Dr. Kevin Kalinsky Covers Targeted Therapy in HER2– Breast Cancer

The treatment landscape for patients with estrogen-driven, HER2-negative breast cancer is rapidly evolving, with a growing emphasis on precision medicine, according to Dr. Kevin Kalinsky, who went on to emphasize that this approach tailor’s treatment decisions based on the molecular characteristics driving an individual’s tumor.

Targeted therapies for ESR1 mutations or for the PI3K pathway alterations provide additional treatment options, he continued; however, the decision to continue a CDK4/6 inhibitor after progression is highly individualized. In an interview with CURE live from the 42nd Annual Miami Breast Cancer Conference, Kalinsky delved into detail about the evolving role of targeted therapies and the clinical decision-making process in managing estrogen-driven, HER2-negative breast cancer.

Kalinsky is a professor and director in the Division of Medical Oncology of the Department of Hematology and Medical Oncology at Emory University School of Medicine, in Atlanta, Georgia. He also serves as the director of the Glenn Family Breast Center and the Louisa and Rand Glenn Family Chair in Breast Cancer Research at Winship Cancer Institute of Emory University.

Transcript:

The field for patients with estrogen-driven HER2-negative breast cancer is really evolving. We are trying to increasingly move to precision medicine, where we make decisions based upon whatever the tumor is being driven by, [such as] mutations, for example. We do have data for patients who were previously on an aromatase inhibitor plus a CDK4/6 inhibitor, [which showed] that for patients who don't have a mutation, there is benefit for potentially switching the endocrine therapy and also switching the CDK4/6 inhibitor. This benefit is also seen for patients that do have mutations, like ESR1 mutations, or alterations in the PI3K pathway. However, this is an individualized conversation. This is because there are other drugs that also target ESR1 mutations, like Orserdu [elacestrant]. There are drugs that target the PI3K pathway, like Truqap [capivasertib] or Piqray [alpelisib].

There are different nuanced conversations that we have that help determine if there is a benefit for continuing a CDK4/6 inhibitor. [However], I would really think about it in the patients who have low volume of disease — maybe it's bone-only — and they were on their hormonal therapy and CDK4/6 inhibitor for a long period of time. Those are the sorts of patients that I talk about continuing with the CDK4/6 inhibitors after progression.

Transcript has been edited for clarity and conciseness.

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