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).
Jack Cuzick, PhD, of Queen Mary University of London, discusses the substantially greater benefits of anastrozole as compared with tamoxifen in terms of preventing breast cancer, with no increase in fractures or other reported serious side effects (Abstract GS4-04).
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).
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?
Rashmi K. Murthy, MD, of The University of Texas MD Anderson Cancer Center, discusses data on the efficacy and safety of tucatinib, trastuzumab, and capecitabine, a treatment regimen under investigation for patients with advanced HER2-positive metastatic breast cancer refractory to standard-of-care regimens (Abstract GS1-01).
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).