Priyanka Sharma, MD, on Postoperative Treatment of Primary Breast Cancer: POTENT Trial
2019 San Antonio Breast Cancer Symposium
Priyanka Sharma, MD, of the University of Kansas Medical Center, reviews new phase III data on adding oral fluoropyrimidine to adjuvant endocrine therapy, the current standard of care, in the setting of hormone receptor–positive, HER2-negative primary breast cancer (Abstract GS1-09).
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).
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).
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).
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.
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).