The case that we&rsquo;re going to talk about today is a 58-year-young female diagnosed in 2014 with stage IV ovarian carcinoma. Her final pathology was a high-grade serous carcinoma from epithelial ovarian cancer. Her initial CA [cancer antigen] 125 was about 460 upon presentation. The CAT scan that was obtained prior to surgeryit was a CT scan to the abdomen, pelvis, and chest, which revealed a 4-cm mass of the left ovary, peritoneal carcinomatosis, and some ascites.

She underwent surgery, which included exploratory laparotomy. She was suboptimally debulked with residual disease greater than 1.5 cm. Postoperatively, the patient received combination intravenous [IV] intraperitoneal chemotherapy with carboplatin and paclitaxel for 6 cycles. She achieved a complete remission with a normalization of her CA 125, CT scans, and physical examination.

Approximately 2 years later, in 2016, she had some symptoms of recurrence, some bloating, and some early satiety. Her CA 125 had risen to 255. She had an ECOG status of 1. At that point, the decision was made for the patient to be treated with chemotherapy. She was treated with carboplatin/paclitaxel for 6 cycles, along with bevacizumab. She had a good partial response at that time and went into remission. She had a good partial response at that time with a CA 125 of 45, and she continued on bevacizumab maintenance.

About a year and a half following the second-line chemotherapywe&rsquo;re now into 2017&mdash;she again presented with symptoms of early satiety and of bloating, as well as some pelvis discomfort. Her CA 125 had risen to 515, and she had an ECOG status of 0. Genetic testing at the time was noted to be germline

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;

Currently, the patient has a CA 125 of 620. Her CT scan shows several small masses within the lung as well as abdomen, and she has an excellent functional status of the ECOG of 0.

I would say this is somebody that&rsquo;s typical, that we see with ovarian cancer. This is a young woman who developed some symptoms of ovarian cancer, and then, unfortunately, presented with that advanced stage disease where she had stage IV disease, based off not just her CT scan findings of abdominal disease but also pleural effusions or something within the liver parenchyma or upper abdomen, such as a pleural effusion.

When we see young women like this that have a good functional status&hellip;I like how they treated her. They treated her very aggressively and took her for primary surgical cytoreduction, which, again, candidates for patients with stage IVat this point a lot of people would consider neoadjuvant chemotherapy, which is 3 cycles of chemotherapy, interval debulking surgery, and then 3 to 4 additional cycles of chemotherapy, and then consider maintenance therapy up front. This patient was treated aggressively with up-front surgical debulking. Unfortunately, she was suboptimal midbulk. That meant that the disease that was left was greater than a centimeter, and a lot of folks would consider any gross residual disease to be suboptimal.

I think this case brings up a couple points. First, she had a primary debulking. It sounds to me like the surgeons felt that could get everything, so they their best to do so. Secondly, with that neoadjuvant chemotherapy, should she get 3 cycles or 4 cycles and then interval debulking? Most people would say 3 cycles of chemotherapy and then interval debulking followed by additional chemotherapy.

I think that in 2019, we have lots of options for these patients. It&rsquo;s about how functional the patient is, what the risk the patient really wants to take is, and then&hellip;the surgical skill and what they&rsquo;re willing to risk for trying to do a primary surgical cytoreduction. In my opinion, when taking somebody to the operating room, I would try to get that patient to microscopic residual. To do a laparotomy, realize that you may not be able to get the patient to complete surgical cytoreduction. Maybe abandoning that and giving them chemotherapy could have been a choice. I think what they did was completely fine.

I think the other thing that was outside of the kind of new way of thinking is giving somebody combination IV/IP [intraperitoneal] chemotherapy who was suboptimally debulked. In most of the studies that we&rsquo;ve done, looking at in the United States, they were with patients who had gross resistant disease of less than a centimeter. You know, GOG-252 is the most recent trial that really showed marked improvements in progression-free survival in the 26, 27, 28-month range, which was a combination of aggressive surgery, a combination IV/IP chemotherapy in 2 arms, and then weekly IV chemotherapy in 1 arm, and then placing the patients on maintenance bevacizumab.

I think what we can say is that this patient was treated very aggressively with primary debulking surgery, given combination IV/IP chemotherapy to achieve remission. Again, she did that. She is like 80% to 90% of folks who come in with this new diagnosis that will achieve remission, which is defined as normal CA 125, normal physical examination, and normal imaging studies such as a CAT scan. I think that this was a very well aggressively managed patient up front.

Case-Based Overview: Pretreated Recurrent Ovarian Cancer

I think in 2019, if this patient would come into the office today, and knowing what we know about the case, I would say that we&rsquo;d look and we&rsquo;d say this patient is stage IV. I think many of us would talk about chemotherapy first, interval debulking, chemotherapy, and then maintenance treatment. With the newer studies showing that PARP maintenance is an important part of that, we would want to do genetic testing. Genetic testing would include looking at the germline status.

We would have the patient see us in the office, talk about chemotherapy, talk about surgery, talk about TT [targeted therapy] guided biopsy to get the patient ready for neoadjuvant chemotherapy. An important part would be having her either see a genetic counselor within the office, or sometimes we&rsquo;ll have to do that type of counseling within the office, because they may not be available to come back. I would recommend some type of panel test to look for any type of genetic predisposition for ovarian cancer. That&rsquo;s very important for this patient in that it&rsquo;s going to help direct her treatments, because I think the treatment has changed since 2014, when this patient presented.

mutation, she would get chemotherapy, surgery, chemotherapy, and then would receive maintenance therapy with a PARP inhibitor at that point.

If she would get genetically tested, there have been many PARP inhibitor studies that have been recently reported.

SOLO-1 looked at patients with advanced-staged ovarian cancer treated with maintenance olaparib. Most recently at ESMO [European Society for Medical Oncology], a study reported by Tesaro/GSK [GlaxoSmithKline] was the PRIMA trial looking at single-agent niraparib for patients with germline mutations, as well as all-comers in another study, PAOLA, that looked at this as well.

In today&rsquo;s 2019 management, we want to know what the germline status is, and then a lot of us would send the tumor off for tumor testing to look for tumor genetic alterations in

, and some of us would look for what is called genomic instability, or HRD [homologous recombination deficiency]. Based off of those test results, you may triage this patient to a different maintenance strategy at that point.

The strategy that we&rsquo;re using now&hellip;and I think that this is very complex, because the results of the ESMO trialsthe SOLO-1 trial the PAOLA trial&mdash;as well as the PRIMA trial all showed clinical benefit. Really, SOLO-1 was with germline mutation patients and somatic mutation patients. When we&rsquo;re in the wild-type realm, it really boils down to: Do clinicians believe in what&rsquo;s called homologous recombination deficiency, or HRD testing?

Personally, I do. I think the HRD test is another way to look and try to capture more patients who may benefit from maintenance therapy. The 2 trials did show that in the HRD-positive patients, those that had the genomic instability type of score, that those patients benefited either from single-agent niraparib or a combination of olaparib and bevacizumab. I look at the patients who have a germline mutation or somatic mutation of

. I would give them chemotherapy and surgery, and then they would be treated with PARP maintenance, whether it&rsquo;s olaparib or niraparib. Then the patients who were noted to be

wild-typetest their tumor. Again, if their tumor is positive, that&rsquo;s a somatic mutation; they would get single-agent niraparib or olaparib. if those were negative, then you look for the HRD testing. If the patients are HRD positive, what many of us are doing, we&rsquo;re going with single-agent niraparib, some people would use the combination of olaparib and bevacizumab. It&rsquo;s very confusing because you can see the same group of patients choosing 2 different potential regimens. Then, in the HRD-proficient patients, or the ones that have a score that shows that their tumor does not have any deficiency, most of us would say we should probably be using niraparib in that group, and then saving bevacizumab for possibly later.

I&rsquo;ve looked at some of these data. I think that if you would ask 4 or 5 different treating medical oncologists as well as GY [gynecologic] oncologists, that you may get different interpretations of the data, and I think it&rsquo;s going to take us a few years to try to figure out how to use this up-front testing. Is combination therapy better than single-agent therapy, or is really single-agent therapy the way to go? Then we&rsquo;re not using our bevacizumab at this time, and we can potentially use that for, unfortunately, when these patients recur. Because as you go through this case, as we know, unfortunately, the majority of these patients with ovarian cancer have advanced stage disease. Ultimately, they&rsquo;ll recur, and with that recurrence, we want to make sure and have more treatment options available at that time.

Gene Testing and Treatment for Recurrent Ovarian Cancer

One of the things I always teach when I talk with the residents and everybody is: Responders respond. There&rsquo;s this group of patients that we may have treated for 6, 8, 10 years, and it seems like each time they come in, they respond. You&rsquo;re going to have that group of patients that, to me, will do well. They&rsquo;ll have a durable response. Then, unfortunately, you have these patients that will develop a recurrence, and so they may have had a treatment-free interval of 12 to 16 months, and then their second treatment was just 2 months, but then they&rsquo;re progressing on each of these lines of therapy.

I think both of those patients are a little bit different, but looking at the newer data that are coming out, I would have to say that that&rsquo;s the big thing. If you look at this patient who is diagnosed in 2014, now we&rsquo;re in 2019. We have a whole host of different clinical trials that are available, as well as these clinical trials that have led to ability for us to use these other agents. I think in this patient and focusing on PARP inhibition today as they go along in their treatment, she didn&rsquo;t receive PARP inhibition up front, and she received bevacizumab in the second or third line, that this would be a patient that we&rsquo;d want to test them molecularly to see; I know that we have a germline that was negative, but we could test more accurately to see if there&rsquo;s a somatic

mutation, or you could elect to send the patient&rsquo;s tumor off to Myriad, which does the myChoice, which is the HRD [homologous recombination deficiency] test.

Or you could potentially choose to send that patient&rsquo;s tumor to Foundation Medicine, which does an LOH [loss of heterozygosity] test, which is similar but not the same. I think one of the key points is, when you look at the QUADRA data, you look at the PRIMA data, they are using the Myriad test. I think that when we&rsquo;re talking about how we&rsquo;re testing patients and we&rsquo;re seeing this patient may have this genetic alteration, we really need to define what test we&rsquo;re using to make sure that everybody&rsquo;s on the same page, since there are different testing modalities and different types of commercial tests out there.

I can see patients going up to 6, 7 lines of therapy. I think sequencing chemotherapy has become very challenging in that you have your platinum-eligible patients that will get repeat platinum doublets, possibly with bevacizumab, to get a response, and then get switch maintenance to PARP inhibition. Those patients will do very well. As you go up further-line therapies, it&rsquo;s hard to say how those patients are going to do. I think when we get up in the further-line therapies, you want to look at agents that may be less toxic, that are easier to deliver, to try not to have a significant decrement on their quality of life.

I would have to say if we look at the percentage of patients who are becoming eligible for that fourth, fifth, sixth line of chemotherapy in the United States, where we treat patients very aggressively, I would say that a number of those patients are increasing.

In general, when I kind of lecture on how to take care of an ovarian cancer patient, kind of from initial diagnosis to potentiallyyou know, unfortunately&mdash;enrolling in that patient in hospice care, one of my thoughts is&mdash;I try to talk with the residents that I&rsquo;m working with&mdash;is that you want to make sure and get a quality surgery for those patients, at least 1 quality surgery for those patients.

Again, if they&rsquo;re young and very functional, I try to give them IV/IP [intravenous/intraperitoneal] chemotherapy like this patient had. Some people don&rsquo;t believe in that treatment anymore, but they need a platinum doublet. Unfortunately, when these patients recur, I think before a patient would eventually end up in the hospice, they really should receive a PARP inhibitor, Avastin, as well as immunotherapy.

These patients that have these durable responses, I could see them being on treatment for a significant period of time, then combinations of what we just talked about: niraparib with bevacizumab; niraparib with immunotherapy. I think are other options down the line that we may be able to safely deliver to these folks.

I think the percentage of patients living to the fourth, fifth, sixth line is there. Those are conversations we have to have with our patients. Some patients are deconditioned at that time, and they may not feel like they want further therapy. On the QUADRA trial, you saw it was opened up in 20-some odd sites, and they accrued 460 patients. These patients are all greater than third-line therapy to get that. A significant portion of these patients were 6-line or greater. I think it&rsquo;s going to be something that we see more and more often as we take this disease from an acute illness to a chronic disease, and we&rsquo;re trying to manage it with medications to help prevent the cancer from growing or coming back.

I think for this patient, again, she was wild-type for germline. I want to test the tumor. You know for this patient, if she had HRD positivity, because you know the new QUADRA data are HRD positive and platinum sensitive, you can go ahead and treat those patients with single-agent niraparib, and I think that that would be a fine choice at this time. The patient had been treated with combination IV/IP chemotherapy; she had received bevacizumab. She received platinum doublets once again. I would have to look at quality of life and say, &ldquo;Is this somebody that we could use the QUADRA data for, which would be single-agent niraparib? Or is this somebody that, you knoware they functional and want to try something else if they&rsquo;re not HRD positive and not germline?&rdquo; I think the TOPACIO data, which are combination immunotherapy with niraparib in a highly platinum-resistant patient population, had 65% disease control rates. To me that was amazing. In a lot of these patients, we may try different ways of starting single-agent and then use in combination to see if we can get a response for them. A lot of it will depend upon their functional status. In this patient&rsquo;s case, she had an excellent functional status. She&rsquo;s young with a functional status, an ECOG status of 0, meaning we&rsquo;re going to try to be as aggressive as possible.

Considerations for Managing Recurrent Ovarian Cancer

As we start to move more to biologic agents, there&rsquo;s no doubt about it that at this past ASCO [American Society of Clinical Oncology Annual Meeting], the AVANOVA data were utilized in patients instead of using chemotherapy. These patients were randomized to niraparib with bevacizumab versus single-agent niraparib. What we saw in that patient population is that you can substitute biologic therapy instead of chemotherapy.

Combining it with Avastin, you had to bring the patient in, and they had to have some chair time to get their infusion. I think one of the nice things about PARP inhibition is that it&rsquo;s an oral drug. If you have a patient who has an excellent functional status who doesn&rsquo;t want to be coming in for chemotherapy infusionssay, their blood counts are fine and they want to get their medications. Then, to know I live in Pittsburgh, say they want to go down to Florida. This way they can fly down to Florida, we can check their labs while they&rsquo;re in Florida, and then refilling other medications, and fly back once a month, once every other month to have their medications refilled and to make sure their toxicities aren&rsquo;t there.

I think it releases them from their chair time. A lot of these adverse effects are managed over the phone with our nurse and a PA [physician assistant] to help in taking the medication in the evening. I think helping fatigue with medications are all positive interventions. I think chemotherapy has adverse effects. PARP inhibitors have adverse effects. They&rsquo;re different profiles. It&rsquo;s a nice alternative for the patients, and I think it gives them choice. I think when we&rsquo;re interacting with a patient, the more options and choices we have for those patientsI think that that sounds odd, but that&rsquo;s comforting, knowing that if this doesn&rsquo;t work, we have these choices. The patient doesn&rsquo;t feel pain and say, &ldquo;This is my only option at this time. I have these other options. I kind of like how this sounds. I can take a pill for a while and not have to worry about chair time,&rdquo; and so the patients are doing well.

I think this is the conversation that each patient&rsquo;s going to have. I don&rsquo;t know, it&rsquo;s what always I tell the residents, &ldquo;The science of medicine is understanding the capacity of data, the QUADRA data, the AVANOVA data. The art of medicine is applying that time for each patient, realizing that, you know, I saw 4 patients today, and each of them is receiving treatment for recurrent therapy and each is slightly different. That is just because that&rsquo;s what the patient said: &ldquo;Hey, this works better for me and my lifestyle.&rdquo;

PARP Inhibition in Recurrent Ovarian Cancer

I think the QUADRA Trial was really important in that it had 460-some-odd patients that were heavily pretreated. What I think we were trying to do with the QUADRA data is&hellip;we had development of PARPs, which started in treatment of patients who had

-mutated tumors, it was germline, and then expanded into germline and somatic BRCA treatment. Then we kind of switched, and we had all the good data coming out with maintenance therapy.

There was this gapcan we use PARP inhibition in all-comers? QUADRA looked at all-comers, and then they kind of took out some data points looking at patients who had

mutations and patients who had HRD [homologous recombination deficiencies] genomic scaring, and then all-comers. Really, what they did is, when they looked at it and they saw the patients who had

mutations treated at fourth line or greater, they had excellent response rates for platinum sensitive, platinum resistant, as well as platinum refractory. They had really good response rates in all-comers with

mutations, and then again when expanding the indication using HRD in patients who had the HRD genomic scar, but not a

mutation, and those patients who were platinum eligible, those patients had durable responses, as well, with respect to having PARP inhibition at that time.

I think these data are definitely practice changing. What it does is, it&rsquo;s taken our portfolio of PARP inhibitors where we should use them and expanded it to additional therapy and then expanded it to HRD. Again, the label is fourth-line therapy or longer. If you had a patient who came in at second- or third-line, she had a

mutation, platinum-sensitive recurrence, this is somebody who said, &ldquo;Tom, I drive an hour and a half from West Virginia. I really do not want to be driving back and forth for chemotherapy. It&rsquo;s something that I would prefer.&rdquo; Sometimes their co-pays may be higher for the chair time and, so, the oral agent.

I used the PARP inhibitor on a patient who couldn&rsquo;t make the drive, and she just wanted to come in once a month for labs, and she thought that that was a better way to go. There were many clinical trials at that time looking at this. I think the QUADRA data are practice changing in that they show that it&rsquo;s expanding the indication. They show that you can use it in heavily pretreated patients because in the QUADRA trial, there was a significant portion of these patients who had 6 lines or greater. To say somebody&rsquo;s had fourth-line, fifth-line therapy, we shouldn&rsquo;t use PARP inhibitorsniraparib has shown that you can use that at the 6-line treatment for these patients. I think it&rsquo;s been a nice addition to a portfolio that gives us choices and options to give to patients when we&rsquo;re sitting down talking with them in, in the clinic.

I think that, looking at the data&hellip;using a biomarker in this heavily pretreated patient group is appropriate. Do I think that if they would have used it in less pretreated patients, would they have had different responses? I think anybody would say yes as we move these drugs up in drug development. I think that this met an unmet need. This is something that we&rsquo;re starting to see more often, in that patients are living longer; we&rsquo;re having to figure out what can we give them for fourth-, fifth-, sixth-line therapy. I think that&rsquo;s a very nice addition.

I also think that it&rsquo;s looking at molecular signals. We have to pay attention. Is the patient

positive? Did we have this HRD test? I think it&rsquo;s really trying to take the biomarker and apply it to the patient even further down the line when most of us would say at fifth-line therapy or sixth-line therapy, the chance of response is 5% to 10%. When you&rsquo;re looking at the response rates in QUADRA, they&rsquo;re much higher than that, especially for BRCA in the 40%, 30% range. To me, those are pretty remarkable response rates.

I kind of, you know, quoted some of the TOPACIO data, which I think are very important; combination niraparib with IO [immuno-oncology], getting a good disease control rate in a very challenging group of patients to treat. I think that those are very good studies done by Tesaro/GSK [GlaxoSmithKline], which has given us options to talk about with our patients. The more options we have for our patients, that means the more treatment that we could, hopefully, give them later on.

So, I think in the platinum-resistant or platinum-not-eligible patients, in the QUADRA trial, they looked at BRCA. So you had to have a

, germline or somatic mutation. And I agree with that. I think if you have that, you should be able to use single-agent niraparib. I would also say that if you didn&rsquo;t have those mutations and you didn&rsquo;t have the HRDbecause in the platinum-ineligible or platinum-resistant patient, that&rsquo;s when they would use the HRD tests. So, HRD-positive test, platinum&mdash;you had to be platinum sensitive. But if you had the HRD test and you&rsquo;re platinum insensitive, it&rsquo;s not an indication. I would take those patients and I would say that it&rsquo;s not that single-agent niraparib cannot be used. It didn&rsquo;t bear out in the QUADRA data, but what I would say is, take the TOPACIO data, which is combination niraparib and immunotherapy; use that combination for those folks at that time, because I think that would get you a good disease control. Because when you look at that trial, those patients were heavily pretreated

Recurrent Ovarian Cancer: QUADRA Trial

Those are 2 really important abstracts looking at a dosing of niraparib, because when we think of oral agents, I think a lot of us clinicians, as well as patients, thought an oral agentit&rsquo;s not going to have the same adverse effects, or there are adverse effects we won&rsquo;t have to worry about like we did for chemotherapy, and that&rsquo;s not true. Niraparib has done a fantastic job of going from phase I to phase III, and it&rsquo;s a very exciting compound with how it&rsquo;s excreted by carboxylesterase. It has high bioavailability, good tissue penetration. To me, all that is very exciting to treat tumors. At one point, you know, you had to worry about the adverse effects&mdash;fatigue, nausea, vomiting&mdash;as well as thrombocytopenia.

Looking at the weight-based dosing and looking at the criteria that they use to look at the patient&rsquo;s baseline weight, as well as baseline platelets, I have to be honest with you: I think ifwhen we use those criteria, about 70% of patients at our clinic are going to get dosed at that lower dose at about 200 Q day&mdash;that if you talked with nurses, myself, the PAs [physician assistants], and the patients&hellip;I think the number of adverse effects that decreased&mdash;the thrombocytopenia has decreased, the fatigue has decreased, some of the, some of the nausea&rsquo;s decreased.

In generalwhen we start somebody on PARPs, in general in niraparib, we&rsquo;ll tell them to take it at night, we&rsquo;ll give them prescriptions to help with diarrhea, prescriptions to help with constipation, as well as nausea and vomiting. I&rsquo;ve heard some people are trying to use just some baseline antiemetics consistently for about 2 months to not let the cycle develop. I typically haven&rsquo;t done that because I think taking it at night will help with that, and then treat those patients as needed. I&rsquo;ve used some low-dose steroid. I put a patient on low-dose steroids for like 2 weeks, and that really helped her nausea, and she&rsquo;s been doing fine after that.

I think there are many different ways that we can try to tweak that. I would say that starting at the lower dose, we&rsquo;ve seen the decrease in the adverse effects. It&rsquo;s hard to say. You know we want to make sure that everything stays as effective. We haven&rsquo;t seen any patients that had seemed like they&rsquo;ve had a rapid falloff with respect to recurrence or anything other than what we&rsquo;ve seen within the literature.

It&rsquo;s something that we need to pay attention to. The FDA dose is 300 down to 200. There are many drugs that I would have to say that we use in GYN [gynecologic] oncology that the FDA dose may be higher than what&rsquo;s the typical dose that we use when we treat patients. But, to me, niraparibusing the weight-based dose, the individualized dose&mdash;I think, you know, I await the FDA&rsquo;s review of that to see if they&rsquo;re going to approve that. I think in clinical practice&mdash;so, phase IV data&mdash;using the drug in clinical practice, it has definitely borne out, and it was definitely very helpful. So the abstracts by&mdash;I think it was

We have a lot of interesting single-agent compounds that we&rsquo;re now starting to do the combinations. I mentioned TOPACIO; I think that&rsquo;s the tip of the iceberg, that we&rsquo;re going to do many of these types of combination therapies. I also think that the amount of molecular data that we&rsquo;re going to need to interpret when we see these patients is going to become more complex. I also think that we&rsquo;re in the era of 5% medicine, which means, you know, we may have to send off 20 tests to find 1 test [so] that we can make a significant change in therapy that may make a significant change in outcome.

I think that the next 5 years are going to be very exciting, just like these past 5 years. We have other drugs. Hopefully, they&rsquo;ll be coming out with some antibody-drug conjugates, combinations of many of these therapies. The first trial, which is combination Avastin, dostarlimab(?), as well as nirapariban up-front setting for maintenance therapy, I think, is going to be a very important trial, because we talked about BRCA, we talked about HRD [homologous recombination deficiency]. Unfortunately, most patients are HRD negative, and that&rsquo;s where we&rsquo;re struggling right now with our treatment, so as we can come up with better combinations&hellip;

I do think that combination immunotherapy with PARP inhibition is going to be very important. I look forward to the dostarlimab data with niraparib. There [are] other trials being done out there that are going to be looking at that from Clovis as well as AstraZeneca. All these companies, I think, are benefiting our patients with the rapid drug development and the development of these combinations, which is a huge change compared to 10 years ago. We have so many clinical trials available for patients; the change is rapid, which is excellent for them.

Managing A Case of Heavily Pretreated Recurrent Ovarian Cancer | Case Based Peer Perspectives

EP 1: Case-Based Overview: Pretreated Recurrent Ovarian Cancer

EP 2: Gene Testing and Treatment for Recurrent Ovarian Cancer

EP 3: Considerations for Managing Recurrent Ovarian Cancer

EP 4: PARP Inhibition in Recurrent Ovarian Cancer

EP 5: Recurrent Ovarian Cancer: QUADRA Trial

EP 6: Ovarian Cancer: PARP Dosing and Future Outlook