C. Kent Osborne, MD, Director of the Dan L. Duncan Cancer Center at Baylor College of Medicine, Houston, and moderator of a press conference where the EMBRACA findings were presented, shared his thoughts on the study. While a few months’ improvement in the risk of disease progression may seem modest to patients, it is proof of activity that can be built upon, he noted.
“I look at the findings as one of the first steps in addressing DNA repair as a target for treatment. The poly ADP-ribose polymerase (PARP) inhibitors have had a difficult road in breast cancer…, but compared to early attempts, there are better drugs in development now, even beyond olaparib (Lynparza) and talazoparib, which have produced positive results,” he said.
“The concept of PARP inhibition has been shown to work in some patients, and that’s the important finding from the talazoparib and olaparib trials. Now, the trick is to determine who will respond best and identify the mechanisms of resistance. In some cases, tumor cells can repair BRCA in an attempt to survive. Without a BRCA mutation, the drug won’t be effective. Understanding mechanisms of resistance such as this, and then trying to overcome them, is important,” he continued.
“We have a start. We know these drugs work in some patients, and some even produce a prolonged response. Trying to refine who to treat and how to reverse the resistance are the next steps. If we can do that, these drugs will be a major advance in the treatment of breast cancer,” Dr. Osborne concluded. ■
DISCLOSURE: Dr. Osborne is on the advisory board of AstraZeneca and Tolmar and has received a grant from Ventana.
In patients with BRCA-positive advanced breast cancer, talazoparib reduced the risk of disease progression or death by 46% vs chemotherapy, according to the phase III EMBRACA trial presented at the 2017 San Antonio Breast Cancer Symposium.1Error loading Partial View script (file:...