Nicholas C. Turner, MD, PhD, on ctDNA Testing to Direct Targeted Therapies in Advanced Breast Cancer
2019 San Antonio Breast Cancer Symposium
Nicholas C. Turner, MD, PhD, of The Royal Marsden NHS Foundation Trust, discusses findings from the plasmaMATCH trial, which showed that circulating tumor DNA testing offers accurate tumor genotyping to identify patients with rare HER2 and AKT1 mutations and may enable matching them with targeted treatments (Abstract GS3-06).
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).
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).
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).
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).
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).
