Abstract
Mutation identification via circulating tumor DNA (ctDNA) to select appropriate therapy has demonstrated clinical utility in metastatic breast cancer (MBC). SERENA-6 demonstrated the efficacy and tolerability of camizestrant in HR + /HER2-, ESR-1 mutated MBC after an AI/CDK 4/6 inhibitor. However, it remains unclear whether switching therapy at the time of ctDNA-detected emergence of ESR-1 mutations (“molecular progression”) improves long-term outcomes over switching therapy at the time of traditional anatomic/clinical progression.