The SERENA-6 trial showed a 56% reduction in risk of disease progression or death with the camizestrant-CDK4/6i combination. How impactful is this in real-world clinical decision-making for HR-positive breast cancer with emerging ESR1 mutations?

SERENA-6 was the first pivotal trial to integrate ctDNA surveillance for early detection of ESR1 mutations. How does this proactive approach reshape the treatment paradigm in advanced breast cancer?

Patients receiving camizestrant experienced a median 23-month delay in deterioration of global health status versus 6.4 months on aromatase inhibitors. How significant is this outcome in terms of patient-centered care and daily functioning?

Camizestrant demonstrated benefit regardless of which CDK4/6 inhibitor was used. What does this suggest about its versatility as an endocrine backbone and the potential for broader application?

With Grade ≥3 adverse events occurring in 60% of patients in the camizestrant arm, primarily due to CDK4/6i-related cytopenias, how do you evaluate the overall safety profile relative to current endocrine strategies?

Although PFS2 and OS data are still immature, SERENA-6 showed early signals of durable benefit. How much weight should we give to these interim results when considering treatment sequencing?

The study intervened before radiographic progression upon ESR1 detection. Could this fundamentally change guidelines around when to switch therapies, especially in light of growing resistance data?

Given its Breakthrough Therapy Designation and robust data, how soon do you anticipate camizestrant could become a standard-of-care in ESR1-mutant HR+ disease—and what hurdles might slow adoption?