform strategies to optimize outcomes for all patients with AML.

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Conflict of interest statement

Conflict-of-interest disclosure: S.M.L. received honoraria from Syros, Agios, Daiichi Sankyo, Jazz Pharmaceuticals, Brystol Myers Squibb (BMS), Acceleron, Astellas, and Pfizer, and research funding from Onconova, Celgene, Biosight, Hoffman-La Roche, and Kura. E.O.H. received research funding from Tmunity Therapeutics and Blueprint Medicines, and had membership on an entity's board of directors or advisory committees for Blueprint Medicines and PharmaEssentia. N.V.F. was a consultant for Sana Biotechnology, Kite Pharma, and Syndax Pharmaceuticals, and received research funding from Novartis. D.L.P. received honoraria from the American Society for Transplantation and Wiley and Sons Publishing; had membership on an entity's board of directors or advisory committees for American Society of Hematology, Decart, Incyte, Janssen, Kite/Gilead, National Marrow Donor Program, and Novartis; is a current equity holder in Genentech; and has patents and royalties with Unity. S.G. has licensed intellectual property with Novartis; received research funding from Novartis, Carisma Therapeutics, and Interius BioTherapeutics; and is a current holder of stock options in Carisma Therapeutics and Interius BioTherapeutics. I.M. received research funding from Genentech and Regeneron, and has reserved on an entity’s board of directors or advisory committees of Garuda Therapeutics. A.E.P. received research funding from Fujifilm, Daiichi Sankyo, Astellas, Arog, and AbbVie, and was a consultant for Daiichi Sankyo, Sumitomo Dainippon, Astellas, BMS/Celgene, Genentech, Loxo, Onconova, Syndax, Forma, Actinium, Roche, and AbbVie. K.W.P. has consulted for AbbVie, Agios, BMS, Astellas, and Novartis; received honoraria from AbbVie, BMS, Astellas, and Celgene; and received research funding from AbbVie, Astellas, and Millenium. C.L. served as a consultant for Taiho, Pfizer, Jazz, AbbVie, Rigel, BMS, Genentech, Novartis, Daiichi Sankyo, and Astellas, and has received research funding from Jazz. The remaining authors declare no competing financial interests.

Figures

None
Graphical abstract
Figure 1.
Figure 1.
CONSORT diagram of patient allocation. APL, acute promyelocytic leukemia; MPAL, mixed-phenotype acute leukemia; w/o, without.
Figure 2.
Figure 2.
OS by treatment era across race/ethnicity. (A) Unadjusted Kaplan-Meier curves by treatment era (reference, Pre era). (B) Predicted OS curves by treatment era after adjusting for age and comorbidity (reference, Pre era). (C) Predicted OS curves by race/ethnicity between treatment eras after adjusting for age and comorbidity (reference, NHW patients).
Figure 3.
Figure 3.
OS of patients who received venetoclax-based low-intensity frontline therapy (reference, NHW patients). (A) Unadjusted Kaplan-Meier curves by race/ethnicity. (B) Predicted OS curves by race/ethnicity after adjusting for age and comorbidity. (C) Unadjusted Kaplan-Meier curves of patients without venetoclax-unfavorable mutations (TP53, KRAS, NRAS, and FLT3-ITD) by race/ethnicity. (D) Predicted OS curves of patients without venetoclax-unfavorable mutations (TP53, KRAS, NRAS, and FLT3-ITD) by race/ethnicity after adjusting for age and comorbidity.
See this image and copyright information in PMC

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