Addressing Treatment Gaps in HER2+ MBC

EP: 1.Global Trends in HER2+ MBC

EP: 2.Standard Treatment Approaches in HER2+ MBC

EP: 3.Updated Data From DESTINY-Breast03 in HER2+ MBC

EP: 4.Subgroup Analyses of DESTINY-Breast03 in HER2+ MBC

EP: 5.Managing TRAEs Associated With Novel HER2+ MBC Therapies

EP: 6.T-DXd for HER2+ MBC and Interstitial Lung Disease

EP: 7.Novel Combination Approaches for HER2+ MBC

EP: 8.Updates to HER2CLIMB in HER2+ MBC

EP: 9.Updates in the Management of HER2+ MBC With Brain Metastases

EP: 10.ADCs Under Investigation for HER2+ MBC

EP: 11.Therapeutic Sequencing in HER2+ MBC

EP: 12.Optimizing Therapy in HER2+ MBC Across the Globe

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EP: 13.Addressing Treatment Gaps in HER2+ MBC

Volkmar Müller, MD, PhD: Thank you all for the great discussion. I have 1 last question for everyone. What’s an important question you have in the field of HER2 [human epidermal growth factor receptor 2]–positive metastatic breast cancer? Dr Criscitiello, you can start.

Carmen Criscitiello, MD, PhD: An important and interesting question for the near future would be to understand optimal sequencing of treatments, not only for the drugs that we have available and those that will be available soon, but also those for which we have less evidence. Another important issue will be to understand, in light of new drugs, potential effects on brain maps. We may remodulate the way we use local treatments for patients with brain metastases and HER2+ breast cancer.

Giuseppe Curigliano, MD, PhD: We have drugs in the metastatic setting that may dramatically affect the outcome. This is quite important. Many of these agents in the early breast cancer setting will increase dramatically to the number of patients that could be cured. The question is how to differentiate a treatment in a special population of patients, like the brain metastases population. They have metastatic disease. Why not the triple-positive system? Treatment of any ER [estrogen receptors]–positive HER2+ in the future will be different from patients who are ER- and HER2+. The future will differentiate niche patients with HER2+ disease, but the treatment algorithm that we have today will be different.

Volkmar Müller, MD, PhD: Dr Traina, what do you think?

Tiffany A. Traina, MD: I’ll echo what my colleagues have said. I also considered where else there might be gaps. It would be wonderful to find an opportunity to de-escalate some of our poly-drug, poly-chemotherapy, and targeted-therapy regimens in the early stage setting, to refine who needs to escalate therapy based on failure of [inaudible]. Is there a simpler approach with some of these amazing new drugs as a monotherapy, with an antibody-drug conjugate in a de-escalation strategy. Brain metastases remain an area of unmet need. The third area would be, how do these agents combine with checkpoint inhibitors? We know PD-L1, after triple-negative breast cancer, is highly expressed in HER2+ breast cancer. Could there be an opportunity to see how these drugs partner with checkpoint inhibition?

Volkmar Müller, MD, PhD: It’s difficult from the last 1, the combination with anchor therapy. That’s aligned with de-escalation toxicity, which is something that could be explored. I’d love to see more trials that have a focus on that. Thank you for this great discussion. It was inspiring. I hope those who watch it give us feedback and tune in again.

Transcript edited for clarity.