HR+ Breast Cancer: Incidence, Prognosis, and Risk Stratification

Transcript:

Sara Tolaney, MD, MPH: Hi, and welcome to this OncLive® Insights® discussion titled “My Treatment Approach: Hormone Receptor–Positive Breast Cancer.” My name is Sara Tolaney. I’m the chief of the division of breast oncology at Dana-Farber Cancer Institute [in Boston, Massachusetts]. Today I’m joined by my colleague Dr Massimo Cristofanilli. Thanks so much, Massimo, for joining me. I’ll pass it to you to introduce yourself.

Massimo Cristofanilli, MD: Thank you, Sara. I’m Dr Cristofanilli. I’m the chief of breast medical oncology at Weill Cornell [Medicine] in New York [New York]. I also direct the Englander Institute for Precision Medicine. It’s great to be here. Today we’re going to discuss how we manage and approach patients with hormone receptor–positive breast cancer both early and metastatic, so let’s get started.

Sara Tolaney, MD, MPH: Thank you for that introduction. Before we dive into some cases, tell us how you think about a patient who presents, for example, with early stage hormone receptor–positive disease. What factors are you taking into consideration when thinking about what their risk is for having a recurrence?

Massimo Cristofanilli, MD: As you know, this is a very common disease. The majority of patients are screen-detected or have a small palpable tumor. Most of them—50% to 60%—are hormone receptor–positive breast cancer. It’s important to define the clinical risks but also the potential additional biomarker and molecular certification pathway that we can use when deciding on treatment. For many years, there’s been endocrine therapy and chemotherapy based on size and clinical patterns. Then we had the opportunity to de-escalate treatment with new molecular tests, particularly in postmenopausal patients.

The first criteria will be tumor size, nodal involvement, and clinical factors like Ki-67 to define proliferation. What should always be considered is when menopause started. When you’re defining clinical factors, we have the opportunity with predictive molecular testing to identify patients and spare them from chemotherapy, vs premenopausal or postmenopausal patients who need not only chemotherapy but also additional adjuvant therapy and combination therapies. At every conference we have updates from a number of clinical trials, looking at the long-term outcome of patients who’ve been enrolled in molecular-driven certification studies. New agents are being introduced in metastatic [disease] or being validated in early disease. It’s an exciting opportunity to treat these patients. We can stratify these patients very well. I think we’ll be serving our patients even better [in the future].

Sara Tolaney, MD, MPH: That’s an excellent overview about thinking specifically of clinical pathological risks but also other characteristics. One thing you brought up that’s interesting and maybe a little controversial is Ki-67 testing. Are you actually getting Ki-67 in your patients with early stage hormone receptor–positive [breast cancer]?

Massimo Cristofanilli, MD: That’s a good question. Every time we present data about various clinical trials…the question is whether your institution is doing validated Ki-67. This has been more important in the context of the new FDA approval. At our institution, we’re lucky enough to have had potential Ki-67 reported in every case. I’d like to consider this as another pathological predictive biomarker. This is true for academic institutions, but it may not be true for community oncology. They have to deal with this information and refer to them from pathology practices. But this has been controversial. In this case, is more than 20% enough to provide information for patients’ benefit from additional therapies with CDK4/6 inhibitors?

Sara Tolaney, MD, MPH: That’s interesting. Our pathologists are a little tough about this. At my institution, we don’t routinely get Ki-67 because it [may not be] reproducible enough. Given the International Working Group guidelines about the challenges with the validity of Ki-67, particularly in that 5%-to-30% range, [it may not be] reproducible in that range. We haven’t been getting them routinely, but we’ll dig into that more because this does come up a lot when we discuss data from monarchE.

Transcript edited for clarity.