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).
Luca Gianni, MD, of the Fondazione Michelangelo, discusses findings from the NeoTRIP trial on pathologic complete response to neoadjuvant treatment with or without atezolizumab in triple-negative, early high-risk, and locally advanced breast cancer (Abstract GS3-04).
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).
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).
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).
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).