In this seventh episode of OncChats: Immunotherapy and You, John Nakayama, MD, of the Division of Gynecologic Oncology, Allegheny Health Network, and assistant professor of OBGYN at Drexel University, and Ali Amjad, MD, medical hematologic oncologist, Allegheny Health Network, walk through a timeline of FDA approvals of immunotherapy approaches in gynecologic oncology and discuss associated toxicities to be aware of as well as how to manage them.


Wonderful. Now that we've talked about [the difference between] mismatch repair–deficient [and] mismatch repair–stable [disease], can you take me through the timeline of FDA approvals?

: In 2018, we saw the first approval in gynecologic oncology with pembrolizumab [Keytruda] used as a second-line treatment in cervical cancer. Since then, we've seen other approvals where combination immunotherapy with a TKI, lenvatinib [Lenvima], has been approved for endometrial cancer.

Dostarlimab [Jemperli] is another PD-1 agent that is approved for endometrial cancer, in a biomarker-selected population, as a single agent. Then, more recently, we've had a combination of chemotherapy plus immunotherapy and an antiangiogenic, bevacizumab [Avastin], approved in cervical cancer.

: I think now you can see this. This is the progression, right? We were looking at this relatively small population, this population of 20% to 25%, that was mismatch repair deficient, and then this trial came out that looked at a TKI plus pembrolizumab. Can you tell me about KEYNOTE-775? Tell me a little bit about who [the patients] were and what was being looked at. 

: KEYNOTE-775 was a phase 3 clinical trial for patients with endometrial cancer who have progressed on platinum-based chemotherapy. [Patients] were enrolled to [1 of] 2 arms: 1 arm being the combination of pembrolizumab and lenvatinib, and the other being standard-of-care chemotherapy with doxorubicin or paclitaxel.

The results were really exciting, and we now have the overall survival [OS] data, as well. Patients who go on this combination of lenvatinib and pembrolizumab live longer compared with [those who go on] chemotherapy alone. I also want to point out the response rate, which is twice as [high] as the response rate [achieved with] chemotherapy alone.

This matters a lot for patients, because when these patients [come in,] they're really sick; they have a lot of pain, bleeding, weight loss, abdominal symptoms, [and other] gastrointestinal problems. When you talk about the response rate being twice as high as chemotherapy, these patients start feeling better right away, and more of them start feeling better. That is important to remember in the beginning.

[There are adverse] effects [AEs], but they may be different from traditional chemotherapy, where patients have alopecia and nausea; patients may have less of a problem with [the immunotherapy] combination.

: I think you're 100% right about that. The overall response rate was really interesting. The fact that we got OS improvement is massive, because a lot of the times we're just working off of [what we know about the] progression-free [survival benefit]. The other thing that I couldn't fit onto the slide is that a lot of people on this trial had high-grade serous, clear cell cancer.

At least in my practice, I have found those people to be harder to treat and to have more aggressive disease than [others]. In [your practice,] have you seen similar responses to what this trial shows in [patients with] those high-risk histologies?

: Yeah, certainly. This was a good trial where they included those rare histologies, as well. Clear cell [tumors], as we know, are really tough to treat, and all of them did have a response with this combination.

: Awesome. Great. So, you mentioned it before, this regimen does have some AEs. Most people will have a grade 3 or 4 AE, and there were some grade 5 AEs and fatal AEs. In your practice, what do you think are the most common AEs and what is your way of dealing with those, in terms of dose interruptions and whatnot? 

Yeah, we know that when we combine these 2 therapies, immunotherapy and a TKI, they have some overlapping toxicities, but they have different sets of toxicities, as well. Hypertension seems to be a common AE from lenvatinib; that may not necessarily bother patients, but we do follow that closely. Fatigue seems to be a big AE. Myalgias, muscle aches, [and then] weight loss is a common AE from lenvatinib treatment. Of the overlapping toxicities, diarrhea is a common one, and that is sometimes hard to tease out because immunotherapy can cause diarrhea from immune inflammation or colitis, and lenvatinib was a diarrhea just from a cytotoxic effect, as well.

It's always tricky to see which [drug] is causing which [toxicity]. I'm pretty open in terms of trying to hold the lenvatinib, reducing the dose, so that we can continue that treatment and restart the treatment as soon as the patients have recovered from the toxicity. As you can see, on these clinical trials, most of these patients had to have a dose reduction and some of them even had to discontinue treatment because of toxicity.

: I think you made a couple of really great points there. I've always found the diarrhea to be the hardest [toxicity] to deal with, because you don't know if it's immune or if it's the TKI. You don't want to be the person who kept them on treatment and let the immune colitis get worse, so that is a clinical conundrum.

I'm curious, what I do in these people is, when I'm starting the combination, I make sure that they're well set up with their primary care doctor. I basically tell them that they're going to get hypertension, and that they need to be ready for that. I don't know about you, but I also try to make sure that they have an antiemetic prescription, and even sometimes antidiarrheals. Is that the approach that you take or do you do anything extra?

: You have to be preventive with these treatments and toxicities, and [ensure that] patients are prepared for it. I typically call them back in 1 week after they start, just to check in and see how things are going, because it's really in the first [or second week that] they [will experience] these toxicities. We have a low threshold to hold treatments. Hydration, nausea control, certainly education, and our nurses come in handy. They do call these patients very frequently to check in on them. As we get in the flow, after the second or third month, patients know how to handle them and they do report anything out of the [ordinary].

I think that's super important. I love that check-in idea; I think that could be very helpful, because we know that they're going to have AEs with this and managing them is absolutely critical. In traditional cytotoxic chemotherapy, we give it every 3 weeks, every 2 weeks, every 4 weeks. Just the fact that [patients need to] take the TKI every day, I wonder if people have an issue with just that lack of a break. I do use dose interruptions every so often for that. What do you think about the lack of a break? What do you think about dose interruptions?

: I'm open to those concepts of reducing the dose and stopping it for a little bit. That is kind of how practice runs. In clinical trials, patients did have dose reductions, as well. So those are things that can help keep them on the medicine because the last thing you want to do is to have a toxicity that [makes the] patients [never want to try something] again. So starting low, and then maximizing the dose, is what I usually do. 

: Dr Amjad, I really want to thank you for taking the time to chat today. At least for me, my takeaways of what you've taught me is that immunotherapy is becoming another important line of treatment within cancer care. What is your takeaway of immunotherapy, not just in gynecologic oncology, but in oncology altogether?

: Immunotherapy is a new way to treat cancer. We're trying to move away from traditional chemotherapy and trying to use immunotherapy as an alternative way to treat cancer. It's here to stay. We'll see further developments and further refinements of agents, harnessing different checkpoints to help the T cells work against the cancer.

: That's wonderful. Well, thank you everyone for listening to this episode. We'll catch you with our next series. 

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In this seventh episode of OncChats: Immunotherapy and You, John Nakayama, MD, and Ali Amjad, MD, walk through a timeline of FDA approvals of immunotherapy approaches in gynecologic oncology and discuss associated toxicities to be aware of as well as how to manage them.

FDA Approvals of Immunotherapy in Gynecology Oncology 

In this sixth episode of OncChats: Immunotherapy and You, John Nakayama, MD, of the Division of Gynecologic Oncology, Allegheny Health Network, and assistant professor of OBGYN at Drexel University, and Ali Amjad, MD, medical hematologic oncologist, Allegheny Health Network, highlight the success seen with checkpoint inhibitors in gynecologic cancers, biomarkers of interest, and recent approvals in the space.

: At this point, we've talked about mechanism action and a little bit about the history [of checkpoint inhibition], but I think [providing] an example might [make it] a little bit easier [to understand]. Since I'm a gynecologic oncologist, and I can't help myself, I think using [looking at this field] as an example would be good because we're very early in the process [of utilizing this approach], and we're trying to catch up to many of the medical oncologists [who are leveraging these agents].

In gynecologic oncology, [specifically] in ovarian cancer, it has been generally disappointing. We have had a lot of negative trials. There has been 1 trial that was sort-of positive but [data have not] been fully published yet. In cervical [cancer], we're really starting to see [the benefits of these agents]—especially [in those who have a] combined positive score of greater than 1%. When the trial that was looking at 4 different agents in cervical cancer [came out, I asked myself], is that the most you can get in any tumor? Is that a lot? How do these people tolerate this?

: That is certainly a lot. Certain [patients with this kind of] cancer are generally younger, so they have good organ function and they can tolerate all of it. However, since we have an effective combination, it's time to try to see whether we can do less and cut back to some degree [to achieve] a similar effect. [To that end,] there are clinical trials [that are] evaluating less cytotoxic chemotherapy and more immunotherapy and targeted treatments. Antibody-drug conjugates [are also] being evaluated in combination with immunotherapy.

: Sure, and I think we will hit this with our next slide. Let's talk about endometrial cancer beyond [the] first-line [setting]. What is deficient mismatch repair? What is proficient mismatch repair?

: Mismatch repair deficiency by mismatch repair proteins are coded by genes called mismatch repair genes and these genes code for these DNA repair proteins, which are considered spell checks. As such, they would fix any errors in DNA replication. When a tumor is deficient in these proteins, DNA repair is not effective so new mutations develop. With those news mutations, there's neoantigens. Deficient mismatch repair seems to be a biomarker [that tells us that patient has] a better chance of responding to immunotherapy.

: That has always made a lot of sense to me. I think a lot of this, if [a patient has] really poor DNA repair, [they are] spilling these antigens everywhere. As such, the antigen-presenting cells come along, and just have a lot more options to work with. That's the way it works. In my mind. Do you think [about this in a] similar [way]?

: Alright, and I see the percentages here. It looks like the majority of patients are mismatch repair proficient, which makes sense; everybody wants their DNA to work right.

The other really interesting thing that you brought up with this, is that we are looking at these 4 genes: MLH1, MSH2, MSH6, and PMS2. We actually screened every [patient with] endometrial cancer for that at the time of their surgery and their pathology to look for something like Lynch syndrome. Have you noticed that this changes your practice? Do you feel like everybody should be screened? Do you think we should be looking at tumor testing as opposed to looking at the mismatch repair genes?

: With this biomarker getting an FDA approval with tissue-agnostic treatments, every solid tumor should get tested for mismatch repair either [with immunohistochemistry] or next-generation sequencing. That is...what we do these days for almost all cancers.

Check back next Wednesday to view the next segment in this series.

In this sixth episode of OncChats: Immunotherapy and You, John Nakayama, MD, and Ali Amjad, MD, highlight the success seen with checkpoint inhibitors in gynecologic cancers, biomarkers of interest, and recent approvals in the space.

Immunotherapy and You: Checkpoint Inhibitors in Gynecologic Cancers 

In this fifth episode of OncChats: Immunotherapy and You, John Nakayama, MD, of the Division of Gynecologic Oncology, Allegheny Health Network, and assistant professor of OBGYN at Drexel University, and Ali Amjad, MD, medical hematologic oncologist, Allegheny Health Network, discuss PD-1 blockade, potential biomarkers of response to treatment with immunotherapy, and the potential for these agents in the neoadjuvant setting.

: We've talked a bit about checkpoint inhibition at this point, but I don't think we've really gone over exactly how it works. I put together this little slide, and I would love your take on it, as well. I feel like PD-1, PD-L1, is kind of the prototypical immune checkpoint, and the way that I look at it, is you're turning that amp up to 11. You're just really turning off the 'off.' As such, you have this double-negative situation and you're ramping up the immune system. Do you have a different way that you think about it?

: Well, my patients ask me all the time, 'How does this work, and how is it different from chemotherapy?' We can talk about biomarkers and how they are the targets and how the receptors work, but the simplistic way to think about this is: We have a cancer cell on 1 side and we have the T cell on the other and they're supposed to recognize and interact but then, there's a curtain in between. That curtain is actually created by the cancer cell; that curtain, we call PD-1 or PD-L1. The T cell is just behind that curtain, but it doesn't know the cancer is right there as well. So these blockers actually lift that curtain away, so that the T cell can interact with the foreign cancer cell and eradicate it. These are checkpoints, as we discussed before; these are 'stop' symbols that are created [as] a part of the immune response. We just have to sometimes release those 'stop' signals so that the T cells don't have a false sense of security that nothing is wrong, when the cancer is right there in front of them.

: Yeah, I couldn't agree more. You mentioned biomarkers a couple of times, and how that's so important because patients who don't have the right biomarkers are much less likely to respond to these agents. Could you talk to me a little bit about what some of those biomarkers are and how they influence who gets treatment with immunotherapy and who doesn't?

: Yeah, so these biomarkers are not perfect either. We know that immunotherapy will work when the T cell will recognize something that is not a self antigen. Whenever that creates neoantigens or new molecules that are considered foreign, would in theory, be addressed by the immune system. There are things like mismatch repair deficiency [and] tumor mutational burden [TMB] that tend to create neoantigens. We'll talk more about that; it becomes pertinent in [tumors] like endometrial [cancer or] colon cancer. Certainly, TMB is also a good biomarker. [It makes sense that] PD-1 or PD-L1 expression would be a biomarker for this, although in many cases, we do see that patients who have tumors that are PD-L1 negative [can] also respond to immunotherapy in some cases.

: Yeah, and it's not as easy as you would think. It's not [a situation where you just check if they] have PD-1 or PD-L1 or whatnot when [you] look at [the] tumor. They actually will sometimes make these combined positive scores [CPS], and there are other scoring systems that will assign a percentage. Have you seen that in your practice, as well?


: Yeah, we have. There's a lot of ways in which we can assess this biomarker. Again, the thing to recognize there is that this biomarker is also dynamic. We use the tissue specimen from a few months, few weeks, sometimes a few years ago, to make a decision on what's happening right now with the cancer itself. [That being said,] PD-L1 can be inducible; it can go away. [As such,] there's another whole layer of complexity that comes with it. However, things like CPS [and] tumor proportion score, we [use these to] try to see this biomarker in the cancer cell and the surrounding cells and come up with a percentage or an estimate of how effective the blockade will be with these agents.

: It seems like, at least in most of [the] cancers [that I see], they [respond to these agents if they have a PD-L1 expression of] at least a 1%. However, [a] higher percentage seems to be correlated with a higher response rate. Is that what we see with other tumors, as well?

: We do. For the most part, 1% or higher is considered a positive score. You know, in lung cancer, for example, 50% or higher would mean that they can try to skip chemotherapy altogether and use immunotherapy alone. However, we haven't quite seen that in other cancers yet.

: That's actually a really great point, and were talking about this the other day. At this point, we've been talking about how [immunotherapy is] used in the adjuvant setting, so after [a patient has undergone] surgery for [their] cancer or after something else [has been done]. Do you see these [agents] moving forward in the lines? Do you see this moving toward maybe before [a patient gets] surgery or replacing chemotherapy altogether?

: Certainly. We have had some approvals this year earlier. Nivolumab [Opdivo], for example, is approved in the neoadjuvant setting for lung cancer. As such, there will be situations where you can try to maximize response before a complex surgery so that the patients can [get to] surgery more easily. [Immunotherapy] has replaced chemotherapy in some situations, as well. We will have to see if we can, in the future, somehow also replace surgery altogether, with something like immunotherapy.

In this fifth episode of OncChats: Immunotherapy and You, John Nakayama, MD, and Ali Amjad, MD, discuss PD-1 blockade, potential biomarkers of response to treatment with immunotherapy, and the potential for these agents in the neoadjuvant setting.

Immunotherapy and You: Understanding the PD-L1 Blockade 

In this fourth episode of OncChats: Immunotherapy and You, John Nakayama, MD, of the Division of Gynecologic Oncology, Allegheny Health Network, and assistant professor of OBGYN at Drexel University, and Ali Amjad, MD, medical hematologic oncologist, Allegheny Health Network, highlight long-term survival data reported with immunotherapy approaches in patients with gynecologic cancers.

: Dr Amjad, I know you put together a little slide for us looking at [immunotherapy approaches in] a variety of cancers that have had more long-term data, as opposed to some of the [data] that I might be more familiar with. Could you take us through what was first? Why it was so important? What do you see [in terms of] survival with immunotherapy?

: Yeah. As you can see in the slide, this is a recent update from the 2022 ASCO Annual Meeting, which describes the longest follow-up for these patients with combination immunotherapy of ipilimumab [Yervoy] and nivolumab [Opdivo]. Here are just 3 examples. 

As we know, melanoma was the first cancer where immunotherapy was implemented and discovered, and we now have 7-year and beyond survival [information]. As you can see, approximately 1 in 2 patients who would otherwise have survived only a few months, when they went on these clinical trials with combination immunotherapy, are now doing well. Many of these treatments were stopped at 2 years after they started, based on protocol requirements. These patients are off therapy, and they're doing well many, many years after they were diagnosed with a stage IV, life-limiting illness. Similarly, in lung cancer, we have a good outcome. We had a recent update at 5 years [which showed that] 1 in 4 patients are alive. Also, in kidney cancer, again, we see tremendous improvement in survival. In the pre-immunotherapy era, you can see survival [outcomes in these populations] were poor.

: That's wild to me. I remember the days of vulvar melanoma, where people were getting interleukin-2 [IL-2], and were just really, really sick and just did not have very good outcomes. Is that what you have seen, as well? [Immunotherapy] is probably less toxic and works better.

: Yeah, IL-2 was, again, a unspecific way to stimulate the immune system, and that had been used for a long time in melanoma in general. In that crossfight between the inflammation that is induced by IL-2, and the cancer and the host, we used to have some success with a small number of people—[only] single digits. However, with these more refined immunotherapies, we now see a lot more patients responding and staying in response for a long time.

In this fourth episode of OncChats: Immunotherapy and You, John Nakayama, MD, and Ali Amjad, MD, highlight long-term survival data reported with immunotherapy approaches in patients with gynecologic cancers.

Long-term Survival Data With Immunotherapy in Gynecologic Cancers 

In this third episode of OncChats: Immunotherapy and You, John Nakayama, MD, of the Division of Gynecologic Oncology, Allegheny Health Network, and assistant professor of OBGYN at Drexel University, and Ali Amjad, MD, medical hematologic oncologist, Allegheny Health Network, review the 5 C's to consider when conducting research in gynecologic cancers and beyond.

: When we were talking earlier, you came up with these 5 C's of cancer research. Could you explain to our audience what you mean by that? 

: Yeah, so this is something that I think about a lot. Being in medical oncology, we have to have a framework of how research develops and how our treatment paradigms are created. [To this end,] I have this 5 'C' model of cancer research.

. Many times, we have to have a new discovery. In the context of immunotherapy, we have created 7 to 8 checkpoint inhibitors. Once we have an effective therapy, we always try to 

 it with other therapies to see whether the efficacy can be improved. We have plenty of examples where immunotherapy can be combined with either chemotherapy, other immunotherapy agents, TKIs, [and other agents]. Those combinations, many times, do work better than just the single agents. 

Once we have an effective single agent or a combination, we try to 

 or sequence them in a way that we can improve efficacy. Many of these cancer treatments are developed in the advanced-stage setting—third-line, fourth-line treatments—and then they get moved to an up-front setting [for analysis]. Like we discussed before, immunotherapy is now being utilized in the adjuvant setting to improve disease-free survival, [for example]. Then, we have effective therapies, we to see if we can 

 on them to see whether we can [still achieve] a similar effect. We [see if we] can identify biomarkers that can select a population [for whom] we can just [give] less than the traditional treatment. For example, if we use chemoimmunotherapy in lung cancer, how about if we use a biomarker to select a population that will do equally good or even better with immunotherapy alone? That is always the goal for us: to do less and get more. Obviously, as doctors and researchers, we want to 

So that seems to be my 5 'Cs,' a simplistic way for thinking about cancer care.

In this third episode of OncChats: Immunotherapy and You, John Nakayama, MD, and Ali Amjad, MD, review the 5 C's to consider when conducting research in gynecologic cancers and beyond.

Immunotherapy and You: The 5 Cs in Gynecologic Cancer

In this second episode of OncChats: Immunotherapy and You, John Nakayama, MD, of the Division of Gynecologic Oncology, Allegheny Health Network, and assistant professor of OBGYN at Drexel University, and Ali Amjad, MD, medical hematologic oncologist, Allegheny Health Network, discuss the safety and efficacy of immunotherapy vs standard chemotherapy in patients with gynecologic cancers.

: You mentioned checkpoint inhibition before. I think a confusion that a lot of people have is that there is more than one kind of immunotherapy, right?

: That's correct. Immunotherapy is a general term. Checkpoint inhibition is just 1 subset of immunotherapy. People call vaccines immunotherapy, as well. Monoclonal antibodies can also be [referred to as] immunotherapy. However, we have seen a wave of checkpoint inhibitors being approved, [and these agents] improve the efficacy of the immune system. That is what immunotherapy refers to, for the most part.

: So, at least from my standpoint, when I think about immunotherapy, I think about checkpoint inhibitors. [These agents] attack [the cancer] in a in a very different way, as opposed to cytotoxic chemotherapy. Could you talk a little bit about this, in terms of efficacy, from a patient's perspective?

: When we have a patient [with cancer who] comes to the office, the first question that they have for us—and the doctors think this way, as well—is [can their] cancer can be killed, and what will it take? Many times, when we talk about cancer treatments, [we think of] removing a cancer [and] addressing where it is right now. [We consider the] main treatment that can provide a cure for that cancer, and that would involve surgery or radiation treatments.

Then, there are adjuvant treatments, where you treat cancer after curative-intent surgery so that the risk of recurrence can be minimized. That's where, traditionally, we've used cytotoxic chemotherapy a lot. We still do, but recently, we've seen some studies that have shown immunotherapy as a very effective adjuvant treatment. In many cancers, [we have seen immunotherapy [perform] better than chemotherapy. To give you a few examples in lung cancer, in melanoma, in kidney cancer, and bladder cancer, we have immunotherapy approvals as adjuvant treatments.

Many times, these patients have cancers that are not curable; they are stage IV. The first thing that comes to mind from the patient's perspective, is that they want to start feeling better; they want to try to stay well and live longer. This is something that we [see] day in and day out. On clinical trials, when when we study these concepts, we capture a response rate. When tumors shrink, patients start feeling better. [With] immunotherapy, in many cases, if we have the right biomarker, [we] can [achieve] a very impressive response rate. In some cases, [the responses are] better than [what is seen with] chemotherapy. When these patients stay on therapy, and they have minimal adverse effects [AEs], they can be well for a long time and survive cancers for many years—even [those] with stage IV disease.

: You mentioned something really interesting about toxicity. Have you found immunotherapy to be less toxic, the same, or more toxic, than standard cytotoxic chemotherapy?

: Certainly, [immunotherapy] is better tolerated. I tell my patients, 'When you're getting this cancer treatment, 8 or 10 times you will not notice that you are getting a medicine for cancer.' Patients certainly don't have the alopecia, nausea, and fatigue that comes with chemotherapy; [immunotherapy] does not affect the blood counts. However, there are going to be some patients who can have severe and unpredictable AEs from it; that can range from 2 to 3 out of 10 patients. Many of these AEs can be mild and manageable. As the saying goes, if anything ends with 'itis,' it can happen with immunotherapy. [Effects] like colitis, thyroiditis, endocrinopathies, pneumonitis [are being watched for] really, really closely. However, for the most part, patients do really well on this treatment.

: Yeah, that has been my experience. I'm a kind of a simple guy, and way that I think about it, [is] like you said, [in terms of] the -itises, inflammation or whatnot. My wife has has autoimmune disease, and in my mind, somehow it's like you're turning up that immune system a little more and it's almost like an autoimmune kind of thing. I recognize it's not the same, but you're turning it up, and you can have that -itis, that inflammation, anywhere; it can be any organ system. Maybe that's too simplistic, but that's the way that I think about it.

: No, I think you're right. The immune system has checks and balances. There are stop signals everywhere, and that's how the immune system is designed. If you have an infection, once the infection is eradicated, the immune system is supposed to calm down. As such, what we try to do here, is activate the immune system against the cancer, which can go the wrong direction, as well. The T cells can activate against the normal antigens, too; that is a real risk.

: [Earlier, you were] talking about duration of response [with immunotherapy]; that caught my attention. I feel like, at least in gynecologic oncology, we have seen relatively low response rates. However, what has kept everyone super interested is the people who respond seem to have really long durations [of response]. Is that in other cancers as well, or is this a gynecologic phenomenon?

: No, that is true. You know, when you [use] immunotherapy, many times you create this equilibrium between the cancer and the tumor cells, to the degree that we sometimes see disease on a scan that seems to be dormant and doesn't seem to activate or progress as if a cancer would progress. So somehow, we change the behavior of a cancer and the cancer can live with the the body without having any major AEs. 

: I think it makes sense, those checks and balances, because tumors create an immunosuppressive environment. If you can alter [those] checks and balances, maybe you can keep it in check, like you are saying.

: That is correct. We'll talk more about PD-L1 and PD-1 blockers, but what happens is, cancer cells know how to hide from the immune system, and all we have to do is to try to expose them to the T cells, and that does the job.

In this second episode of OncChats: Immunotherapy and You, John Nakayama, MD, and Ali Amjad, MD, discuss the safety and efficacy of immunotherapy vs standard chemotherapy in patients with gynecologic cancers.

Immunotherapy and You: Gynecologic Treatment Efficacy From a Patient’s Perspective 

In this first episode of OncChats: Immunotherapy and You, John Nakayama, MD, of the Division of Gynecologic Oncology, Allegheny Health Network, and assistant professor of OBGYN at Drexel University, and Ali Amjad, MD, medical hematologic oncologist, Allegheny Health Network, explain how immunotherapy has changed practice for the treatment of patients with gynecologic cancers.

: Welcome to OncChats, I'm Dr. Nakayama. Today, I am joined by Dr. Ali Amjad; he's a hematologist oncologist at Allegheny Health Network. Dr. Amjad, would you mind introducing yourself to everybody?

: Thank you, Dr. Nakayama. It is a pleasure to be here, with you, today. I'm a medical oncologist, board certified in hematology and medical oncology. My practice here, at Allegheny Health Network, is a mix of tertiary care referral, as well as community practice. I mostly specialize in gynecologic medical oncology, in my main center. I [also] have 2 satellite offices, where I see a mix of the usual lung, prostate, breast, and other cancers. Thank you for having me.

: Thank you for being here. The thing that we're trying to do with this series is get an idea of where immunotherapy has been, where we are right now, and where we're going. You know, from my standpoint, as a gynecologic oncologist, this is all really new. However, for you guys, this is old hat. How have you seen immunotherapy change in your practice in the past few years?

 You're right; immunotherapy has changed the landscape of our treatments for cancer care in general. Traditionally, we used to think of chemotherapy or cytotoxic chemotherapy, where we were focusing on trying to kill the cancer to chemicals. However, now we realize that with immunotherapy, we can harness the body's own immune system to do the job for us. There are ways to to unleash the immune system onto the cancer, and there are ways to enhance the immune system—all of that [falls within] the realm of immunotherapy.

We saw the initial hint of immunotherapy working in 2010, more than a decade ago, and since then, we have had a lot of immunotherapy approvals. You may have heard about checkpoint inhibitors, and we'll talk more about them. We have 6 or 8 checkpoint inhibitors now approved by the FDA for a variety of cancers.

In this first episode of OncChats: Immunotherapy and You, John Nakayama, MD, and Ali Amjad, MD, explain how immunotherapy has changed practice for the treatment of patients with gynecologic cancers.

Ali Amjad, MD

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