BIOM-04. METASTATIC BRAIN CANCER FROM BREAST CANCER CNS ADHESION MOLECULE BIOMARKER ANALYSIS STUDY

Abstract Breast cancer, characterized by its heterogeneity, presents a substantial challenge when metastasized to the brain. Despite the prevalence of breast cancer brain metastases (BCBM), the molecular mechanisms facilitating tumor cell invasion into the central nervous system (CNS) remain inadequately understood. This study seeks to elucidate the genomic profiles and key molecular interactions, that contribute to the metastatic propensity of breast cancer subtypes. We conducted a comprehensive genomic analysis of 43 breast cancer samples collected from patients at Chungbuk National University Hospital. These samples, representing four major breast cancer subtypes—Luminal A, Luminal B, HER2-enriched, and triple-negative breast cancer (TNBC)—underwent differential gene expression (DEG) analysis. High-throughput next-generation sequencing (NGS) was employed to determine the expression profiles that distinguish metastatic from non-metastatic states. Bioinformatics tools identified DEGs that were linked to CNS adhesion molecules and other related pathways. The DEG analysis identified several genes such as HER2, BRCA1, BRCA2, and P53, whose expression profiles were significantly altered in the context of BCBM. A range of CNS adhesion molecules including DSG1, PKP1 were also frequently upregulated and potentially facilitated the metastatic process. TNBC samples showed pronounced genomic alterations, indicating a more aggressive metastatic behavior and underscoring the subtype’s distinct molecular vulnerabilities. Our study observed and indicated significantly altered key genes underlying the genomic mechanisms of BCBM. Therefore, by highlighting these key molecular interactions and pathways, our findings offer potential avenues for the development of targeted therapies aimed at preventing or mitigating BCBM.