Dr. Konecny Discusses the Role of PARP Inhibitors in Ovarian Cancer

Gottfried E. Konecny, MD
Published: Wednesday, Jun 06, 2018



Gottfried E. Konecny, MD, associate professor of medicine, University of California, Los Angeles, discusses the role of PARP inhibitors in the treatment of patients with ovarian cancer.

Konecny says that 50% of patients with ovarian cancer harbor a deficiency in DNA damage repair, making them susceptible to DNA-damaging agents such as platinum or PARP inhibitors. Currently, there are 3 PARP inhibitors approved by the FDA for use in patients with ovarian cancer—niraparib (Zejula), olaparib (Lynparza), and rucaparib (Rubraca).

Initially, PARP inhibitors were used in patients with germline BRCA mutations and somatic mutations. Konecny says that there are 4 key lessons that have been learned across all the different experiences with PARP inhibitors. First, the activity of PARP inhibitors extends beyond patients that have a germline or somatic mutation. Second, the activity of PARP inhibitors go hand-in-hand with platinum sensitivity, as both are associated with DNA damage repair deficiencies. Third, Konecny says that the better the response a patient has to platinum, the better the response they will have to the PARP inhibitor. Lastly, the earlier that a patient is treated with a PARP inhibitor in their treatment course, the better the response will be.
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Gottfried E. Konecny, MD, associate professor of medicine, University of California, Los Angeles, discusses the role of PARP inhibitors in the treatment of patients with ovarian cancer.

Konecny says that 50% of patients with ovarian cancer harbor a deficiency in DNA damage repair, making them susceptible to DNA-damaging agents such as platinum or PARP inhibitors. Currently, there are 3 PARP inhibitors approved by the FDA for use in patients with ovarian cancer—niraparib (Zejula), olaparib (Lynparza), and rucaparib (Rubraca).

Initially, PARP inhibitors were used in patients with germline BRCA mutations and somatic mutations. Konecny says that there are 4 key lessons that have been learned across all the different experiences with PARP inhibitors. First, the activity of PARP inhibitors extends beyond patients that have a germline or somatic mutation. Second, the activity of PARP inhibitors go hand-in-hand with platinum sensitivity, as both are associated with DNA damage repair deficiencies. Third, Konecny says that the better the response a patient has to platinum, the better the response they will have to the PARP inhibitor. Lastly, the earlier that a patient is treated with a PARP inhibitor in their treatment course, the better the response will be.



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