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).
Jack Cuzick, PhD, of Queen Mary University of London, discusses the substantially greater benefits of anastrozole as compared with tamoxifen in terms of preventing breast cancer, with no increase in fractures or other reported serious side effects (Abstract GS4-04).
Nadine M. Tung, MD, of Beth Israel Deaconess Medical Center, discusses cisplatin vs doxorubicin/cyclophosphamide (AC) as neoadjuvant treatment in BRCA-mutation carriers with HER2-negative breast cancer. Although cisplatin as a single agent shows activity in this setting, the pathologic complete response with this agent alone is not higher than that with standard AC chemotherapy (Abstract GS6-03).
Luca Gianni, MD, of the Fondazione Michelangelo, discusses findings from the NeoTRIP trial on pathologic complete response to neoadjuvant treatment with or without atezolizumab in triple-negative, early high-risk, and locally advanced breast cancer (Abstract GS3-04).
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).
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).
