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).
Javier Cortes, MD, PhD, of the IOB Institute of Oncology, discusses study findings that suggested pembrolizumab offered a prolonged survival benefit compared to chemotherapy for a subset of patients with previously treated metastatic triple-negative breast cancer. In the trial, high tumor-infiltrating lymphocytes were significantly associated with better clinical outcomes with the checkpoint inhibitor.
Tari A. King, MD, of Brigham and Women’s Hospital and Dana-Farber/ Brigham and Women’s Cancer Center, discusses retrospective findings from the AURORA U.S. Network on molecular differences between primary tumors and metastases, a better understanding of which may help lead to more effective treatment of metastatic breast cancer (Abstract GS3-08).
Hongchao Pan, PhD, of the University of Oxford, discusses an analysis of 86,000 women in the Early Breast Cancer Trialists’ Collaborative Group database, which showed that the risk of distant recurrence 20 years after a diagnosis of node-negative, estrogen receptor–negative early-stage breast cancer in women who discontinued endocrine therapy at 5 years is likely to be about a third lower now than in his group’s previous report (Abstract GS2-04).
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).
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).
