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Molecular differences in the profiles of low grade serous ovarian cancer (LGSOC) and high-grade SOC substantiate the need to find unique, differentiated treatment options for each epithelial ovarian cancer subtype, according to Kathleen N. Moore, MD, MS.

CancerNetwork® spoke with Moore, Virginia Kerley Cade Endowed Chair of Cancer Development, associate director of Clinical Research at the Stephenson Cancer Center, director of the Oklahoma TSET Phase I Program and professor in the Section of Gynecologic Oncology the University of Oklahoma Health Sciences Center, about distinguishing low grade serous ovarian cancer from other types of ovarian cancer, current treatment options and clinical trials evaluating new regimens, as well as managing treatment in younger patients with or those seeking to preserve fertility.

Moore began by differentiating LGSOC from high grade SOC, stating that this disease typically occurred in younger patients and was primarily characterized by MAP kinase alterations, specifically 

mutations. She then discussed the emergence of endocrine therapies in this indication owing to the presence of estrogen receptors.

Additionally, first line treatment was discussed, with the standard of care defined by primary cytoreduction followed by paclitaxel and carboplatin. She then highlighted multiple clinical trials assessing alternative treatment in this indication, particularly involving the use of letrozole (Femara).

Other clinical trials evaluated the use of CDK4/6 inhibition plus fulvestrant or 

 inhibition with letrozole, with Moore emphasizing the potential for these studies to shift the treatment paradigm in the frontline setting. Furthermore, she suggested that CDK4/6 inhibition may help enhance responses in patients with recurrent LGSOC.

Moore then highlighted treatment concerns for younger patients and those seeking to preserve fertility, while expressing the importance of understanding a patient’s goals, which may help optimize outcomes. She concluded by reiterating the importance of designing trials and tailoring treatment considering the molecular profile of LGSOC.

Foundation for Women’s Cancer

Low grade serous ovarian cancer, a rare epithelial ovarian cancer subtype, requires differentiated treatment from its high-grade counterpart.

Redefining the Treatment Paradigm in Low Grade Serous Ovarian Cancer

 Biennial Ovarian Cancer Research Symposium, being held September 13–15 at the University of Washington in Seattle, we are speaking with Dr. Dmitriy Zamarin, MD, PhD, a medical oncologist who specializes in the care and treatment of women with cervical, ovarian, and other gynecological cancers at the Memorial Sloan Kettering Cancer Center in New York City. At the conference, Dr. Zamarin presented data from a phase II trial at Memorial Sloan Kettering, of a peptide vaccine called TPIV-200 in combination with durvalumab, an anti–PD-1 checkpoint inhibitor antibody, in patients with platinum-resistant ovarian cancer. 

Can you first describe this peptide vaccine, what it targets, and the rationale for its use as a therapy for advanced ovarian cancer?

 Absolutely. One of the limitations of cancer vaccines against shared antigens in different cancers in general is that the overexpression of some of these antigens is restricted to only a subset of tumors. The nice thing about the vaccine against the folate receptor alpha that we are using is that folate receptor alpha is overexpressed in the majority of ovarian cancers. In the metastatic setting, it has been reported that 80% or more of these tumors express folate receptor alpha. In addition, spontaneous immunity against the folate receptor alpha has been previously reported in breast and ovarian cancer patients which suggests that this target can actually be immunogenic.

 suggested that folate receptor alpha is an attractive target for vaccination and generated the rationale for this vaccine. In this case, the vaccine is called TPIV-200 and is composed of five long peptides that each target different regions of the folate receptor alpha. Those specific peptides were previously identified to elicit T-cell responses in breast and ovarian cancer patients that were vaccinated with this product.

These peptides are HLA Class II restricted, which means that there is not much of a restriction of use in specific patients as its estimated that over 85% of women express the HLA that would recognize at least one of these peptides and that eliminates the need to screen for specific HLA expression in the patients to assess their eligibility. In addition, the vaccine includes GM-CSF as an adjuvant to stimulate dendritic cells.

It sounds like this is not the first clinical trial to use this vaccine. Can you tell us about the design of this trial and also the rationale for combining these two immunotherapy approaches in ovarian cancer?

Sure. And you are absolutely right, this is not the first trial to use this vaccine. It has been previously tested for immunogenicity in breast and ovarian cancer patients. That study was not designed to look for outcomes, it was designed to test whether patients respond to this vaccine or not. And in that that study, which was published in 

a few months ago, vaccination had elicited T-cell responses in virtually every single patient that received the product. This was one of the findings that led us to try this vaccine in patients with advanced ovarian cancer.

That leads me to the design of this trial. Studies with various vaccines in cancer to data have, unfortunately, demonstrated rather underwhelming efficacy results. This is due to the fact that even once tumor-antigen specific T cells are generated via vaccination, these T cells might not be effective in clearing the tumor because of the multiple inhibitor–mechanisms that are present in the tumor microenvironment.

To overcome these mechanisms, there has been development of novel immunotherapy agents over the last few years including immune checkpoint blockade antibodies with those that target PD-1 or PD-L1 being the prime examples. While in some cancer types, such as melanoma, these antibodies are effective as single agents, in ovarian cancer, these anti-PD1 and anti-PDL1 antibodies have unfortunately not been very effective. Only about 10% of ovarian cancer patients respond to these drugs. Studies in animal models have indicated that combinations of tumor vaccines with agents targeting PD1 or PD-L1 can be very effective in instances when single agents don’t work.

In this trial, we decided to use a combination of this folate receptor alpha targeting vaccine and an agent targeting PD1, an antibody called durvalumab. This was a phase II study using a 2-stage design with 27 patients accrued to the first stage and then another 13 patients accrued to the second stage. The decision to proceed to the second stage was based on the response rate in the first stage.

We reported results on the first stage of the trial. This was a very heavily pre-treated patient population who received a median of four prior lines of chemotherapy and 33% of the patients received five or more lines of prior therapy. To provide a historical perspective, patients with platinum-resistant disease and two prior lines of therapy have a median overall survival of approximately 12 months, so ours is a much more heavily pre-treated population in this trial.

What are the key efficacy and safety results from this trial?

To start with the safety, this combination treatment was very well tolerated. The majority of the adverse events that were seen on the study were grade I or II and the most common adverse event was a grade I injection site reaction from the vaccine. This was seen in approximately 40% of the patients. Interestingly, this injection site reaction persisted for a long time, even after discontinuation of the vaccination which was probably reflective of an ongoing response to the vaccine. There were only two grade III/IV immune adverse events that were thought to be clinically significant.

One of the patients developed an immune-related thrombocytopenia and a second patient developed type I diabetes. But overall, the treatments were very well tolerated. With regards to the efficacy results, only 1 patient met the criteria for a partial response and 7 patients or 26% exhibited stable disease. Interestingly, several patients had pretty durable disease stabilization with 22% of patients being on the study beyond 24 weeks.

Based on these findings, the study was closed after the first 27 patients because it did not meet the criteria for the response rate that was needed to activate stage II of the study and the number of patients that benefited was, unfortunately, not higher than what would be expected for those patients treated with an anti-PD1 or anti-PD-L1 antibody alone.

Although the population treated on our study were more advanced and heavily pre-treated than those reported in previous studies. As I mentioned, in this heavily pre-treated patient population, the overall survival is expected to be pretty dismal and in prior recent trials of patients with platinum-resistant disease and two prior lines of therapy, the median overall survival was reported to be approximately 12 months.

In our study, what is interesting is that despite the poor response rate, the median overall survival was 21 months which is much higher than we would expect in this patient population. Because this was a single institution study, we had the opportunity to look at subsequent therapies that the patient received and saw significant responses even to standard chemotherapy, often to drugs that patients had already received. 

Many of the patients went on to receive several lines of therapy and had durable benefit from each of these therapy lines. These findings, while from a relatively small cohort, highlight that cancer immunotherapies can make a durable impact on tumor biology even without an objective response and may affect responses to subsequent treatments.

Is there a next step that is planned for this combination for ovarian cancer patients or either drug on its own? Will there be additional clinical trials conducted? And you mentioned that this vaccine could potentially affect subsequent therapies, so what are the implications of that?

 We are in the process of performing translational studies to delineate whether the responses to the vaccine or the vaccine-immunotherapy combination were predictive of clinical benefit during the trial and perhaps, predictive of the benefit to subsequent chemotherapies.

We are also trying to understand whether the subsequent responses to chemotherapies were affected by the vaccine alone or by the addition of durvalumab. For this, we are looking at other patient populations that have been treated with immune checkpoint blockade alone.

In general, while the vaccine had a relatively modest efficacy in tumor shrinkage on its own, we believe that it does alter tumor biology and it may be that the tumor microenvironment of advanced tumors is resistant to vaccine-specific T cells and that the vaccine needs to be tested in an earlier setting.

We have initiated a trial of this adjuvant TPIV-200 vaccine in ovarian cancer patients that have completely upfront chemotherapy. Basically, these are the patients that have finished chemotherapy and had a partial or complete response after the upfront treatment and then they receive the vaccine as a maintenance therapy. This trial is currently ongoing.

In addition, given our findings of subsequent chemotherapy responses, it would also be prudent to evaluate the vaccine in combination with chemotherapy to see if responses to chemotherapy, or perhaps, the durability of chemotherapy benefit could be improved with this combination.

The findings also suggest that we should continue to prospectively collect information on the patients that discontinue from our immunotherapy trials because we often come across findings that we otherwise would not be able to capture.

Thank you so much for joining us today Dr. Zamarin!

Dr. Dmitriy Zamarin speaks with Cancer Network about the findings of a phase II trial in platinum-resistant ovarian cancer patients.

Target Folate Receptor Alpha in Ovarian Cancer? 

 Biennial Ovarian Cancer Research Symposium, being held September 13–15 at the University of Washington in Seattle, we are speaking with Dr. Ranjit Manchanda, MD, MRCOG, PhD, a clinical senior lecturer and consultant gynecological oncologist at the Barts Cancer Institute, which is part of the University of London in the United Kingdom. Manchanda studies ways to risk stratify patients with gynecological cancers to both predict the onset of these tumors and to help prevent them. At the meeting, he will give a talk titled “Population testing for ovarian cancer gene mutations for primary prevention.”

First, specifically for ovarian cancer, what are the major questions on primary prevention? What do we know, if anything, about potential ways to prevent this tumor type?

The most effective way to prevent ovarian cancer is through an operation or surgical procedure, which involves removal of both the tubes and the ovaries once a woman has completed her family. This is typically done for women who are at high-risk of developing ovarian cancer, and it is often done through keyhole surgery and is effective in preventing ovarian cancer.

Taking a contraceptive pill for about 5 years can also help decrease the risk of ovarian cancer. These are two important ways of preventing ovarian cancer that are currently used. A relatively new method is removal of the tubes alone, which is called a salpingectomy. In a recent study of high-risk women, we are looking at a two-step procedure which is removing the fallopian tubes as a first step and the ovaries later to prevent ovarian cancer.  The removal of ovaries in premenopausal women can have detrimental effects on long-term health, including osteoporosis and risk of cardiovascular disease, neurocognitive impact, and sexual dysfunction.

What exactly is the population testing approach in cancer?

The way we identify people who are at increased risk of developing ovarian cancer currently in clinical practice is based on taking someone’s family history of cancer, which is usually a three-generation family history. Using the descriptions of the cancers in the family and the age of onset, we calculate the probability of the individual carrying a cancer-risk gene. If individuals with a family history of cancer fit these criteria or have cancer themselves, a number of them have access to gene testing.

The common genes that are tested are the 

 genes, which are associated with about a 40% and 17% risk of developing ovarian cancer over a lifetime, respectively. Additionally, some newer genes have been identified including 

, each of which has an associated ovarian cancer risk of between 6%–11%.

This gene testing based on family history is offered in clinical practice; however, a number of people may not carry a strong family history of cancer but may carry a faulty gene, and so this system is not perfect and can miss up to half of the people who are at risk. The only way to identify these people who don’t fill the family criteria is by offering testing to everyone. Hence, we propose population testing. [Which means] testing everyone to identify additional people who are at risk to more effectively prevent cancer in the future in many more individuals.

Could you describe the specific population approach you and your colleagues use for your studies of primary prevention of ovarian cancer in the context of what data you will present at the conference?

We undertook a randomized, controlled trial in London in a Jewish population. A lot of the population studies have been done initially in the Jewish population and in London. Our trial compared a clinical criteria-based approach to population testing for the 

 gene mutations in an unselected population. We showed that it is possible to do

population-based testing outside the hospital in a community-based setting and that this was acceptable and feasible and did not cause detrimental psychological or quality-of-life consequences.

Over 50% of people we identified as being at-risk would not have been identified by standard clinical family criteria. We also undertook a cost-effectiveness analysis and showed that this would be cost-saving in most scenarios and not just cost-effective which means it would save lives 

We also did an analysis for both the UK and the US healthcare systems which showed that this population-based approach would be cost-effective in both of these healthcare systems. Studies done in Israel and in Canada have also demonstrated the feasibility, acceptability, and utility of population-based testing among the Jewish female population.

We’ve also done a study in London evaluating current rates of testing across a large, 16 million population and found that only a very small proportion of 

 carriers have been identified since this genetic testing has been going on. If we continue to identify those at risk at current rates in this clinical, family-history focused way, we will never be able to identify all of the people who are at risk. The current system has a number of limitations, and the way that the genetic testing technology has progressed and the falling costs of testing enable us, technically, to be able to do large-scale testing on a population basis. This provides the opportunity to identify far more people at risk and to offer them options of primary prevention.

We are currently undertaking a pilot study of population testing for ovarian cancer in a primary care setting in London that is ongoing and will be reported in the next year or so. We have also done a cost-effectiveness analysis and evaluated costs and consequences of doing population testing in the UK and US populations for breast and ovarian cancer gene mutations and found that this approach could save thousands more lives and prevent thousands of cancers in both healthcare systems. So, we’ve done a number of such population testing studies over the last 8–9 years.

In your talk, you’re going to discuss ovarian cancer gene mutations that could confer risk of developing ovarian cancer. What do we know so far about what mutations do confer risk of developing this type of cancer, and you did mention that there are certain groups of women that are more likely to develop ovarian cancer?

The most common and most widely studied genes are the 

 gene confers about a 40% risk of developing ovarian cancer over a woman’s lifetime, and the 

gene confers a 17% risk. The newer genes are 

, which have, depending on the gene, a risk of about 6%–11% of developing ovarian cancer. It’s about 6% with the 

 genes. Then there are other genes, including the Lynch Syndrome genes, which have about a 6%–14% risk of developing ovarian cancer. These are the current, well-known, moderate- and high-risk gene mutations. There are a number of other low-penetrant genetic variants, known as SNPS [single nucleotide polymorphisms], which have been identified and linked to ovarian cancer, and these are now being used in risk models with epidemiological factors that can also impact ovarian cancer risk.

The models are being built to predict ovarian cancer risk and to stratify the population. We have been involved in this with other colleagues. The aim is to ultimately have validated risk models that can use a large number of these factors to stratify people into different risk categories and identify those above a certain risk threshold that could benefit from primary prevention of ovarian cancer. Additionally, we defined the risk threshold for offering primary prevention, have published a few papers on this [topic], and feel that it is justifiable over about 5% lifetime risk of ovarian cancer.

Thank you so much for joining us today Dr. Manchada.

Dr. Ranjit Manchanda speaks with Cancer Network about using population testing to predict and prevent gynecologic cancers.

Population Testing to Prevent Gynecologic Cancers

As part of our coverage of the 2017 American Society of Clinical Oncology (ASCO) Annual Meeting, held June 2–6 in Chicago, we are speaking with Gordon Mills, MD, PhD, chair of the department of systems biology and professor of medicine and immunology at the University of Texas MD Anderson Cancer Center in Houston, about ways to incorporate homologous recombination markers into clinical practice for ovarian cancer. 

First, what is the link between ovarian cancer and homologous recombination deficiency? Do most ovarian tumors harbor this defect? 

I think it’s important to remember that when we talk about ovarian cancer, we frequently focus on high-grade serous ovarian cancer, the most common and most lethal type of ovarian cancer. Homologous recombination deficiency is actually very common in high-grade serous ovarian cancer. If you look at the most clear indication of homologous recombination deficiency-loss of 

 cancer genes, either in the inherited germline or the tumor itself-that number is close to 25% of ovarian cancers. If, however, you look at the pathway more broadly and look at any defects in enzyme involved in homologous recombination, those numbers increase the percentage to somewhere between 50% and 70%. Indeed, at least in part, the abnormalities in homologous recombination deficiency have contributed to the very outstanding responses to platinum therapy and very striking new data with PARP (poly [ADP-ribose] polymerase) inhibitors.

What are the ways to test for this deficiency of homologous recombination in patients with ovarian cancer? Is this something that is now readily done in the clinical setting?

There are a number of approaches to test for homologous recombination deficiency. I think the one that is done most commonly right now is testing for the breast cancer genes, 

. These tests are quite widely available either from commercial resources or within hospitals. Testing for additional genes in the pathway and in a number of pathways is done through a number of commercial resources; the only other clinically relevant test is the homologous recombination defect assay, which is commercially available from Myriad Genetics. [Dr. Mills has disclosed that he holds part of the technology associated with that particular assay and patent.]

In terms of the use of PARP inhibitors, the first two PARP inhibitors that were approved required testing for 

 deficiency as a co-clinical test from the US Food and Drug Administration (FDA) for approval. However, the most recent approval of niraparib came through without any restrictions in terms of having additional tests done to indicate that there may sensitivity. This was due to an observation that there were strong responses in patients with 

 abnormalities, responses that were intermediate in patients with the homologous recombination defect assay. But, even the patients without either of those abnormalities had a modest improvement in progression-free survival with PARP inhibitors. The FDA decided in this case that the benefit was sufficient to warrant approval of the drug without requiring any additional biomarker testing. This is controversial, since the amount of benefit in those patients without either abnormalities in the pathway or in the homologous recombination defect assay are really quite modest, and whether this warrants the toxicity of the PARP inhibitors in these circumstances will require additional study.

You mentioned the clinical utility of testing for homologous recombination deficiency. What else do we know about understanding how homologous recombination deficiency as a marker can guide clinical practice? Are these markers prognostic and do they tell clinicians about potential eligibility of other types of therapies, including those under development?

Patients that have defects in homologous recombination-and the data are clearest with 

 abnormalities-do have an improved prognosis. However, that improvement in prognosis is not sufficient to warrant changing management for those individuals. I think that the exciting opportunity here is to go beyond using PARP inhibitors alone in patients in a recurrent or maintenance setting and to move those upfront to where they may have more activity. That will require a completely new set of clinical trials, and it’s my expectation that the benefit is going to be most marked in those individuals with clear evidence of homologous recombination deficiency.

The PARP inhibitors that we use, although they have a very high response rate, the vast majority of patients will still recur. We need to add something to the active drug, the PARP inhibitors, a rational combination to identify ways to give patients a greater benefit. Whether that will be restricted to patients with a homologous recombination deficiency or all ovarian cancer patients is probably going to depend on the particular combination. In either case, it will be very important both upfront and as we look at combination therapies, to determine which patients optimally benefit and if they are the patients with defects in homologous recombination who should be tested for genetic changes with the functional homologous recombination defect assay that I mentioned earlier. Also, a number of new homologous recombination defect assays have been recently released, including one from the Sanger Institute called HR Detect that may be even more effective in identifying patients with abnormalities in homologous recombination.

What are the important questions that still need to be addressed? Are there gaps in our knowledge on what we know and how we define homologous recombination deficiency? Are there other genes that we have not identified yet, or is there anything else that still needs to be addressed or studied further in regard to this biomarker?

I think that there is an enormous amount that we need to understand. Although the response rate to PARP inhibitors is really quite remarkable, particularly in those with defects in homologous recombination, it is clear that the majority of these patients will still recur. We need to understand the mechanisms of resistance to PARP inhibitors to potentially identify patients who are going to recur quickly and who will not benefit significantly from them. But even more important is to understand the mechanisms sufficiently enough to be able to come up with rational combination therapies to increase both the frequency of benefit and the duration of benefit from PARP inhibitors. We have this wonderful first step for a drug that is highly effective in a significant population of patients, and we now need to convert that step into prolonged responses. Hopefully that will approximate cures or will greatly extend the survival of ovarian cancer patients.

Thank you so much for joining us today, Dr. Mills. 

Thank you. I am pleased to talk to you and I hope that this will help both my colleagues and patients. I think it is important to emphasize that the activity of PARP inhibitors in high-grade serous ovarian cancer is one of the most exciting events that has happened in this disease over the more than 30 years that I have been working in this setting.

ASCO Annual Meeting: Gynecologic Cancer

As part of our coverage of the 2017 ASCO Annual Meeting, we discuss homologous recombination deficiency in ovarian cancer and PARP inhibitors.

Homologous Recombination Deficiency and PARP Inhibition in Ovarian Cancer

As part of our coverage of the 2017 Society of Gynecological Oncology (SGO) Annual Meeting, held March 12–15 in National Harbor, Maryland, we are speaking with Robert Neff, MD, a gynecologic oncology fellow at the Ohio State University Medical Center in Columbus. Dr. Neff 

 data at the meeting that compared the cost-effectiveness of an enhanced recovery program compared with usual care following patients who had surgical cytoreduction for their ovarian cancer.

First, can you describe this type of surgery. Is this a standard type of surgery that patients with ovarian cancer undergo, and 

First, thank you for the offer to discuss this topic. In 2016 ovarian cancer will be diagnosed in about 22,000 women, and the majority of those women are diagnosed at an advanced stage, stage III or stage IV. This is important, because that means the disease has spread outside of the ovaries and is now throughout the abdomen and pelvis. When we talk about ovary cancer in the upfront treatment setting, the two main pieces for treatment include surgery and chemotherapy, and there is somewhat of a debate regarding the order of each at this point. But historically the primary treatment, and it still is today, is primary surgical management or a debulking procedure. The procedure is essentially an attempt to remove all of the visible disease from the abdomen and pelvis to get the patient down to a no gross residual disease, essentially no disease visible to the surgeon. The reason that’s important is that it has been shown over a number of studies that this increases the overall survival of patients who are able to have primary cytoreduction surgery.

The surgery, as you might imagine, can be long and entails a number of different procedures, which can include bowel resection in addition to removing the ovaries and the uterus, basically removing any organs or tissue that have cancer involved. Because of the size and complexity involved in these surgeries, these patients are often hospitalized for a prolonged period.

I think it’s important to note that really anyone who is diagnosed with ovarian cancer is eligible for this surgery. It is up to a board-certified gynecologic oncologist to make a determination as to whether they should proceed with surgery prior to doing chemotherapy, or if they feel that there is a better chance for them to get all of the disease out during surgery by starting with chemotherapy. So sometimes the patient starts out with chemotherapy, and then has surgery. Either way, the surgical procedures, in both cases, are similarly complex and involve a prolonged hospitalization, which is why this topic has grown in interest in our field.

How does an enhanced recovery program differ from the usual pre- and post-operative care?

So enhanced recovery after surgery (ERAS) is essentially made up of pre-op, intra-op, and post-op changes to the way that we care for patients undergoing surgery. This movement toward enhanced recovery kind of began in the 1990s in the surgical field-it probably has been best studied in the colorectal surgery literature. You are attempting to preserve the pre-operative body state through the surgical course-essentially, trying to reduce the overall stress that these big surgical procedures put on the body in order to facilitate or improve the outcomes for the patients. And what is interesting is that in literature within the colorectal surgical field, they have actually shown that when you put patients into a program like this, you actually decrease the overall complication rate as well as decrease the amount of time the patient spends in the hospital. So it kind of has a twofold benefit, both for society and for patients.

In the colorectal surgical literature, they found that patients overall do better. From a society standpoint, where we are more concerned with the overall cost of care, the ability to affectively get a patient out of the hospital in a safe manner and in a quality manner for the patient, is a way to allow for some cost-savings into the system. The way that it’s basically different from older or usual care in the perioperative setting is that it standardizes the care that is given to the patient.

For anyone who has been through a surgical training program, they know that a lot of what goes into the care of a surgical patient is based on the historical experience of the institution they trained at-how the providers pass down what they know to their trainees. And it’s not always with a keen eye on what the research is that backs up those means of caring for the patient. So a lot of what is great about ERAS is that it standardizes what you do for the patient. For all patients that come through, it says, “What are we going to do for you prior to surgery and how are we going to keep you going during the surgery?” and “What are the things we will do to maximize your post-operative period in the hospital so that you are back up and functional in a more timely fashion?”

I think what it starts with, and the biggest difference to the older way of thinking, is that you are setting expectations with the patient. So when you meet with the patient prior to surgery, you are letting them know what to expect, and what you are going to provide for them with this enhanced recovery and discussing questions upfront, “How are we going to manage your pain and how are we going to manage your diet after surgery?” and “When are we going to allow you to eat and how often do we want to get you walking?” Those types of things.

In this interview we discuss the idea behind an enhanced recovery program for patients undergoing cytoreductive surgery for ovarian cancer, as well as some of the potential cost savings.

Ovarian Cancer

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