The other question is, why don’t you use both? Why don’t you use bevacizumab [Avastin] and PARP inhibition together? We had that published in the 

, and the approval is in process. Sharyn, tell us about the study that we call PAOLA-1. There’s a 1 after it just like SOLO-1, because it’s a first-line study. Go ahead.

 PAOLA-1 was 1 of the groundbreaking discussions that started at ESMO [European Society for Medical Oncology Congress]. This was a trial that enrolled women with stage III and stage IV epithelial ovarian cancer. Patients were enrolled regardless of surgical outcome, which was a little different from PRIMA. Women who were eligible for the study all had to have either a CR [complete response] or a PR [partial response] following carboplatin, paclitaxel, and bevacizumab therapy. This was a European trial. It was enrolled throughout 8 different countries. Bevacizumab was utilized in the frontline setting with chemotherapy and then as maintenance. These women were then randomized, if they had a CR or PR, to either bevacizumab alone or olaparib and bevacizumab. The bevacizumab arm was continued for 15 months and the olaparib was continued for up to 24 months, or until there was some type of unacceptable toxicity or progression.

The primary end point on this study was time from randomization until investigator-assessed disease progression or death. Certain subgroup analyses included PFS [progression-free survival] by BICR [blinded independent central review] and PFS2 [progression after the next line of therapy]. There are also secondary end points, and tumor was analyzed for HRD [homologous recombination deficiency] via myChoice CDx. In total, over 800 patients were enrolled. Baseline characteristics were well balanced between the groups. It’s interesting that about 30% of patients had stage IV disease. Most of the patients were actually NED [no evidence of disease], going to either a complete cytoreduction or having a CR after frontline therapy. It was very interesting.

The duration of investigator-assessed PFS was significantly longer in the olaparib and bevacizumab arm than in the bevacizumab alone arm, with a median of 22 months versus 16.6 months. That led to a hazard ratio of 0.59. There was essentially a 41% risk reduction of progression or death if receiving the combination of olaparib and bevacizumab versus bevacizumab alone.

Looking at the various subgroups, for patients who had HRD-positive 

-mutated tumors, median PFS was amazingly 37 months with the combination of olaparib and bevacizumab versus only 17 months in the bevacizumab-alone arm. That was a hazard ration of 0.33. If you’re looking at patients who had HRD positivity without a tissue 

 mutation, the median PFS was 28 months in the combination arm versus 16 months in the Avastin-alone arm. That was a hazard ratio of 0.47. Interestingly enough, in the patients who were negative for HRD or had an unknown status, we saw that the median PFS was the same between the 2 groups: 16 months in both arms, and the hazard ratio was 0.92.

We did not see any new safety signals. As I mentioned, the trial did meet its primary end point. It was very impressive to see the response of the 2 drugs together—bevacizumab and olaparib—in these patients.

Videos

 PAOLA-1: Combination Maintenance Therapy in Ovarian Cancer 

Let’s just assume, Katie, that you saw a patient who comes into your office and says, “I responded to my frontline chemotherapy. I had a serious advanced ovarian cancer, and my doctor did this HRD [homologous recombination deficiency] test; here it is.” And she says, “My doctor is not very passionate about recommending that I get PARP maintenance, and I don’t have a 

Would you say—with the same passion you had for SOLO-1—to this patient that this is a no-brainer. You need PARP maintenance, you have a molecular marker, as Tom alluded to. This would be more than a doubling of the median progression-free survival. The median for an HRD-positive patient, excluding 

, has a hazard ratio of 0.5—Tom, what you said—going from 8.2 to 19.6 months. It is more than doubling of the progression-free survival. What would you tell that patient, Katie? I’m going to ask you, Tom Krivak and Sharyn Lewin, the same question.

 You asked me about my passion. I do believe that PARP inhibitors are the standard of care with shared decision-making for patients who have 

-associated cancers. For patients without 

-associated cancers, they are a standard of care, but there’s a spectrum in there. This would be on the stronger edge of evidence. The HRD group was 1 of the analytical subgroups of PRIMA, and it met its end point. I believe that, and we’ll get into the debate later. I would strongly counsel this patient regarding the potential benefit of use of niraparib, and then the known risks and benefits. I would especially talk about what the gains would be in terms of progression-free survival and what that means, without an overall survival end point that we won’t have for quite a while; though in PRIMA, we may get it much earlier than on some of the other studies. Then it would be shared decision-making between the patient and me.

I think this is a little different in that there are options for both. Some patients just want to do surveillance. I don’t know if I’d beg someone to start maintenance, which I do with 

-associated cancers. But I would strongly recommend this. I think it makes a lot of sense. We know these patients are going to recur. We just have to stop talking about all these cured high-stage patients. They don’t exist. I really wish they did, but they don’t. Try to prolong response as long as possible. I just don’t know why you wouldn’t.

I like this idea of shared decision making. But let’s face it, when you give the patient the option of taking a pill that might have some adverse effects versus going on vacation—trust me, you can go on vacation and take a PARP inhibitor too—they have a tendency to take the easy way out. It’s just human nature, right? Every patient thinks they’re cured. You say they don’t exist. Every patient thinks they’re the exception, and I don’t know why the doctor thinks they’re the exception, but there are many care providers who do.

 If you present observation as an equivalent option—and it’s listed like that in the NCCN [National Comprehensive Cancer Network] Guidelines, which is mind-boggling—then they’ll think, “Oh, I could do something or not do something? I’m going to not do something.” We invoke the counseling.

That’s what I’m trying to discuss here. It’s the strength of the recommendation in everything we do. Whether it’s a Gardasil 9 vaccine or PARP maintenance, it’s the strength of the recommendation. Sharyn, how strong would you recommend this? HRD in hand, a patient who didn’t receive bevacizumab and responded to frontline therapy comes to you and says, “Dr Lewin, you have a great reputation. Do I need maintenance niraparib?”

 Honestly, I agree with everything that Katie said. I want to take a minute to highlight the importance of frontline germline testing, which unfortunately not 100% of women with ovarian cancer receive. There were data at the SGO [Society of Gynecologic Oncology] Annual Meeting showing about 60% do. I don’t know why it’s not quite 100%. But I agree, it really is shared decision-making. I am a big biomarker believer. I know the inherent problems with the subgroup analyses. But I think if the patient does have HRD—and of course if she has a 

 somatic or germline mutation—I’m going to strongly encourage PARP maintenance.

Tom Krivak, how strong is the recommendation? HRD in hand.

 We talk about financial conflicts. What I can say is that I have a biomarker conflict too, in that I believe in HRD and I believe in maintenance. When I give talks, I automatically say that I graduated fellowship in 2002. I thought Maurie Markman’s trial of 12 monthly cycles versus 3 maintenance paclitaxel was great, and I’ve used maintenance therapy ever since. It’s important because what’s really moved the needle has not been the up-front 6 cycles of whatever therapy we give: the maintenance therapy has moved the needle. To me, if somebody has an HRD-positive tumor, I would strongly recommend maintenance, whether it’s single-agent niraparib or a combination therapy. But I would have to say part of my bias is that when I see folks with advanced-stage ovarian cancer, I’m going to recommend some form of maintenance therapy, and I don’t believe in active surveillance in that group.

People want to know what your conflict of interest is. Trust me, your conflict of interest is not because someone paid you to go to work, whether it be a drug company or your hospital. Your conflict of interest is that you have seen patients benefit and stay alive and live better with maintenance therapy. I get that. In my mind, it’s evidence and evidence based. For the audience, I’ve got 4 panelists here and myself to offer—with a strong recommendation—a maintenance PARP inhibitor in 

mutated disease. With an HRD molecular signature, you can maybe soften it a little. Your head doesn’t have to explode, to quote Katie Moore, but my head would explode if someone says, “Well, I don’t know.”

Practical Applications of PRIMA in Ovarian Cancer Management

mutations, maybe two-thirds or three-quarters of those are germline. We want to go beyond 

, and clearly PARP inhibitors work beyond 

: we’ve shown that in the recurrent setting. There’s now a third study that was also published in the 

by Antonio González-Martín called PRIMA. Tom, tell us about PRIMA and what the opportunity is here beyond 

 It is also known as GOG-3012, right? We can’t forget that. This compared maintenance niraparib with placebo, and niraparib was given as maintenance for 36 months in this trial after patients completed primary chemotherapy. Eligible patients had stage III with gross residual disease after primary surgery or had stage IV disease, and this trial included patients who had neoadjuvant chemotherapy as well. Both serous and endometrioid histologies were included in this trial, importantly, and to be eligible, you had to have a response, either partial [PR] or complete [CR], to previous chemotherapy.

Brad, you’ve shown this with your weights-and-plates work in the past in terms of impact, especially on thrombocytopenia, for those patients who had a platelet count less than 150,000 permm3 or who weighed less than 77 kg. You actually reduced the dose. That happened about two-thirds of the way through this trial. That’s important in terms of interpreting some of the toxicity data.

The patients were randomized 2 to 1. There were 733 patients who were randomized in total. Importantly, they used hierarchical step-down in terms of the statistics. They actually did stratification based on whether you received neoadjuvant chemotherapy or not, what your HR [homologous recombination] status was, and whether you had CR or PR. Those were the 3 stratification factors. The primary end point in this was homologous recombination deficiency [HRD], and we can get into discussing what exactly that is and what that means. But the primary end point was the HRD population. If that was positive, then they were able to go on to the other populations, and the second population they looked at was the entire intent-to-treat population. That’s important to understand. The primary end point that they used within these groups or cohorts was progression-free survival [PFS] as determined by BICR: they had radiological blinded independent central review to determine if you actually had progression or not.

In their first assessment for the group that had HRD, they found a significant improvement in the median. The PFS was 21.9 months for the group that received niraparib and was 10.4 months for the group that had placebo. The hazard ratio was very impressive, 0.43, so there was a 57% reduction in the hazard of either relapse or death. If you look at it in the intent-to-treat population, it was still impressive: 13.8 versus 8.2 on the medians, with a hazard ratio of 0.62. That’s in all comers who were in this study. The phase 3 patients had to have residual disease, so they were a fairly difficult group. When you’re looking at the medians, you have to be cognizant of what the patient population was.

Then there were a number of subgroup analyses that were looked at as well, getting back to what Katie just talked about. If you look at the 

 group, you’re down into the 0.3 range. If you break it out—Brad, you had data at the SGO [Society of Gynecologic Oncology] Annual Meeting this year looking at 

1 showed a slightly higher hazard ratio of 0.39. It was a little lower, 0.35, for our 

 and look at just the HRD, the hazard ratio is still impressive, 0.5. That’s interesting. If you look at your HR [homologous recombination] proficient patients, you still had a positive hazard ratio. It did not cross 1, and the hazard ratio was 0.68, that’s very impressive in terms of what you’re seeing with this data. Now, the medians were not very different. The difference was about 2.7 months, so you’d have to include that in how important you think that difference is.

I don’t think there were any significant new safety signals from this trial. We continued to see anemia, nausea, and thrombocytopenia—the big 3—largely as grade 1 and 2 events. But we still saw 28% nausea that was grade 3 or higher. In terms of thrombocytopenia, the amount definitely dropped down a little, but we still saw a significant amount of grade 3 or higher events that were present at about 29%. We still saw some of those safety signals that were the same.

What does this mean, Brad? It means you have a patient population where you could argue you could use a PARP in any of these subpopulations. I’d love to hear about these subgroup analyses that really aren’t powered and what they mean. I think people have different interpretations of what that means and how they’re going to apply it clinically. But I do think many people are going to look at these data and say, why wouldn’t I use it on everyone?

I wanted a comprehensive answer, and that was comprehensive. The impact of this study deserves a comprehensive assessment as you just provided. I’m not going to debate yet—we will—whether HRD testing should be performed.

PRIMA: Frontline Niraparib Maintenance Therapy in Ovarian Cancer 

-associated disease. We have Katie Moore here, who was the first author published in the 

 related to the approval in December 2018. Tell us about that study and what that has meant to our practice in the frontline setting.

 As you know, I love to talk about SOLO-1. SOLO-1 was a randomized phase 3 study that enrolled only women with 

-associated cancers, predominantly germline mutations in 

. They had to have advanced cancer, an attempted cytoreductive surgery, and at the end of platinum-based chemotherapy, complete or partial response to chemotherapy. At this point they were randomized 2 to 1 to receive olaparib tablets versus placebo until progression or toxicity or the 2-year mark. The primary end point was investigator-assessed progression-free survival [PFS].

That took a long time to reach, but it finally resulted and demonstrated a ratio of 0.3, which translated to a difference in the median progression-free survival—counted from the end of chemotherapy, importantly&mdash;of 13.8 months in the control arm and not yet reached in the arm that was treated with olaparib, but it is somewhere around 47 to 49 months. The PFS2 [PFS after 2 lines of therapy] was positive as well. There have been several subsequent exploratory analyses in all the different surgical and residual disease subgroups, demonstrating equal magnitude of benefit regardless of how you analyze it. That appropriately led to a change in the standard of care for these women.

, I define that as what reasonable physicians would do in a similar setting. It doesn’t mean it’s the only standard of care. Tom Krivak, is this the only standard of care if you have a 

, but I know we use it a lot. Given how the question is phrased, I would say that you must have a reason not to give it. To me, when you look at those data, they’re just so impressive that I completely agree. Sometimes there’s a slow adoption, but to not be on this therapy with the germline mutation as well as somatic mutation, I get nervous. I think if you would show patients some of these Kaplan-Meier curves when they say, “I don’t think I really need it,” and you ask if they want to be on the top line or bottom line, there is such separation that most patients would say, “I don’t understand why you aren’t making me take this.”

 I would say that you really have to have a strong reason not to be using a PARP inhibitor in a patient who has a 

Katie, I know you like to talk about this, and we like to listen to you. That’s a great opportunity. You presented this all around the world, and we love it. Do you ever present it and people say, “Well, I’m not sure”? Never, right?

Why do people say that? Tell us. That’s what I’m trying to discuss here.

 The save-it-for-later crowd. I had the opportunity to debate someone who is really a believer in that at the NRG Oncology Semiannual Meeting this year. I’ve been convinced there’s just no rationale for that. I’ve stopped being nice about it because I don’t want it to even be considered an equivalent option. We should have learned that message from the bevacizumab story, which you just demonstrated. The argument is you look at SOLO-1 and SOLO2 and the hazard ratios are both 0.3, so someone says, “Well, I can use it here and now or later, and I get the same benefit,” which assumes you’re going to let your patient recur. I don’t know why you would let your patient recur, No. 1; and No. 2, those are 2 completely different lines of therapy. If you look at the same thing with bevacizumab but lined up frontline and second line—such as OCEANS or GOG-0213 and then AURELIA&mdash;and use that rationale, you would say, “Well, I would use only it in the AURELIA setting,” which is asinine. Why would you wait in your highest-risk population? It is a good drug there, but your frontline is where you have the opportunity to cure somebody. It makes no sense, and the argument makes no sense. It makes my head explode.

Before we offend too many people, I’m going to stop you there. But that’s great. Thank you for your hard work on that. I look at it as an unprecedented result. Whatever the definition of standard of care is, we have an obligation to discuss that with our patients. The obligation begins with germline and somatic testing, because if you don’t test, you won’t have the opportunity.

SOLO-1: Frontline Olaparib Maintenance Therapy in Ovarian Cancer

® titled, “Ovarian Cancer: Evolving Concepts Around Systemic Therapy.” My name is Brad Monk. I’m a gynecologic oncologist from Phoenix, Arizona, at both the University of Arizona and Creighton University, as well as The US Oncology Network. Joining me today in this discussion are my colleagues: Tom Herzog, from the University of Cincinnati Cancer Institute in Cincinnati, Ohio. Welcome, Tom.

 Brad, it’s a pleasure to be with you today, and I look forward to a great discussion. Thanks for having me.

Dr Tom Krivak from the University of Pittsburgh Medical Center and Allegheny Health Network in Pittsburgh, Pennsylvania. Go Steelers! Thank you, Tommy.

 Thanks for having me here, I’m looking forward to a great discussion.

Dr Sharyn Lewin from Holy Name Medical Center in Teaneck, New Jersey. Thank you, Sharyn, for joining us.

And Dr Katie Moore from the Stephenson Cancer Center at University of Oklahoma in Oklahoma City, Oklahoma. I want to recognize Dr Moore for her contribution to the Society of Gynecologic Oncology [SGO] as the program chair this year. She was able to seamlessly transition from an in-person meeting to a virtual meeting. I thank you for that. The scientific exchange was very exciting and informative, and that’s 1 of the reasons we’re here today. We’re here today to talk about new presentations, new indications, new studies, new research, and innovation from the Society of Gynecologic Oncology 2020 Annual Meeting.

We’re here because of 2 indications in ovarian cancer beyond 

in 2019 and presented at ESMO [European Society for Medical Oncology Congress] 2019. We’re going to take a deep dive into what PRIMA and maintenance niraparib means to you and your patients. PAOLA-1 was also presented in Madrid at ESMO 2019 and published in the 

in 2019. We’ll discuss what that study means to you, starting with bevacizumab and bevacizumab maintenance therapy but adding olaparib to it in the maintenance space. Hopefully when you’re done here, you will know what you missed at the SGO meeting if you did miss it. If you didn’t miss it, we’ll hopefully add some context. We’ll discuss some opportunities with these new approvals.

I’m going to begin here by talking about bevacizumab. Bevacizumab was the first targeted therapy to be approved in 2014. We’re going to begin by talking about first-line treatment. Bevacizumab was approved in June 2018 as first-line therapy. Tom Krivak, tell us about GOG-0218 and how that led to FDA approval.

 GOG-0218 was a large randomized trial of about 1800 or 1900 patients with 3 arms. It was designed by you and Dr Robert Burger a long time ago when we were learning about targeted therapies, and it’s undergone many publications. The most recent publication was the final publication looking at overall survival. Comparing all 3 groups, there was no difference in the overall survival. However, when we look at this publication, there are a couple of things that are really important to note. The stage IV group did show an improvement in overall survival of 10 months: 33 months versus 43 months in the patients who received bevacizumab with bevacizumab maintenance. I also think it’s really important that as we go through these discussions, we’re going to be talking about HRD [homologous recombination deficiency] and some other biomarkers.

The trial and this publication did try to look at HRR [homologous recombination repair] genes, but it was only in 1200 of the patients. But to me, I think that as we take some small steps with molecular medicine, we’re going to need some of these trials to look at how this may affect patient selection for molecular-targeted therapy for up-front treatment. The label with the PFS [progression-free survival] improvement of 6 months while receiving maintenance bevacizumab is what it was approved on, and the overall survival final paper showed that there was no improvement in overall survival. I think that’s the summary for this paper at this time.

It’s been an important step forward. It was not a big step, but it was an initial step. Six months of progression-free survival when bevacizumab is added to chemotherapy and in maintenance for a total of 15 months. In some people’s minds this is impactful, certainly in the high-risk subgroup. It’s most important today, though, because it’s a path toward other treatments. We’re adding PARP inhibitors to bevacizumab, and if you don’t start bevacizumab, you can’t add it to it. There will be a study imminently, which we’ll talk about, that adds immunotherapy to bevacizumab. We’ll talk about what that means in the setting of combination therapy. Tom Herzog, what percentage of patients do you think receive frontline bevacizumab in the United States today?

 As best I can tell, it’s about 40% right now.

 I would think it’s a little higher, but 40% may be correct. The market data that I’ve heard have it around 50%, maybe a little higher. But that’s a ballpark estimate.

 Agreed. The market data that I’ve heard as well are between 40% and 50%.

One of the things that’s interesting is that the medical oncologists use it a little more. The medical oncologists were earlier adapters because of the use in colorectal cancer and lung cancer. I really don’t have any evidence of that, but certainly that has been my observation.

GOG-0218: Frontline Bevacizumab in Ovarian Cancer

Thomas Herzog, MD, a professor of obstetrics and gynecology and deputy director at University of Cincinnati Cancer Institute, discusses the data that led to the FDA approval of the combination of olaparib (Lynparza) and bevacizumab (Avastin) for the maintenance treatment of patients with advanced ovarian cancer who are in complete or partial response to first-line platinum-based chemotherapy with bevacizumab and whose cancer is associated with homologous recombination deficiency (HRD)—positive status defined by either a deleterious or suspected deleterious 

Data from the pivotal phase 3 PAOLA-1 trial served as the basis for the approval. The results, which build on data from the phase 3 SOLO-1 trial, showed that the combination led to a 41% reduction in the risk of disease progression or death compared with bevacizumab alone in this patient population (HR, 0.59; 95% CI, 0.49-0.72; 

 <.001). After a median follow-up of 22.9 months, the median progression-free survival (PFS) was 22.1 months and 16.6 months with the combination and bevacizumab alone, respectively.

The benefit with the combination was seen in all-comers, says Herzog. However, data demonstrated that patients with tumors that tested positive for HRD, including tumors that had 

 mutations derived the most benefit with olaparib (HR, 0.33; 95% CI, 0.25-0.45). In this subgroup, the median PFS was 37.2 months and 17.7 months with the olaparib combination and bevacizumab alone, respectively.

In those who had HRD-positive tumors without 

 mutations, the median PFS was 28.1 months with olaparib/bevacizumab and 16.6 months with bevacizumab alone, respectively (HR, 0.43; 95% CI, 0.28-0.66). 

Thomas Herzog, MD, discusses the data that led to the FDA approval of the combination of olaparib and bevacizumab for the maintenance treatment of patients with advanced ovarian cancer who are in complete or partial response to first-line platinum-based chemotherapy with bevacizumab and whose cancer is associated with homologous recombination deficiency–positive status defined by either a deleterious or suspected deleterious BRCA mutation, and/or genomic instability.

Dr. Herzog on the FDA Approval of Olaparib/Bevacizumab as Frontline Maintenance in Ovarian Cancer

Thomas Herzog, MD, professor of obstetrics and gynecology, deputy director, University of Cincinnati Cancer Institute, discusses the use of hyperthermic intraperitoneal chemotherapy (HIPEC) in ovarian cancer.

 on the use of HIPEC in patients with ovarian cancer by Willemien J. van Driel, MD, PhD. The trial boasted an approximate 1-year overall survival advantage by giving neoadjuvant carboplatin and paclitaxel, and cytoreductive surgery with or without HIPEC at a single dose of 100 mg/m

 with cisplatin. Patients had slightly less than a 4-month advantage in progression-free survival, and immature data showed an approximatel 1 year improvement. Additionally, the toxicity profile was much less than what has been traditionally observed.

The data from this trial, explained Herzog, contradicts the data that was reported at the 2017 ASCO Annual Meeting, which showed no advantage with HIPEC and more toxicity. Physicians need more randomized data in this area to understand HIPEC’s role in ovarian cancer, states Herzog.

Dr. Herzog on the Use of HIPEC in Ovarian Cancer

Thomas Herzog, MD, professor of obstetrics and gynecology, deputy director, University of Cincinnati Cancer Institute, discusses the impact of recent clinical trials in ovarian cancer.

Herzog says physicians owe all the progress observed in the treatment of patients with ovarian cancer to clinical trials. More than a decade ago, clinical trial data led to the adoption of paclitaxel-based chemotherapy into treatment, which has significantly improved outcomes. Phase III trials have also made a difference in allowing gynecologic oncologists to take a cumbersome inpatient regimen and turn it into a convenient outpatient regimen with the addition of carboplatin. Paclitaxel infusion time has also been adjusted from 24 hours to 3 hours.

Herzog adds that the GOG-178 trial showed an improvement of progression-free survival with maintenance therapy after paclitaxel-based chemotherapy for patients with advanced disease. Studies of dose-dense regimens are ongoing to see if patients can receive more therapy over a shorter period of time.

Dr. Herzog on Impact of Recent Clinical Trials in Ovarian Cancer

Thomas Herzog, MD, professor of obstetrics and gynecology, deputy director, University of Cincinnati Cancer Institute, discusses novel therapies in ovarian cancer.

Biologics have been the main source of progress in ovarian cancer, says Herzog. The biggest development has been with antiangiogenics, specifically bevacizumab (Avastin). Bevacizumab now has an approval in frontline ovarian cancer based on the data from the GOG 218 and ICON7 trials. Now, physicians have an indication in the frontline, platinum-sensitive, and platinum-recurrent settings. However, physicians are still determining where they can leverage the agent the most.

The future will likely rely on combinations, biomarkers, and understanding how to categorize patients correctly, explains Herzog, which will be important in minimizing toxicity and maximizing outcomes. Additionally, using biomarkers and a patient’s genomic profile and signature will be important, so that physicians can put the patients who are going to benefit from angiogenesis inhibitors in one group, immunotherapy in another, PARP inhibitors in a third, and potentially some type of novel combination between those 3 or additional therapies will emerge.

Dr. Herzog on Novel Therapies in Ovarian Cancer

Thomas Herzog, MD, professor of obstetrics and gynecology, deputy director, University of Cincinnati Cancer Institute, discusses the optimal use of bevacizumab (Avastin) in patients with ovarian cancer.

In June 2018, the FDA approved bevacizumab for use in combination with carboplatin and paclitaxel followed by bevacizumab monotherapy, for the treatment of patients with advanced ovarian cancer following initial surgical resection. Now, bevacizumab has 3 indications in ovarian cancer, and deciding in which patients to use it depends on several factors, explains Herzog.

Herzog explains that bevacizumab is very effective in getting patients with plural effusions and large volume ascites off of having to be tapped, either through arthrocentesis or paracentesis. Additionally, a subgroup analysis from the ICON7 trial looked at patients with high-volume disease and a high risk of relapse, and showed that those patients had a significant improvement in progression-free survival and perhaps an overall survival advantage, says Herzog.

Whether it should be considered in all-comers is still up for debate, though many physicians will, says Herzog. Herzog believes that its use will likely increase following the approval, as insurance may be more likely to cover the agent.

Thomas J. Herzog, MD

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