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).
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).
Marie-Jeanne T.F.D. Vrancken Peeters, MD, PhD, of the Netherlands Cancer Institute, discusses an interim study analysis showing that ultrasound-guided core biopsies of the breast in patients with excellent response on MRI after neoadjuvant systemic therapy may not be accurate enough to safely select patients with pathologic complete response for omission of surgery (Abstract GS5-06).
Nadine M. Tung, MD, of Beth Israel Deaconess Medical Center, discusses cisplatin vs doxorubicin/cyclophosphamide (AC) as neoadjuvant treatment in BRCA-mutation carriers with HER2-negative breast cancer. Although cisplatin as a single agent shows activity in this setting, the pathologic complete response with this agent alone is not higher than that with standard AC chemotherapy (Abstract GS6-03).
Hope S. Rugo, MD, of the University of California San Francisco Comprehensive Cancer Center, discusses trial data on margetuximab plus chemotherapy, which improved progression-free survival in patients with previously treated HER2-positive metastatic breast cancer when compared with trastuzumab plus chemotherapy. Maturing data comparing overall survival also provides new insights (Abstract GS1-02).
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).