Breast Cancer Treatment: Sequencing With Antibody-Drug Conjugates

Kevin Kalinsky, MD, MS: In the remaining minutes, I want to go around the Zoom room and have everybody conclude with 1 clinical pearl or takeaway for those who’ve checked in [late]. I’m going to start with Allison, then go to Kandra, and then I’ll end with Komal.

Allison Butts, PharmD, BCOP: That’s a lot of pressure with 1 pearl. I was thinking sequencing and how the algorithm is going to fall into play is what’s interesting to me. These drugs keep moving earlier into the treatment algorithm, so we’ll see potentially targeted therapy be our first-line approach. Even in the neoadjuvant space, getting rid of chemotherapy as we know it and seeing where we go with more targeted agents.

Kevin Kalinsky, MD, MS: Kandra?

Kandra Horne, DNP, MSN, WHNP-BC: I’m excited about seeing some of the promising trials looking at triple-negative [breast cancer] and the impact with the target therapies. Also, the patients with hormone receptor–positive breast cancer with the HER2 [human epidermal growth factor receptor 2] new and negative components and the impact of that. That’s exciting. There’s more room to grow and impact our patients.

Komal Jhaveri, MD, FACP: I second both comments from Allison and Kandra. This is a very active class of agents. They’re here to stay. We’re trying to get version 3 and 4 to improvise their use, to tackle their toxicities better—how can we improve outcomes by combining them better? With the DESTINY-Breast03 trial, for example, there were 16 complete responses in those patients. We’re beginning to cure some patients with this class of agents and these novel agents. In combination with, say, I/O [immuno-oncology], even in the first line or the utility up front they can help us achieve that, so I’m looking forward to a bright future. Hopefully we’ll see even better outcomes for our patients.

Kevin Kalinsky, MD, MS: I totally agree with these assessments. This question about the HER2-low population is a really interesting question. Going back to 1 of the things Allison said early on, we know that some of these targets are active targets, like HER2 and TROP2, and how the structure of the ADC [antibody-drug conjugate] can lead to different toxicities and adverse effects. This is an ever-evolving field, and where we are now is going to be different from where we’re going to be in 3 to 5 years. This is a moving target, and that’s exciting for us and our patients.

I want to thank Komal Jhaveri, Allison Butts, and Kandra Horne for joining us. This has been a great and active conversation. Thank you, everybody, for joining this panel discussion.

Transcript edited for clarity.