Formal discussant of this trial, Robert Bruce Montgomery, MD, Clinical Director of Genitourinary Medical Oncology, Seattle Cancer Alliance, said, “The rationale for checkpoint inhibition and [poly ADP--ribose polymerase (PARP)] inhibitors is strong in patients with underlying homologous recombination–deficient ovarian and breast cancers, but in patients who do not have underlying homologous repair deficiency, it’s a little less clear how PARP inhibition will actually help. You can’t generate a BRCA-ness signature by treating a nondeficient tumor with a PARP inhibitor,” he said.
“However, it has been shown that exposure to a PARP inhibitor will increase [programmed cell death ligand 1] expression, and in preclinical models, that does, in fact, lead to better responses with these various therapies,” Dr. Montgomery continued.
“The responses and progression-free survival were compelling in this early study, especially in view of the limited toxicity, although the high frequency of homologous recombination tumors limits the interpretation,” he concluded. ■
DISCLOSURE: Dr. Montgomery reported no conflicts of interest.
Error loading Partial View script (file: ~/Views/MacroPartials/TAP Article Portrait Widget.cshtml)
The combination of the poly ADP-ribose polymerase (PARP) inhibitor olaparib (Lynparza) and the programmed cell death ligand 1 (PD-L1) inhibitor durvalumab (Imfinzi) produced positive preliminary...