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).
Ian E. Krop, MD, PhD, of Dana-Farber Cancer Institute, discusses phase II trial findings on trastuzumab deruxtecan, a HER2-targeting antibody-drug conjugate, in patients with HER2-positive metastatic breast cancer who were previously treated with trastuzumab emtansine (Abstract GS1-03).
Ivana Sestak, PhD, of Queen Mary University of London and the Centre for Cancer Prevention, discusses study findings that confirm the prognostic ability of the Clinical Treatment Score at 5 years (CTS5) for late distant recurrence, specifically for patients older than 50 years and/or for those deemed to have intermediate- or high-risk hormone receptor–positive, HER2-negative, node-negative breast cancer. The CTS5 is less prognostic in women younger than 50 who received 5 years of endocrine therapy alone (Abstract GS4-03).
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).
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).
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).