Gerardo Antonio Umanzor Funez, MD, on Metastatic Breast Cancer: Comparing IV and Oral Formulations of Paclitaxel
2019 San Antonio Breast Cancer Symposium
Gerardo Antonio Umanzor Funez, MD, of Liga Contra El Cáncer, discusses phase III findings on intravenous (IV) paclitaxel and oral paclitaxel plus encequidar (a novel P-gp inhibitor), the first orally administered taxane regimen shown to be superior to the IV formulation in terms of response and survival with less neuropathy (Abstract GS6-01).
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).
Javier Cortes, MD, PhD, of the IOB Institute of Oncology, discusses study findings that suggested pembrolizumab offered a prolonged survival benefit compared to chemotherapy for a subset of patients with previously treated metastatic triple-negative breast cancer. In the trial, high tumor-infiltrating lymphocytes were significantly associated with better clinical outcomes with the checkpoint inhibitor.
Icro Meattini, MD, of the University of Florence, discusses study findings that showed the less-invasive partial-breast irradiation using intensity-modulated radiotherapy after surgery may be an acceptable choice for patients with early breast cancer, as it is cost-effective, safe, and efficacious when compared with whole-breast irradiation (Abstract GS4-06).
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).
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).
