(sorry for the drive-by posting, but had to share. I know there's a specific SABCS thread, but didn't want to double-post)
DNA Repair Company Announces New Clinical Findings Which May Help to Guide Breast Cancer Treatment
BOSTON--(BUSINESS WIRE)--The DNA Repair Company (DNAR), an early-stage company focused on personalized approaches to cancer treatment, announced today that it has identified a promising set of protein biomarkers that may aid in the treatment of a particularly aggressive form of breast cancer. These findings were presented at the CTRC-AACR San Antonio Breast Cancer Symposium.
The DNAR study was conducted in collaboration with investigators from the Dana-Farber Cancer Institute and Beth Israel Deaconess Medical Center, both in Boston. The lead author of the study, Brian Alexander, MD, physician resident at the Harvard Radiation Oncology Program and currently a White House Fellow, was selected as a recipient of the prestigious AstraZeneca Clinical Scholars Award in recognition of the merits of the study.
The study was conducted using clinical data with so-called “triple-negative” breast cancer, a form of the disease that is not responsive to therapies targeting estrogen receptors, progesterone receptors, or the HER2 receptor. The prognosis for triple-negative breast cancer is poor, due in part to the more limited set of treatment options available.
Clinical biopsies from 143 patients were examined to determine whether the modulation of various DNA repair proteins might have an impact on disease progression. DNA repair pathways correct DNA that has been damaged by many common forms of cancer treatment (e.g. chemotherapy and radiation) and play a central role in making tumors resistant to therapy.
With clinical samples from half of the patients, the investigators discovered a statistically significant correlation between the presence of four DNA repair proteins and recurrence-free survival. Investigators were then able to validate the correlation with progression-free survival seen in this cohort by testing the four proteins in the second group of patients. The marker panel distinguished a high risk group of patients with a medium time to recurrence of 14 months from low risk patients with median time to recurrence of >10 years. Even though a number of DNA repair markers produced statistically significant results individually, results observed with the four DNA repair marker panel were superior to those seen with a number of single markers.
These findings are significant, because they suggest that monitoring DNA repair protein profiles in patients with triple-negative breast cancer will contribute important insights as prognostic or predictive tools. In addition, DNA repair pathways may provide a promising target for developing novel therapies for the disease.
“These findings provide intriguing evidence that the activity of certain DNA repair pathways play an important role in determining how patients with triple-negative breast cancer will respond to therapy, and further validation will help focus drug development on approaches most likely to succeed,” said lead investigator Judy E. Garber, MD, MPH, Director of the Cancer Risk and Prevention Program at Dana-Farber and Associate Professor of Medicine, Harvard Medical School. “The frequently poor prognosis for patients with this form of breast cancer lends increased urgency to understanding the molecular basis of the disease, and its implications for treatment and new drug development.”
DNAR is leveraging its deep knowledge of the role that DNA repair pathways play in cancer to create new tools that give physicians unprecedented data-driven insights into which course of treatment will work most effectively for an individual patient. DNAR aims to improve patient care by improving physicians’ ability to prescribe the most effective treatments the first time from the host of therapeutic options available. DNAR is advancing a major goal of personalized medicine – to identify the right therapy for the right patient, and to reduce the need for “trial and error” medicine.