Luca Gianni, MD, on the Neoadjuvant Treatment of Triple-Negative Breast Cancer
2019 San Antonio Breast Cancer Symposium
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).
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).
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).
Joerg Heil, MD, PhD, of the University Hospital Heidelberg, discusses findings on how accurately this technique can diagnose residual disease and pathologic complete response after neoadjuvant chemotherapy in patients with breast cancer. These data may help tailor, de-escalate, and potentially avoid unnecessary surgeries (Abstract GS5-03).
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).