Within the spectrum of ovarian tumors, notable players include fibromas, thecomas, and granulosa cell tumors, alongside germ cell tumors such as mature cystic teratomas, dysgerminomas, mixed germ cell tumors, and yolk sac tumors. Metastases to the ovaries are also plausible, particularly in patients with a cancer history, necessitating vigilance in differential diagnosis.

Serous tumors, classified into benign, borderline, and malignant based on clinical behavior, require careful evaluation beyond cell type determination. Low-grade serous cancer (LGSC) poses specific diagnostic challenges, often overlapping with serous borderline tumors. Pathological examination becomes pivotal, with micropapillary or cribriform features signaling potential aggressiveness and a resemblance to LGSC behavior. Micro-invasion, defined as foci less than five mm in size, is present in serous borderline tumors but doesn't classify as LGSC unless the morphology aligns with the latter. Lymph node involvement by serous borderline tumors is distinct, not considered metastatic. In the differential diagnosis, distinguishing low from high-grade serous carcinoma is crucial, as they represent distinct diseases with varying molecular profiles.

Molecular profiling emerges as an opportunity for LGSC patients, especially those with advanced-stage disease. Tumor profiling using next-generation sequencing often reveals 

 mutations, indicating oncogene activation, while lacking p53 loss of function mutations and homologous recombination deficiency. Molecular insights aid in confirming the LGSC diagnosis, identifying treatment targets, and preventing misclassification. Overall, meticulous pathology review, awareness of potential mimickers, and molecular profiling enhance diagnostic accuracy and guide treatment strategies in the complex landscape of ovarian tumors, specifically focusing on the nuanced aspects of low-grade serous carcinoma.

Summary is AI-generated and reviewed by OncLive editorial staff.

Videos

Expert oncologist Ian Hagemann, MD, PhD, shares insight into the process of making a differential diagnosis of low-grade serous ovarian cancer in light of adjacent disease and available IHC testing. 

Making a Differential Diagnosis of Low-Grade Serous Ovarian Cancer  

Dr. Thomas Herzog: So I'm going to talk a little bit about HRD testing in ovarian cancer, the guideline, recommendations, and we'll get into typical workflow if there is such a thing. Hopefully, there's some consensus, but it's not even the same in our group. Depending on sort of how the patient got into the system, it can be different. So I think that we'll find some of those things will be the same. So in terms of thinking about NCCN guidelines, other organizational guidelines, and so forth, there've really been- there's a section, for example, with NCCN that looks at the pathologic principles in terms of ovarian cancer and so forth. And one of the parts of that is the tumor molecular analysis. And they really do stress the importance of looking upfront at a minimum to optimize identification of molecular alterations that can inform someone about the interventions that have demonstrated benefit in these settings. And so, just what Dr. Krivak was just talking about in terms of some of these trials that we mentioned where PARP inhibitors have really shown amazing hazard ratios. That's one of the things that I think has probably been the most transformational thing for the GYN oncology world, is to go from hazard ratios for successful studies from something that's slightly below 0.7 to 0.3 and below and now are approaching 0.2 in some of the subsets. So, pretty crazy in terms of the benefit or the magnitude of benefit that we're seeing with this. So, we brought up both upfront and in the recurrent setting. I personally believe that knowledge is power and that it gives you the best opportunity to plot that patient's journey in terms of the treatment choices you're going to make as you go through their ovarian cancer treatment landscape with them. And so, I think that having that information upfront is important. If you don't have it, and they get into your system later, getting in at recurrence is important. It's nice to know some of the other things about the tumor. We have a number of trials coming out. We've just had a trial reported at ASCO, DUO-O, looking at combinations with checkpoint inhibitors along with PARPs. And we have three other trials that'll report in the future looking at various combinations with IOs and PARP inhibitors. So, things such as PD-L1 status, tumor mutational burden, MSI status, and so forth are all, I think, important. Knowing some of these other less frequent mutations in the recurrent setting is important as well, such as NTRK fusions, BRAF. Now, folate receptor alpha is with a new approval at ASCO that- well, with an approval for accelerated approval before ASCO, and then the definitive trial report that came out of the ASCO, we'll probably see movement on that in terms of final FDA action hopefully soon. And so, this whole idea of understanding the molecular background, I think, is really important in terms of what we look at. I think one of the things that often gets lost in all this for our lower volume treaters out there who may only see one or two cases of ovarian cancer in a year or less, and then they get a case and they're like, well, what am I supposed to do? Things have changed really rapidly. Don't forget to do germline testing and make sure we know where we stand with germline testing. Not only so we have the somatic which can be an additional group up to, say, 5, 7% and some of the higher numbers that we've seen in terms of prevalence can have somatic mutations, and then you have that 15% or so that are germline for BRC1 or 2. I think what gets lost there is the fact that not only is it prognostic and then predictive of whether we can use these therapies, that opportunity to be able to do cascade testing on the family is really an opportunity to save lives. And I really want to stress that, and I don't know if Ian or Tom, you want to say anything about that, but I find people, some of the lower volume treaters get caught up in some of these other advanced tests, sort of forget some of the basics, and all our groups agree on that. So ASCO guidelines, SGO, NCCN and so forth. Any comments on that?

Dr. Ian Hagemann: Oh, yeah. No, it's lifesaving. The patient herself may be at risk for additional cancers too. So the presenting cancer-


Dr. Ian Hagemann: Could be ovarian and not breast for-

Dr. Thomas Herzog: It is a very different treatment strategy perhaps but also surveillance strategy for the patient within that patient that you find for other cancers. Correct.

Dr. Thomas Krivak: I think it's been tremendous, Tom. I completely agree. I think we do risk-reducing surgery. And when we look at the numbers, it seems like ovarian cancer fell below 20,000. It's 19,750, I think, in the most recent. So it seems like we've dropped 1,500 cases, whether that's COVID and people not going to the doctor or potentially us starting to see the effects of risk-reducing surgery and OCPs. It's tremendous.


Panelists discuss clinical guidelines recommendations for HRD testing in ovarian cancer and how they inform their practice.

HRD Testing in Ovarian Cancer: Clinical Guidelines Recommendations

Dr. Thomas Herzog: So we're going to talk a little bit about leveraging HRD testing results in ovarian cancer. Tom, can you take us through this a little bit?


Dr. Thomas Krivak: Absolutely. Thanks for asking. Again, looking at HRD and ovarian cancer, to me, we wanted to look at that. Ian did a great job of saying we have BRCA, let's look for a test that may give us that BRCA phenotype and looked at how these companies have gone through and developed these tests. And what does that mean? And how can that actually increase the number of patients who may be exposed to medication? And so what you can see here is this is looking at PAOLA and looking up to, again, 50% of patients with advanced stage ovarian cancer and can be positive for an HRD test without a BRCA mutation. So, we had SOLO come out and it showed excellent responses for patients in an upfront setting. Prolonged PFS, now we have OS data that was very good. And then, how can we expose, how can we identify patients who may best tolerate additional maintenance therapy and have good outcomes? And so looking at HRD positive patients, and again, PAOLA looked at that and saw that upwards of 50% can be HRD positive and increasing the number of patients who may get exposed to maintenance medication from roughly 20% up to 45 to 48%. Not novel by any means, because we knew in NOVA, we saw the HRD, we saw when they did study 19 how they looked at different, going back looking at germline, looking at somatic mutations. ATHENA as well as other trials have showed this. But the bottom line is that you look at- When you look at BRCA mutations and you look at patients who have tumor tested for HRD, it does increase the number of patients who may get exposed to this medication. So you can see here, PAOLA was Olaparib/bevacizumab versus bevacizumab/placebo. And you can see the number of patients who fell out who are HRV positive or BRCA positive with these- With this type of test. And in PAOLA I think it was myriad for these folks. And what does that mean clinically? Go ahead.

Dr. Thomas Herzog: I was just going to say just for our audience SOLO-1 was done in those patients who had BRCA mutations almost exclusively but not completely germline and a few somatic scattered in, And then PAOLA-1 and PRIMA came out looking at a wider group, inclusive but the labels were somewhat different there in terms of how that got labeled when those were presented in 2019.

Dr. Thomas Krivak: And, to me, if we could go on to the next slide which really is trying to say - Ian said it really nicely, what's the outcome? What are we seeing here with these tests? And when you look at BRCA mutation, positive, negative, positive, negative, and then HRD, mutation, negative, negative, positive, positive, really what you're seeing when you look at Olaparib versus bevacizumab versus bevacizumab alone, what you're seeing in those patients if they are HRD positive, and you can see whether they were BRCA mutation status negative or positive. And again, to me, that BRCA negative HRD positive is going to be that score that's an LOH score above 16%, or an HRD genomic instability score above 42, Caris, how they define it. But when you look at that, then you look at the patients who had a BRCA mutation and they were classified as HRD mutation status negative but when you look at positive mutation status and then positive, positive in the HRD group and you look at Olaparib versus bevacizumab, you're seeing that clinical relevance that Ian was talking about. BRCA mutations, hazard ratio by adding Olaparib to bevacizumab of.31. And then you look at the HRD positive, basically BRCA mutated patients again,.33. And then looking at this group that are HRD negative or HRD positive of BRCA wild type, you're still seeing a significant hazard ratio of.43. So in those positive groups you're seeing a really strong reduction of risk of recurrence for those patients. And again, just like we were talking about earlier, PRIMA was similar looking at HRD. So to me, this looks like it's a predictive marker as well as a prognostic marker for these patients. So I think what PAOLA-1 did really was, nicely, was had an enriched population for high grade CRS, high grade endometrioid, showed that you can increase the number of patients who may be exposed to maintenance therapy and then showed in that HRD test positive patients as well as BRCA patients, you really had a decrease in the chance of recurrence. And again, with PAOLA we did see an overall survival benefit. So it's really nice this year to see overall survival benefit in SOLO as well as an overall survival benefit in PAOLA. Again, we need to wait for statistical significance but the trend is there in our HRD positive patients.

Discussion centered around data from the PAOLA-1 trial, highlighting the prevalence of BRCA1/2 mutations and HRD status in ovarian cancer, and how patients with these alterations may benefit from PARP inhibitor treatment.

Leveraging HRD Testing Results in Ovarian Cancer: Clinical Data

Dr. Ian Hagemann: There's a number of tests available. I was mentioning just a moment ago, there is not very good standardization. And so we have to be careful when we're reading the results of trials that have been done with HRD as a covariant because you got to understand how that trial was characterizing the tumors for HRD. There are two tests that have an FDA label currently. The FoundationOne assay and Myriad myChoice CDx are both FDA approved in a specific context, and they all take a little bit different approach. I won't necessarily go through the whole detail, but all four of the tests that are listed here. So, there's also Caris Molecular Intelligence reports out HRD and Tempus also does. These are all feasible on formal and fixed paraffin-embedded tissue, so your routine clinical tissue. They have a little bit different approach to measuring HRD. They all look for BRCA mutation, but then the myChoice assay looks at LOH, TAI, and Large State Transitions. The others that are listed here look primarily for loss of heterozygosity as a form of genomic scarring. And there are also a number of what I would call take-home kits. So there's a TruSight sequencing platform or sequencing assay that can be done on the Illumina platform that can be used to report out a genomic instability score. And so some labs will run this in their own institution. There's an Oncomine assay from Thermo Fisher, which is Ion Torrent platform. And then SOPHiA Genomics is also offering a kit that's able to detect mutations in 28 homologous recombination genes and also report out a genomic integrity index. So, I'm not here to say that any of these are good or bad. The commercially available assays are certainly easier to obtain, and they all come with their caveats.

Dr. Thomas Herzog: Ian as a pathologist, at WashU, do you have - do you do a lot of this in-house now, or do you cooperate with the commercial labs, or is it a hybrid, or something different, or do you use mostly commercial for determining HRD, for example?

Dr. Ian Hagemann: Yeah, to be candid, we do not have an in-house HRD assay at this time. So, these are sent out to the clinician's choice, and one of the assays that's mentioned here is used preferentially by our gynecologic oncologist. I think that's sort of a matter of preference. But, yeah, it's not an assay that we run in-house. We do have sequencing platforms and probably could bring it up, but that's been a matter of crosstalk between the clinicians and the path lab.

Dr. Thomas Herzog: Yeah, I think it's always challenging because you need such economies of scale to be able to do this where you're not losing money, because these efforts all take a lot of capital, both number of employees and so forth and maintenance.


Dr. Thomas Herzog: Dr. Krivak, what do you do in terms of do you do it centrally in-house or do you send it out commercially or how does that work?

Dr. Thomas Krivak: So we send it out. I completely agree with you. I think it's economy of scale, and we want to make sure that we do it well. I do think that how I use HRD and a lot of folks at our institution it's a critical time point for upfront, how we're going to do maintenance therapy. And so, my preference is again, I'm not here to say this is better than this. I've just been very comfortable with the Myriad test and up front we'll recommend the Myriad test up front. Some of my partners will use Foundation, and again, a lot of people will like Caris and Tempus. I do think the Illumina is a very interesting thing to do in-house. And we've started with our molecular path about talking about doing that test. It has a quick turnaround, but I think the first time that we do the Illumina test, we're probably going to send it out to Myriad or to Foundation to make sure we have some agreement. But I completely agree. I think turnaround time, I like the Myriad test because it gives us a BRCA mutation. And if we have a germline-negative patient and we have a somatic mutation, I generally always go back and make sure that that mutation was looked at in the germline to make sure that we're not getting fooled with respect to that. So, we send out and, again, I think all these tests are good, but to me, my bias has been Myriad.


Dr. Ian Hagemann: You're making me think of something, Tom, there's no gold standard in this space. The gold standard is probably a patient-related endpoint. So, until we have a gold standard, it's going to be hard to define a best test.

Dr. Thomas Herzog: Yeah. No, I understand and-

Dr. Ian Hagemann: They're going to reach the-

Dr. Thomas Herzog: Different capabilities in terms of how many SNPs they have across the genome and so forth. We use a lot care at our institution because we're a center of excellence that allows us. I know you are, I think, too in WashU for the POA. You're able to do some of that, but all these things are you weak side things rather than the central quality of the test itself, we think, but we'll hopefully get more information on that with patient-driven outcomes. Great.

Dr. Thomas Krivak: I think clinically it's important to define it. And what I mean by that is patient 65 years young, stage three C, high-grade serious cancer, BRCA germline negative, HRD test negative by what test? And just so when you're looking at this and you're looking at strategies to make sure that everything is lining up. And, again, I think when you do that, you make sure that you've done your germline testing, and if you believed in HRD testing, that you're at least making sure that you check that box, whether it's Foundation, Caris, Tempus, Myriad or whatever.

The panel reviews commercially available HRD tests and expand upon factors that may influence test choice, such as clinical performance, institutional availability, turnaround time, and cost.

Commercially Available  HRD Tests for Ovarian Cancer

Dr. Ian Hagemann: There are signatures associated with the presence of a homologous recombination defect, cells that have HRD deficiency. So, we've agreed that they often have BRCA1 or BRCA2 mutations, and I implied that they might have difficulty repairing double-strand breaks. If you look at the genome of a cancer cell that has the HRD phenotype, that has this so called BRCAness phenotype, you can see certain mutational signatures. You can see numerous small insertions or deletions, 50 or greater nucleotides in length that's called mutational signature three in the catalogue of mutation signatures. You can also see loss of heterozygosity, or LOH that's illustrated on this diagram here. That's a phenotype in which instead of being heterozygous at the majority of low sigh that are able to show variation, the cell has lost one of those copies and repaired it by- repair that locus by duplicating the other locus. So, you'll see a loss of heterozygosity, and that can be picked up by sequencing. There's also a phenomenon or a type of genomic scar that's been designated as large scale state transitions, those are basically large rearrangements greater than 10 megabases in size within the chromosomes. And then finally, telomeric allelic imbalance is a form of genomic scar that looks specifically at the ends of chromosomes. And it's the idea of losing either the mothers or the fathers, haplotype, you've lost either one end of the maternally derived chromosome or the paternally derived chromosome. And I think the reason why these scars happen is that at the ends of the- the ends of the chromosomes are a little bit more susceptible to DNA damage. There's also fewer ways for those chromosomes to repair themselves by homologous recombination, because the ends of the chromosome don't have as many places to overlap with the good copy that the cell still has. Anyway, the take home message would be that these three types of scars LOH, LST and TAI can all be present in cancer cells that have homologous recombination deficit, and they can be picked up by certain assays that are available for characterizing tumors.


Dr. Thomas Herzog: Hey, Ian, let me ask you this, I'm going back to what we were just looking at here. So, a lot of people they get these three platforms, if you will, confused and it gets complicated. And as you know, some companies use three of these, some of them use one of these, some of them use two of these in terms of assessing whether there's going to be a likelihood for homologous recombination deficiency phenotype. And so, of these, which is by far the most important and how do we look at that?

Dr. Ian Hagemann: Well, I'll tell you the LOH is the most highly agreed. I think the LOH is used the most extensively. And so, I'd probably put that one in a little bit bigger print, if I had to. It's computationally a little bit easier to detect by sequencing and used by the most assays. In a survey that our professional organization, the Association for Molecular Pathology has done, it seems that LOH is used more extensively. So, that's - more data on that are forthcoming, but there's a fair amount of intellectual property in this space also. And there's a little bit of a lack of harmonization. There really are not professional guidelines from either our pathology societies or from the gynecologic side, from what we would call clinicians professional guidelines to dictate how HRD testing should be done. So, that's an area for improvement. Depending on how extensive the test is, you might find different rates of mutation and you might get a different determination for a particular patient. The baseline, the lowest level of testing, kind of the simplest test would just be to look for BRCA1/2 mutations. But as I was mentioning, a couple of slides ago, there can be mutations in what we might call the rare HRD gene, something like check two or break one that confer an HRD phenotype. The promoter of BRCA1 can be methylated. So, an assay that doesn't look for BRCA methylation might miss the fact that mutation is present. These genes have hotspots. If you look just at the hotspots, you might miss a non-hotspot mutation. And then another kind of hot topic that I might throw in is that these genomic scars, if they're present, they mean that cancer had HRD at some point. But sometimes under treatment will have reversion mutations where the cells reacquire an HR-proficient phenotype. So that's another complication that we have to think about, especially in patients who have had neoadjuvant therapy.

Dr. Thomas Herzog: So, most of the HRD testing is historical and it tells you where the cell has been not necessarily where it currently is, correct?

Dr. Ian Hagemann: Absolutely. Tells you the state the cell is in now.

Dr Hagemann explains how loss of heterozygosity (LOH), large-scale state transitions (LSTs), and telomeric allelic imbalance (TAI) can also contribute to HRD.

Other Causes of HRD: Chromosomal LOH, LST, and TAI

Dr. Thomas Herzog: So Dr. Hagemanm, I'm going to have you start us off here and tell us about defining HRD and its role in ovarian cancer.

Dr. Ian Hagemann: Yeah, of course. It's well known that cancer is a disease of the cellular genome. And in fact, cells even under ordinary circumstances accumulate many mutations or DNA changes per day. Some of them are due to cellular processes, some of them due to environmental insults that they sustained. And so cells have naturally evolved mechanisms to repair all of these. We could talk through some of them. Some of the smaller forms of DNA damage can be repaired by just excising the nitrogenous base, or maybe a whole nucleotide. So bulky adducts of tobacco smoke, where a large molecule gets conjugated to DNA. The cell will clear out a short piece of single strand of DNA and put the correct strand back in. We need a different set of mechanisms to repair double stranded breaks in DNA that can happen due to a cosmic ray or some other process interacting adversely with the DNA. And the cells preferred mechanism for repairing these is to repair the DNA, so the sequence is unchanged. If there is a set of homologous chromosomes after DNA replication in an appropriate phase of the cell cycle, so in the phase where there two sister chromatids present homologous chromosomes, the second copy will be used as a template to repair the first and that's your homologous recombination pathway. There's a wide variety of genes, probably 15, 20 genes that assemble their protein products into an apparatus for homologous recombination. The second mechanism for repairing a double strand break is non-homologous end joining. That's very simple. The cell just sticks the two ends of the DNA back together and has to hope that it stuck the correct ones back together in the right order. So that's a very error prone process. So not surprisingly, it's very desirable for cells to have intact homologous recombination repair mechanisms. Unfortunately, mutations in the genes that are responsible for assembling that complex are not that uncommon in the gene pool. They're also not that uncommon to be acquired somatically by a cancer. So that's some of what we want to kind of talk about next. Mutation. So the most important genes in the homologous recombination repair pathway, the best known best characterized first discovered are BRCA1 and 2, or BRCA1 and BRCA2. Either of these genes can be mutated. Pretty common to see in high-grade serous ovarian cancer or other gynecologic cancers, other serous cancers of the GYN track. But we're really focusing on ovarian high-grade serous tumors here. Depending on the study that you look at, you'll see some variation in the rate of mutation in the BRCA1 or BRCA2 gene. But let's just say it's not rare. Somewhere around 10% of ovarian cancers are going to be related to a germline mutation in BRCA1 or BRCA2. So that will be a variant that was inherited from a parent and you might be able to detect segregation of that cancer predisposition trade in their pedigree if you were to take a family history and draw it out. Depending on not only what series you look at, but how you assay it. You might find higher or lower, but let's say somewhere around 1 in 10. And then besides that, it's not uncommon for serous ovarian cancers to have acquired a somatic mutation in this pathway. That's adaptive for the cancer cells. Because once that repair pathway is knocked out, the cells acquire additional mutations and some of them lead to a selective advantage for the tumor cells. So let's say somewhere in the neighborhood of another 20% of ovarian cancers are going to have a somatic mutation. Somewhere in this pathway, they'll have a deficiency in their ability to carry out homologous recombination repair. So we've summarized a couple of studies here on the slides, but I think that the exact numbers aren't as important as the takeaway points that, A, these variations can be either are coming from the germline. Of course, then they're in every cancer cell or can be acquired somatically. And, B, that they're not rare. C, that there's actually a number of genes that can be implicated, not only BRCA1 and BRCA2. But additional homologous recombination repair genes. So BRIP1, CHEK2, nibrin which is NBN, RAD51 complex components are all genes that can be mutated either in the germline or somatically and confer what we call a homologous recombination repair HRD phenotype on cancers. And if you look at ovarian cancer overall, again depending on your series, the majority will not be abnormal for HRD. Then you'll have a subset that have a germline deficit and then a subset that have a somatic inactivation of the HRD pathway.

Experienced clinicians explain the role of the homologous recombination repair (HRR) pathway in DNA repair and how mutations in HRR-related genes, including BRCA1 and BRCA2, can cause homologous recombination deficiency (HRD) and contribute to the development and progression of ovarian cancer (OC).

Defining HRD and its Role in Ovarian Cancer

Dr. Thomas Herzog: Greetings, welcome to Optimizing Homologous Recombination Deficiency Testing Paradigms in Ovarian Cancer. So our objectives tonight are to define what HRD is from a multidisciplinary perspective and how it relates to ovarian cancer development and disease progression. We also want to discuss the similarities and differences between somatic and germline, homologous recombination deficiency testing, sampling considerations and available methodologies and products, as well as how this all affects treatment decisions. We want to review how changes in the treatment landscape have affected HRD testing paradigms. And finally, we want to share best practices and clinical insight into how and when PR providers should order HRD testing for their patients with ovarian cancer. I'm Dr. Tom Herzog. I'm deputy director at the University of Cincinnati Cancer Center. And joining me tonight are two of my esteemed colleagues, and I'm going to have them both introduce themselves Dr. Krivak, and we're going to probably call each other by first name. It's not to be pejorative, but rather because friends, so we just if we're informal, that's why. Tom.

Dr. Thomas Krivak: I agree. Tom, we're all friends here and thanks for the, the excellent introduction. My name's Tom Krivak, GY oncologist and director of GY oncology research, as well as the division at Allegheny Health Network in Pittsburgh Pennsylvania. So thanks for having me on board. It's good to do this discussion.


Dr. Ian Hagemann: Hi everyone. Uh, my name is Ian Hagerman. Uh, I'm a pathologist at Washington University in St. Louis, Missouri. Uh, my main areas of interest are gynecologic breast and molecular pathology. So I'm here to represent the laboratory perspective as we talk about homologous recombination deficiency testing, and really appreciate the chance to be here.

Dr. Thomas Herzog: I'm really excited to have both of you with us and hopefully we'll be able to have a spirited dialogue that I think will be to the benefit of our audience in terms of learning opportunities.

Thomas Herzog, MD, Thomas Krivak, MD, and Ian Hagemann, MD, PhD open their discussion by introducing themselves and the objectives of the program.

Opening Remarks from Dr. Herzog, Dr. Krivak, and Dr. Hagemann

Ian Hagemann, MD, PhD, assistant professor of pathology and immunology, Washington University School of Medicine, discusses the main take home from his presentation at the 2020 SGO Winter Meeting.

As a pathologist at his institution, Hagemann works very closely with his gynecologic group so that they can make better use of the pathology services. He recommends that physicians continue their conversations with pathologists regularly.

Hagemann hopes that the audience took away that they need to foster closer conversations with pathologists in their institutions to ensure the best practice in gynecologic oncology.

Ian Hagemann, MD, PhD, discusses the main take home from his presentation at the 2020 SGO Winter Meeting.

Ian Hagemann, MD, PhD

Articles

Making a Differential Diagnosis of Low-Grade Serous Ovarian Cancer

HRD Testing in Ovarian Cancer: Clinical Guidelines Recommendations

Leveraging HRD Testing Results in Ovarian Cancer: Clinical Data

Commercially Available  HRD Tests for Ovarian Cancer

Other Causes of HRD: Chromosomal LOH, LST, and TAI

Defining HRD and its Role in Ovarian Cancer

Opening Remarks from Dr. Herzog, Dr. Krivak, and Dr. Hagemann

Dr. Hagemann on Best Practices for Pathology in Gynecologic Cancers

Ian Hagemann, MD, PhD

Articles

Making a Differential Diagnosis of Low-Grade Serous Ovarian Cancer

HRD Testing in Ovarian Cancer: Clinical Guidelines Recommendations

Leveraging HRD Testing Results in Ovarian Cancer: Clinical Data

Commercially Available HRD Tests for Ovarian Cancer

Other Causes of HRD: Chromosomal LOH, LST, and TAI

Defining HRD and its Role in Ovarian Cancer

Opening Remarks from Dr. Herzog, Dr. Krivak, and Dr. Hagemann

Dr. Hagemann on Best Practices for Pathology in Gynecologic Cancers

Commercially Available  HRD Tests for Ovarian Cancer