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).
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).
Hope S. Rugo, MD, of the University of California San Francisco Comprehensive Cancer Center, discusses a retrospective analysis on the effectiveness of the VENTANA PD-L1 SP142 assay, the Dako 22C3 assay, and the VENTANA SP263 assay as predictors of response to atezolizumab plus nab-paclitaxel in patients with metastatic triple-negative breast cancer (Abstract PD1-07).
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).
Miguel Martín, MD, PhD, of the Gregorio Marañón Institute and GEICAM, discusses phase III study findings that showed no improvement in progression-free survival with palbociclib plus endocrine therapy vs capecitabine in patients with hormone receptor–positive/HER2-negative metastatic breast cancer whose disease progressed on aromatase inhibitors—although the drug combination was generally better tolerated than capecitabine (Abstract GS2-07).
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).
