The targeted therapy Herceptin helps women with HER2+ type of breast cancer independent of whether patients have extra copies of chromosome 17, home to the HER2 gene which produces the HER2 protein that fuels cancer growth.
Prior to this report, there were conflicting opinions about whether that was the case, say Mayo Clinic investigators who presented their findings at the San Antonio Breast Cancer Symposium.
The analysis came from the North Central Cancer Treatment Group's clinical trial N9831 which tested the use of Herceptin in combination with chemotherapy in patients with surgically-removed HER2+, early-stage, node-positive or high-risk, node-negative breast cancer. Data from the trial on the long term efficacy and safety of this treatment were presented recently by Mayo Clinic researchers and collaborators as part of a joint analysis with another U.S. trial. They demonstrated the significant benefit of using Herceptin, which is a monoclonal antibody that binds the HER2 protein, shutting down its function.
HER2+ breast cancer accounts for approximately 20 percent of all breast cancer cases, and most oncologists decide whether to use Herceptin based on a test that measures the amount of HER2 protein or the number of extra (“amplified”) genes in a patient's tumor tissue sample. The goal of this sub-study was to see if patients with more than two chromosome 17s (known as polysomy 17) had a different outcome from use of Herceptin.
“Some oncologists thought that patients with non-amplified HER2 gene in polysomy 17 tumors may respond to Herceptin because they may have that many extra HER2 genes resulting in HER2 protein over expression. Others thought they might not benefit because they had far too many HER2 genes from the extra chromosomes, producing too much HER2 protein, which may overwhelm Herceptin's effectiveness,” says the study's lead investigator, Monica M. Reinholz, Ph.D., an assistant professor at Mayo Clinic's campus in Rochester, Minn. “No one knew if they would respond, in general, or not.”