Ralph R. Weichselbaum, MD, of the University of Chicago, summarizes a plenary lecture in which he presented data that could guide future clinical strategies: studies supporting the basis and classification of oligometastatic disease, including breast cancer; and basic and clinical data on radioimmunotherapy (Abstract PL2).
Rashmi K. Murthy, MD, of The University of Texas MD Anderson Cancer Center, discusses data on the efficacy and safety of tucatinib, trastuzumab, and capecitabine, a treatment regimen under investigation for patients with advanced HER2-positive metastatic breast cancer refractory to standard-of-care regimens (Abstract GS1-01).
Hope S. Rugo, MD, of the University of California San Francisco Comprehensive Cancer Center, discusses trial data on margetuximab plus chemotherapy, which improved progression-free survival in patients with previously treated HER2-positive metastatic breast cancer when compared with trastuzumab plus chemotherapy. Maturing data comparing overall survival also provides new insights (Abstract GS1-02).
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).
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).
