Starting Maintenance Therapy for Ovarian Cancer

EP: 1.Molecular Testing and Ovarian Cancer

EP: 2.Sequencing of Biomarker Testing for Ovarian Cancer

EP: 3.Genetic Counseling for Ovarian Cancer

EP: 4.Case Scenario: Stage 3A High-Grade Epithelial Ovarian Cancer

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EP: 5.Starting Maintenance Therapy for Ovarian Cancer

EP: 6.Ovarian Cancer: Significant Clinical Trials

EP: 7.Case Scenario: Stage 3C High-Grade Serous Ovarian Cancer

EP: 8.Ovarian Cancer Maintenance Therapy: Olaparib vs. Niraparib

EP: 9.Ovarian Cancer Maintenance Therapy Clinical Pearls

EP: 10.The Future of Ovarian Cancer Treatment

Chad A. Hamilton, MD: What is your time frame for starting your maintenance therapy after you finished your adjuvant chemotherapy? Let’s say she’s on carbo [carboplatin]/Taxol [paclitaxel] and bevacizumab [Avastin], and she’s completed 6 cycles total. How soon do you start the olaparib [Lynparza]? Or do you layer the olaparib onto the bevacizumab at that point? Is there any eyeballing the patient? Do you have sort of a fixed time frame in your mind?

Robert W. Holloway, MD: I obviously have to see how the patient is healing. I’m a little concerned about adding bevacizumab too quickly if they’ve had GI [gastrointestinal] surgery. So if a patient had a low rectal, I’d probably wait until she’s at least 6 weeks before I’d start this regimen and maybe even a little longer, especially if she was R0 resected. The olaparib is a big driver in an HRD [homologous recombination deficiency] patient and won’t have a problem with the GI surgery. So that’s all about bone marrow, and she’s already been off chemotherapy probably 4 weeks before you went to your interval size reduction. So within a month, you could clearly start the olaparib and then maybe later the bevacizumab and do it the other way, if you had GI surgery. With no GI surgery, you’re just looking at the wounds and vaginal cuff and probably get going within a month is what I would typically do. And then of course, you’re going to look at your toxicity that you had with your chemotherapy coming up to that. If their bone mass still seems a little fatigued, you could layer on the olaparib a little bit later.

Chad A. Hamilton, MD: I’m going to adjust this case just a little bit. Let’s say you did a primary debulking on a patient that didn’t get down to R0 and had residual disease, so you decided to start her on bevacizumab but then shortly after you got testing back, it demonstrated she was HRD-positive. Would you ever bail out on the bevacizumab early on, knowing that you’re going to have part maintenance on the back end? Or I know you talked about the hazard ratio, does that give you enough impetus to continue with the bevacizumab in that scenario?

Robert W. Holloway, MD: I think it’s really patient-dependent. If they’re tolerating the bevacizumab well—not having hypertension or proteinuria problems—that would certainly be 1 issue. If it’s difficult for the patient, if they’re traveling a little bit, or if they express to you that they’re weary, asking “Are we really going to do this for a year? You’re going to come in and take infusions every 3 weeks?” Then I wouldn’t feel it terribly difficult to back off on the bevacizumab and go with single agent niraparib [Zejula] in that setting; switch maintenance, we’ll call it. Or a patient, if they started out on a PAOLA [clinical trial] treatment and they said after 6 months that they just didn’t want to take any more bevacizumab and they were completely resected, and they really don’t seem to be the type of patient who derive the best maintenance benefit from the bevacizumab, then I could even see dropping it. I realized that would be out of guidelines maybe, but probably not. That probably happened in the study, too. They were started on it, maybe they got off the bevacizumab for some reason and they continued the olaparib, so I think you’d have those choices. I think if you look at the hazard ratios with SOLO-1 and PAOLA, they’re rather similar, and it suggests to me, and these certainly BRCA and HRD populations, that the benefit is largely driven by the PARP [poly adenosine diphosphate-ribose polymerase] inhibition.

Transcript edited for clarity.