Abstract PS2-06-28: Clinicogenomic and Immune Profiles of Male Breast Cancer by Race: Insights from a Large Real-World Cohort

Abstract Background Male breast cancer (MBC) is a rare disease with limited data on potential racial differences in clinical and molecular characteristics, despite the fact that such differences are well-recognized in females. Understanding differences in the immune microenvironment and clinicogenomic features of MBC by race could inform future treatment strategies and improve health equity. This study leveraged the largest real-world (rw) cohort of MBC patients (pts) to date to characterize these features in Black/African American and White men. Methods Male pts with primary breast cancer who underwent xF or xT testing in the Tempus multi-modal database (Tempus AI, Inc., Chicago, IL) were identified using Tempus Lens. Statistical comparisons used Kruskal-Wallis and Chi-squared/Fisher’ exact tests where appropriate. Pts with xR testing (RNA) were classified into PAM50 subtypes and immune infiltration was quantified using quantiseq. Hormone receptor status was extracted from clinical documentation within 60 days of sample collection. Tumor mutational burden (TMB; mutations/megabase) and microsatellite instability were assessed by DNA sequencing. Real World overall survival (rwOS) was defined from the time of sample collection to death, last follow-up, or a study cutoff of 7 years, and was estimated using Kaplan-Meier methodology; comparisons used the log-rank test. Results The study cohort included 291 MBC pts: 128 White (44%) and 36 Black (12%). Among pts with available ethnicity, 93% were not Hispanic or Latino. Clinical subtypes were HR+, HER2- (39%), HER2+ (7.6%), triple-negative (7%) and 50% unknown or not otherwise specified. Median age at diagnosis was 63 years, and 87% of staged pts presented with stage IV disease. PAM50 subtyping identified Luminal A (62% of White and 68% of Black) and Luminal B (23% of White and 14% of Black) as the most common subtypes, with no significant racial differences in molecular subtypes (p=0.6). TMB was low (