Ariella B. Hanker, PhD, on Therapeutic Implications of HER2 and HER3 Mutations in Breast Cancer
2019 San Antonio Breast Cancer Symposium
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).
Sara M. Tolaney, MD, MPH, of Dana-Farber Cancer Institute, discusses phase II findings on patients receiving T-DM1 monotherapy as adjuvant treatment for stage I HER2-positive breast cancer, a regimen associated with few recurrences in the study population (Abstract GS1-05).
Joseph Sparano, MD, of the Montefiore Medical Center, discusses three challenges:
- How can gene-expression profiles and other diagnostic tests be used to guide the use of adjuvant systemic therapy?
- Is it time to reappraise active surveillance?
- Are there diagnostic and therapeutic strategies that can identify tumors at highest risk of metastasis, and novel therapies that can block the spread of disease?
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).
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).