Belinda Kingston, MB ChB, on the Genomic Landscape of Breast Cancer Based on ctDNA Analysis
2019 San Antonio Breast Cancer Symposium
Belinda Kingston, MB ChB, of the Institute of Cancer Research London, discusses next-generation sequencing results from the plasmaMATCH trial, including the incidence of gene alterations overall, as well as the associations with clinical and pathologic features that may help direct treatment decisions (Abstract GS3-07).
Gerardo Antonio Umanzor Funez, MD, of Liga Contra El Cáncer, discusses phase III findings on intravenous (IV) paclitaxel and oral paclitaxel plus encequidar (a novel P-gp inhibitor), the first orally administered taxane regimen shown to be superior to the IV formulation in terms of response and survival with less neuropathy (Abstract GS6-01).
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).
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).