Breast Cancer

Dr Matthew Goetz addresses the prospect of utilizing CDK4/6 inhibitors to treat patients with HER2+ metastatic breast cancer, stating early data indicate that CDK4/6 inhibitors may have some antitumor activity in HER2+ breast cancer.
Despite international guidelines and data that show CDK4/6 inhibitors plus aromatase inhibitors can improve overall response rates, overall survival, and progression-free survival in patients with metastatic breast cancer, there is a lasting belief among patients that chemotherapy is the preferable course of treatment. Dr. Hope Rugo attempts to dispel this misconception, citing that endocrine therapy and CDK4/6 inhibitors are well tolerated and don’t have the intensive side effects associated with chemotherapy.
Dr Matthew Goetz reviews what differentiates abemaciclib, the latest CDK4/6 inhibitor FDA-approved for HR+ metastatic breast cancer, from ribociclib and palbociclib.
Dr Hope Rugo provides an overview of some hot topics being covered at SABCS 2017 in the areas of hormone therapy, immunotherapy, neoadjuvant therapy, and more.
In the phase 3 OlympiAD trial, treatment with olaparib significantly improved progression-free survival and reduced the risk for disease progression or death compared with standard chemotherapy in women with HER2-negative, BRCA-mutated metastatic breast cancer.
PD-L1 positivity in all cells in patients with breast cancer may be a useful prognostic marker based on a recent meta-analysis.
A new analysis shows that there is an ongoing, steady risk for metastatic or distant recurrence of cancer from years 5 to 20 among women with estrogen receptor–positive breast cancer.
After accounting for the benefit of pertuzumab, investigators found that >6 cycles of docetaxel did not significantly improve progression-free or overall survival in patients with HER2-positive, metastatic breast cancer.
Abemaciclib offers a new option for women with HR-positive, HER2-negative advanced metastatic breast cancer.
OlympiAD provides proof of principle that breast cancers with defects in a specific DNA damage repair pathway are sensitive to a targeted therapy designed to exploit that defect, said Dr Robson.
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