Tari A. King, MD, on Molecular Differences Between Primary and Metastatic Breast Tumors
2019 San Antonio Breast Cancer Symposium
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).
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).
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).
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).
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.
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).
