Terry P. Mamounas, MD, MPH, on Extending Letrozole Treatment in Hormone Receptor–Positive Breast Cancer
2019 San Antonio Breast Cancer Symposium
Terry P. Mamounas, MD, MPH, of Orlando Health UF Health Cancer Center, discusses 10-year results from NRG Oncology/NSABP B-42, which showed that, for postmenopausal women with hormone receptor–positive breast cancer who have completed previous adjuvant therapy with an aromatase inhibitor or with tamoxifen followed by an aromatase inhibitor, extended treatment with letrozole improved disease-free survival (Abstract GS4-01).
Belinda Kingston, MB ChB, of the Institute of Cancer Research London, discusses next-generation sequencing results from the plasmaMATCH trial, including the incidence of gene alterations overall, as well as the associations with clinical and pathologic features that may help direct treatment decisions (Abstract GS3-07).
Ariella B. Hanker, PhD, of UT Southwestern Medical Center, discusses data showing that breast cancers expressing co-occurring HER2 and HER3 mutations may require the addition of a phosphoinositide 3-kinase alpha inhibitor to a HER2 tyrosine kinase inhibitor (Abstract GS6-04).
Sara M. Tolaney, MD, MPH, of Dana-Farber Cancer Institute, discusses phase II findings on patients receiving T-DM1 monotherapy as adjuvant treatment for stage I HER2-positive breast cancer, a regimen associated with few recurrences in the study population (Abstract GS1-05).
Joerg Heil, MD, PhD, of the University Hospital Heidelberg, discusses findings on how accurately this technique can diagnose residual disease and pathologic complete response after neoadjuvant chemotherapy in patients with breast cancer. These data may help tailor, de-escalate, and potentially avoid unnecessary surgeries (Abstract GS5-03).
Milan Radovich, PhD, of Indiana University School of Medicine, discusses trial findings that show patients with triple-negative breast cancer who are at high risk of relapse after receiving preoperative chemotherapy can be risk-stratified based on the presence of minimal residual disease as determined by circulating tumor DNA and circulating tumor cells (Abstract GS5-02).
