Hi, I’m Professor Phil Cornford of Liverpool University Hospitals in the UK and Vice Chair of the EAU Prostate Cancer Guidelines Panel. This series of videos has been co-created in association with ecancer. We will discuss the current role of PARP inhibitor use in prostate cancer, and what we might expect in the future.
PARP inhibitors treat certain types of cancer by blocking the PARP enzymes in cells. These enzymes help repair DNA damage, so blocking them can prevent cancer cells from repairing. This is known as homologous recombination repair or HRR. As cancer cells have less stable DNA, this causes them to die.
They have so far demonstrated efficacy in ovarian, breast, pancreatic, peritoneal and metastatic castration-resistant prostate cancer, with the greatest effect observed in patients with HRR deficiency.
There are four main PARP inhibitors: rucaparib, niraparib, olaparib and talazoparib. Of these, olaparib and rucaparib are now FDA approved for metastatic castration-resistant prostate cancer. Olaparib is approved for patients with gene alterations in BRCA, ATM and eleven other genes associated with homologous recombination repair following progression on prior enzalutamide or abiraterone.
Rucaparib is approved by the FDA for the treatment of metastatic castration-resistant prostate cancer with gene alterations in BRCA post androgen receptor targeting agents and taxane based therapy.
In Europe, the EMA has approved olaparib for metastatic castration-resistant prostate cancer and BRCA alterations following progression on prior new hormonal therapy.
And in combination with abiraterone and prednisone or prednisolone, in adult men for whom chemotherapy was not clinically indicated.
