Key Findings
- Acquired CDK4/6 inhibitor resistance was associated with expected enrichments in ESR1 and RB1 alterations, confirming known biological mechanisms in a real-world setting.
- Differential gene expression analyses revealed distinct resistance-associated molecular programs that differed by baseline obesity, including immune, metabolic, and growth-factor–related pathways.
- Baseline obesity status emerged as a potential modifier of resistance biology, highlighting a clinically relevant patient characteristic that may inform personalized treatment strategies and warrants further validation.