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).
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).
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).
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).
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).
