Jack Cuzick, PhD, on the International Breast Cancer Intervention Study II: 10-Year Results
2019 San Antonio Breast Cancer Symposium
Jack Cuzick, PhD, of Queen Mary University of London, discusses the substantially greater benefits of anastrozole as compared with tamoxifen in terms of preventing breast cancer, with no increase in fractures or other reported serious side effects (Abstract GS4-04).
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).
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).
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).
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).
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).