Ralph R. Weichselbaum, MD, on Oligometastatic Cancer: The Role of Radioimmunotherapy
2019 San Antonio Breast Cancer Symposium
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).
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).
Ian E. Krop, MD, PhD, of Dana-Farber Cancer Institute, discusses phase II trial findings on trastuzumab deruxtecan, a HER2-targeting antibody-drug conjugate, in patients with HER2-positive metastatic breast cancer who were previously treated with trastuzumab emtansine (Abstract GS1-03).
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).
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).