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Jacob Sands, MD: Hello. I'm Dr Jacob Sands, a thoracic medical oncologist at the Dana-Farber Cancer Institute. Welcome to Medscape's InDiscussion series on lung cancer. Today, we'll discuss immunotherapy in metastatic non–small cell lung cancer. I am very excited to introduce my guest, Dr Stephen Liu. Dr Stephen Liu is an associate professor of medicine, director of thoracic oncology, and head of developmental therapeutics at Georgetown University in Washington, DC. Dr Liu, welcome to InDiscussion.
Stephen V. Liu, MD: Thanks for having me, Jacob. It's a real pleasure to be here. I'm a big fan of the podcast.
Sands: I'd like to start out with a bit about your personal journey. What interested you in focusing on lung cancer?
Liu: I wish I could tell you that I was interested in lung physiology from an early age. But it's not true. To be honest, it was more of a pragmatic decision. During my fellowship, I was at the University of Southern California (USC) in Los Angeles, and all of my fellowship research was in prostate cancer. That's where I had all my publications, my grants, and my mentors, and that's really the career I envisioned for myself. When I finished the fellowship and began applying for jobs, it was important that I stay at USC. My wife was still in training there, and while they offered me a prostate cancer job there, they had a lot of prostate cancer doctors. From the jump, I would have been pretty redundant, which isn't the best career path early on. The options it shook down to were to take a prostate cancer job across town at a different university or stay at USC and work in lung cancer where there was more of a need. I chose based more on location. It was much more of a pragmatic decision.
I can tell you why I decided to stay in lung cancer because I've since changed institutions. What has kept me in the field is the people. This is a very lethal disease, as you know. When you meet patients who are diagnosed with lung cancer, they're often very sick. It's a very special type of relationship because it's a bond that's formed under a lot of duress. It's a very privileged type of relationship that I really enjoy. I know I'm biased, but I think that the lung cancer community, the academics, and the specialists are among the best people out there. Part of it is that when I am at a conference or a meeting and I see you or I see another lung cancer doctor, I know you have probably had a pretty rough clinic. The community is very supportive of each other. You don't see a lot of competitive bickering. It's a very supportive community. I think it's because we know we need that support. This community, maybe more so than in other specialties, really comes together. It's a great place to thrive and to grow.
Sands: That has definitely been my experience, as well. I can certainly say on behalf of many within the academic lung community that we are so grateful you have chosen to stay in in lung cancer treatment or ended up as one of our colleagues within lung oncology. You've certainly been a leader. You're right, the history of lung cancer has been a rough one. There are some really remarkable new advances and we're going to discuss some of them, some of what we're seeing, and some of the more exciting cases being immunotherapy. We also have targeted therapies we talk about in other environments. We're going to focus on immunotherapy today. We're going to discuss various checkpoint inhibitors, but we'll start with the KEYNOTE trials. We had KEYNOTE-024 with pembrolizumab, and KEYNOTE-042. Then, of course, we had the combination chemotherapy/pembrolizumab studies, as well. Do you want to take us through an overview of the pembrolizumab-related KEYNOTE trial?
Liu: Sure. These are hugely monumental studies that changed not just our standard of care and our treatment algorithms but really changed how we perceive the disease and what we're capable of in treating someone with metastatic lung cancer. Early on in my career, we saw the introduction of immunotherapy as salvage treatment or for heavily pretreated lung cancer in the second-line setting, replacing docetaxel. The first-line study that really changed the field was KEYNOTE-024, and Martin Reck presented this at the European Society for Medical Oncology (ESMO) 2016 meeting to a standing-room-only audience. This was a phase 3 study that randomized patients with treatment-naive non–small cell lung cancer, so they had no prior therapy. They were randomized to receive immunotherapy, which was pembrolizumab for a period of 2 years, or chemotherapy. Immunotherapy was clearly better. It was better tolerated. It worked better. It worked for longer. It's our new standard of care. This was for PD-L1 (programmed death-ligand 1)– high non–small cell lung cancer. But at the time, there was a little concern about this study. Some of our colleagues didn't have equipoise because we had learned over many decades of studies that chemotherapy improved survival and immunotherapy didn't work for everyone. The thought here was if we gave immunotherapy as a frontline treatment and it didn't work, the natural history of the disease wouldn't allow some of these patients to get second-line treatment. There were some people who thought it was a risky study and weren't sure if it should go forward. We're glad it did because pembrolizumab was by far the better option of improving survival. Even with crossover built in and even with immunotherapy available as second-line treatment, the median survival doubled from 13 months to 26 months. We now know that the 5-year survival rate is over 30% with pembrolizumab alone. From October 2016, it became below the standard of care to give chemotherapy alone as a first-line treatment for PD-L1–high lung cancer.
We then saw that indication expand. PD-L1–high lung cancers are about a third of metastatic non–small cell lung cancers. What do we do for the other two thirds? For PD-L1–low lung cancer, we saw KEYNOTE-042. Now, KEYNOTE-042 was including people with a PD-L1 score of 1% or greater, so about two thirds of the population. We saw that the study results overall were positive, but in the PD-L1–low group, immunotherapy wasn't convincingly better than chemotherapy. It wasn't necessarily worse, but it was not convincingly better. We wanted something more there, and that came in the form of adding chemotherapy.
Chemotherapy does two things. There is certainly an additive benefit, so you can benefit from the chemotherapy alone and from the immunotherapy alone. There's some suggestion that there might be synergy between them and that giving chemotherapy might allow the release of neoantigens that might invoke an immune response. Clearly, though, the combination is an established option. KEYNOTE-189 was a combination of carboplatin or cisplatin with pemetrexed and pembrolizumab. KEYNOTE-407 was a taxane — either paclitaxel or nanoparticle albumin bound (nab)-paclitaxel — with pembrolizumab for squamous lung cancer. Both of those combination studies showed that when you add the checkpoint inhibitor — when you add pembrolizumab to that platinum doublet — you improve survival. This was seen across PD-L1 strata. Now, for someone that doesn't have a driver mutation, we know immunotherapy has to be part of frontline care. You can't save it for later use, and it's either given by itself or with chemotherapy. It's got to be immunotherapy because that leads to better outcomes in the short term. More importantly, though, there are better outcomes in the long term and the potential for really durable, meaningful, transformative types of responses.
Sands: That's a great, concise overview of a whole bunch of information. KEYNOTE-024 included a PD-L1 expression greater than or equal to 50%, and then KEYNOTE-042 included a PD-L1 greater than or equal to 1%. Then the combination trial of chemotherapy and pembrolizumab included all comers. I highlight that because I sometimes see people forget that in the first-line setting, if the PD-L1 is less than 1%, these patients are still ones that you generally treat with chemotherapy plus pembrolizumab. They're certainly eligible. Within the forest plots of those trials, this did appear meaningful, as well. You mentioned the improvement in median survival and in tolerability. You mentioned a 5-year survival of 30%, and this is a really remarkable statistic in the setting of metastatic non–small cell lung cancer. Can you talk a little bit about the tail of the curve related to these KEYNOTE trials?
Liu: That's really what we look at now. Medians don't tell the whole story. It's not that immunotherapy benefits everyone. It doesn't, unfortunately. If you do get immune-related responses, they can be extremely durable. Some of us use the word "cure" and we have to figure out how we best define that. Thirty percent of people who receive pembrolizumab alone are alive at 5 years, and that's with PD-L1–high lung cancer. Historically, that number would be in the single digits with other therapies. When we look at KEYNOTE-189, which, as you mentioned, was an all-comers study that included chemotherapy, platinum, pemetrexed, and pembrolizumab, the 5-year survival there was about 20%. We've come an extremely long way in a very short period of time when you think that one in five people is alive 5 years later with what not too long ago was a uniformly and fairly rapidly fatal disease with a median survival of less than a year. For a subset of patients, we do achieve meaningful long-term survival that might approach what we would call a cure.
Sands: Let's move on now to nivolumab (NIVO) and nivolumab plus ipilimumab. We've seen a couple of different trials that have led to FDA approvals in the first-line setting. Can you take us through the CheckMate studies?
Liu: I don't think we have enough time to go through the design of CheckMate 227 because it is one of our more complicated studies. At the crux of it, you're looking at dual immunotherapy or dual checkpoint blockade. Programmed cell death 1 (PD-1) and PD-L1 are important checkpoints in a cancer that will prevent immune activation or immune recognition of cancer cells. By blocking these checkpoints, we can restore the anticancer immunity that we normally see. With CheckMate 227 and CheckMate 9LA, we're now incorporating dual checkpoint blockade. So in addition to blocking PD-1, we're blocking CTLA-4. CTLA-4 inhibitors such as ipilimumab in the CheckMate studies, or tremelimumab in the more recent POSEIDON study are used more in priming the T cells, and those have an established role in melanoma and in kidney cancer. While they are associated with a different toxicity profile in lung cancer, they are also associated with extremely long, durable responses. CheckMate 227 was a combination of nivolumab and ipilimumab. This therapy, which showed a benefit, is approved only for PD-1–positive cancer, but it did show a benefit in PD-L1–negative cancer as well. This was across histologies. CheckMate 9LA is that same combination of nivolumab and ipilimumab but in combination with chemotherapy given for only two cycles, and that's maybe to prevent that early progression we can see for those who aren't so immune responsive. That combination is also FDA approved. It really is this embarrassment of riches where we have multiple agents — most recently, the POSEIDON regimen of durvalumab plus five doses of tremelimumab plus four cycles of chemotherapy. There are a lot of subtle differences here. What we have are a lot of options. Now, if the question is, does adding a CTLA-4 inhibitor improve outcomes compared to PD-L1 alone? We don't have the right direct head-to-head comparison yet. We're just left with a lot of different options.
Sands: The balance in this that I hear debated is a CTLA-4 inhibitor raising that tail of the curve where you're getting potentially more durable benefits. Of course, now we're doing cross-trial comparison and even having this discussion, which as we know, statistically, you cannot do. At the same time, when we're meeting with patients, that's exactly what we have to do in deciding what the right regimen is for an individual. On the potential upside, we are looking to raise that that tail of durable responses while accepting a bit more of a toxicity profile. What does that equation look like for you? How do you weigh those out?
Liu: What we really need is a good biomarker for who is going to get that extra benefit from a CTLA-4 inhibitor. Who needs it? If you have someone who's in that 30% from KEYNOTE-024 or who's in that 20% from KEYNOTE-189, we don't need to add a CTLA-4 inhibitor. If I knew upfront that this person was destined for 5-year survival, it's not really worth adding that extra drug, the extra cost, the extra toxicity, and the extra risk. How many people are we converting from a nonsurvivor to a survivor by adding that? We don't know the answer. We can't tell who those people are upfront. For me, a CTLA-4 inhibitor is an attractive option even without a biomarker. I only consider it in the right patient. When we think of what CTLA-4 inhibitor adds, for sure it adds another layer of toxicity, and these are immune-related toxicities that as we know can escalate and get out of hand very quickly.
I don't want to give a CTLA-4 inhibitor to a patient who's going to have an immune-related colitis, and I don't find out about it for a week or two. That could happen if I have a patient who is seeing me for front-line therapy. Everything's on the table, and this person lives very far away or completely on their own, or I have some patients who live quite rurally and don't have phone coverage. I also have patients who aren't complainers and keep things to themselves. Those are the wrong type of populations to think of a CTLA-4 inhibitor for because the risk is a bit higher. On the other hand, there are patients who have a little more support, are a little more engaged, and have a little more access to help, so if there is a toxicity, we can recognize and treat it very quickly. That's my biggest concern.
Sands: I want to highlight that first statement you made about essentially trying to identify patients in whom we can convert what would not have been a really durable response with a PD-1/ PD-L1 inhibitor alone into one of those durable responses. What you're describing is trying to find the population for whom a CTLA-4 inhibitor is going to be the thing that really matters in an individual having a long or ongoing response to therapy. Sometimes I hear people say that the next research should be to figure out how to make the checkpoint inhibitors or immunotherapy work better. The nuance to that is not necessarily to make them work better for those it's working for — because some people are having remarkable ongoing benefits — but how to make it work that well for more people. That's what you're highlighting and also recognizing that we don't currently have a good biomarker for this. It sounds like this is what you're pinpointing as an area of huge need — identifying who would have a benefit by the inclusion of a CTLA-4 inhibitor. This then brings us to the logical conclusion that you believe there is a population that is benefiting from the inclusion of the CTLA-4 inhibitor. In your cross-trial comparison, you're assessing that there is likely a larger number of patients who are benefiting from the inclusion of CTLA-4 inhibition.
Liu: I think there is. A lot of these differences are difficult for us to measure because the numbers are quite small. To me, the leading candidate today might be one with STK11 mutations. We know that this predicts for a relatively immune-refractory population, and some convincing evidence from MD Anderson and Hopkins led by Ferdinandos Skoulidis shows that when you have specific mutation profiles like STK11, those patients don't seem to get a lot of benefit from the addition of immunotherapy. They were all retrospective data but very convincing retrospective data. The bar, though, is a little higher to withhold immunotherapy. Rather than not give those patients immunotherapy, I think a better strategy is to find different immunotherapy strategies. In the POSEIDON dataset, we saw that patients with an STK11 mutation got more relative benefit from CTLA-4/PD-L1 inhibition from the addition of tremelimumab to durvalumab than durvalumab alone. That was shown with tails of the curves at landmarks like 2 years and 3 years that were quite a bit higher in those populations. But as you know, Jacob, those numbers were very small. We're talking about datasets of 12-18 patients, which is relatively small to base a whole strategy on, but it's a start. We need to pool our forces and really identify what those biomarkers are.
Sands: Yes. We have atezolizumab and the IMpower regimens where we have a combination. This was one of the earlier publications that had the inclusion of bevacizumab in that initial statistical analysis. What is your assessment of that? Is this part of your equation? Can you give us an overview?
Liu: Yes. There are a lot of agents out there. If we're talking about only the US-based regimens, it's a long list. When we start getting into other regimens, for example, in Asia, the list grows even longer. Atezolizumab is approved in the frontline setting, and that was based on the IMpower110 study led by Dr Roy Herbst where we saw atezolizumab compared to chemotherapy. Atezolizumab did improve survival compared to chemotherapy in that PD-L1–high group. It is another option in that setting. I don't think it's convincingly better or necessarily worse than pembrolizumab, but it is another option. There are different chemotherapy backbones associated, as well. We have atezolizumab with nab-paclitaxel and carboplatin. That was the IMpower130 study led by Jack West. While that is an approved regimen and the addition of immunotherapy to chemotherapy did improve survival — and I think that's the right answer on a board exam — it's hard to find a use for that specific regimen. Maybe if there was an adenocarcinoma or you couldn't give pemetrexed, there are maybe some niche populations, but that's a regimen that probably hasn't found its home just yet.
The IMpower150 regimen is a little different. That's carboplatin/paclitaxel/bevacizumab as a backbone. Based on the ECOG 4599 study, with the addition of atezolizumab, it did improve survival. It is an approved regimen. To me, what sets that regimen apart is its activity in the EGFR mutation space. What we did see was potentially some benefit in lung cancer patients with EGFR mutations after a tyrosine kinase inhibitor (TKI) that was the initial treatment, whereas you didn't really see that benefit with atezolizumab alone and without the bevacizumab. That fits in with other studies we've seen. We saw that sintilimab plus antiangiogenesis did improve outcomes in patients with EGFR mutations, whereas in more recent data from KEYNOTE-789, pembrolizumab alone did not improve outcomes when added to chemotherapy in patients with EGFR mutations. There might be something to vascular endothelial growth factor (VEGF) inhibition with EGFR mutations. It's still an unanswered question but one that's important to ask. When we talked to our colleagues in Asia, the IMpower150 regimen is hugely popular in Japan, after TKI therapy. There's a lot of patients with EGFR mutations there, so they must know something. It's something that needs a little further study.
Sands: I debated starting this whole interview with a discussion of next-generation sequencing and looking at actionable alterations. The reason I held off was because of these data you're specifying. This is a good segue into genomic testing and how it fits into this whole picture. I personally will do a next-generation sequencing on all patients with non-squamous non–small cell lung cancer. In anyone with a squamous cell cancer without a smoking history or with a particularly limited and distant smoking history, I would also do next-generation sequencing, I consider that to be standard of care. Of course, at an academic institution, we have some patients with a significant smoking history and squamous cell cancer who end up getting tested as part of some of our research studies that are observational. Generally speaking, I'd say standard of care is testing what I initially started with. In most of the actionable alterations with an FDA-approved targeted therapy in the first-line setting, I would treat in those cases. You've highlighted IMpower150 — although it is a first-line trial, it is second line after targeted therapy for EGFR-sensitizing mutations. However, the trials often don't specify what percentage of patients with an EGFR mutation truly had sensitizing mutations as opposed to a nonsensitizing or exon 20 mutation. How does genomic testing fit into all of this in your standard practice? Is IMpower150 a regimen you would consider particularly in that setting, or does it not have to be considered? Do you think there's more benefit to that regimen than others? Is immunotherapy something you utilize after targeted therapies? I've given you a string of questions that all fit together, but I'll let you go through them in whichever way you want to wander through them.
Liu: They do go together. Everyone who walks in my door with a diagnosis of lung cancer gets next-generation sequencing, whether the cancer is early stage or late stage. Regardless of histology, everyone's getting next-generation sequencing. I've been called many things, Jacob, but I've never been called cost efficient. Yet to me, I need to know this information because it helps me not only choose which treatment we're going to do today, but which treatment we're going to do tomorrow. It tells me about the biology and it tells me what treatment to give and what treatment to avoid. While I appreciate that next-generation sequencing is not free and it is an expensive test, it's less expensive than one dose of immunotherapy. If I see someone with an ALK fusion with a ROS1-fusion that I wouldn't have otherwise detected and if it steers me away from a year or 2 years of immunotherapy, it dwarfs the cost of a next-generation sequencing test. I really consider it essential. I understand that I speak from a position of privilege in that we can do these tests, but everyone in my clinic is going to get that treatment.
When do we give immunotherapy to someone with a driver alteration? When we're thinking specifically of the nonsmoking-related mutations like EGFR and like ALK, it's pretty far down the line. For patients with EGFR-mutant lung cancer, it's TKI therapy, and then I'm going to use biopsy to try to guide more rational combinations and trial delivery. My point is that if I'm going to give immunotherapy, I'd like to give it with VEGF and potentially with chemotherapy. If we're going to do that, it's probably the best currently available way to deliver immunotherapy. If we're talking about second-line PD-L1 inhibitor therapy alone, I don't have a lot of excitement about that delivery. If we're going to do immunotherapy, using the IMpower150 regimen makes sense. I'm less excited about it if I need to continue TKI therapy, and that's specifically in patients with brain metastases where there's value in continuing the TKI therapy to maintain central nervous system control. TKI therapy plus immunotherapy doesn't mix well. Those are settings where I'm probably not going to give immunotherapy ever.
Sands: It sounds like the use of these regimens is a bit of an outlier for those with an EGFR mutation. You have other preferences, of course — looking for other targeted options and such — but if you're using it, the IMpower150 regimen would be your choice. Let's use that as a jumping point in synthesizing all of these regimens. We've talked about a lot of different regimens. You've specified some specific subpopulations within them. Can you take us through an overview of your treatment strategy? What do you do when you see someone in clinic and you're talking about the first-line setting? Let's say there are no actionable alterations as far as no targeted therapy given. Yet, this is clearly not done enough throughout the country, so I highlight that again, patients should get next-generation sequencing and end up on a targeted therapy when appropriate. But assuming none of those happens, now what?
Liu: We have a lot of options. We also have cemiplimab monotherapy, cemiplimab plus chemotherapy, and other regimens coming up around the bend. For me, I'm looking at PD-L1 status. I'm looking at burden of disease and comorbidities. If the patients are very fit, I'm more likely to give chemotherapy upfront, especially if there's a large burden of disease. If someone's asymptomatic with PD-L1–high lung cancer, my preference is still monotherapy, and I like to avoid the chemotherapy toxicity. I'm probably using pembrolizumab there alone. There is nothing wrong with atezolizumab or cemiplimab, but there's a lot of inertia, and I don't really see a compelling reason to change practice. Those are reasonable options. If there was a copay difference or a formulary difference, I have no problem switching, but I'm primarily using pembrolizumab alone for patients without a lot of symptoms. If a patient has a lot of symptoms, I'm going to lean toward combinations of chemotherapy with immunotherapy. My general practice is to reach for KEYNOTE-189, again, just because I have the most experience with it. I leave room for individualization and for shared decision-making and talking about the different options. Scheduling is an important consideration, as well. Pembrolizumab alone can be given every 6 weeks, which is a much more favorable regimen. For PD-L1–low and PD-L1–negative cancer, my preference is chemotherapy with immunotherapy, and there, it's a toss-up between KEYNOTE-189 for adenocarcinoma or CheckMate 9LA if I really think of the value in avoiding long-term durable chemotherapy. There are a lot of other regimens that are all reasonable options. I don't think one's shaken up to the top, and I do have allowances for other options based on unique specific circumstances.
Sands: I feel similar. You mentioned cemiplimab, and I'm glad you mentioned that one. I think the data for that were quite compelling but not compelling enough to move out the inertia for pembrolizumab. It absolutely justifies a backbone for ongoing trials and combinations. I feel very comfortable with the control arm of cemiplimab. As you mentioned, if there's a copay issue or some other issue, I feel very comfortable with the idea of prescribing any of these approved regimens. Now you did mention a subpopulation of patients with an STK11 mutation where you might consider CTLA-4 inhibitors. Can we further flesh out any other aspects that would make you more inclined to choose CTLA-4 inhibition aside from your just-mentioned issue of whether or not you'd use longer-term pemetrexed?
Liu: The central nervous system is a consideration, as well. If we borrow from our melanoma colleagues, CTLA-4 inhibition seems to boost the responses in the brain. If someone had a lot of disease in the brain that was an important consideration, I might be a little more likely to lean toward a CTLA-4 inhibitor there, as well.
Sands: With regard to time and duration of treatment for each of these, do you do 2 years and stop? Are you doing any kind of assessment at that time? Is it patient to patient? What duration of therapy are you giving when it is effective and well tolerated?
Liu: I'm highly conflicted here. It's certainly debatable when we think of duration of treatment. There's really only one randomized study that looked at this question, which was CheckMate 153 led by Dave Spigel. This was in the second-line setting with NIVO alone, and it was NIVO for 1 year vs NIVO until progression or intolerance. We saw that there was not only a progression-free survival benefit that you might expect but an overall survival benefit with continuing NIVO longer than 1 year. That doesn't answer the question in the front-line setting, and it doesn't answer the question of 2 years vs indefinite therapy. It's important to set expectations, so I tell patients upfront that we're going to continue the treatment. The tentative plan is do it for 2 years, and if all goes well, if there's not major toxicity, and it keeps working, we're going to plan on the treatment for a period of about 2 years. At 2 years, we are going to have a discussion. I have some patients that get to 2 years and they say they feel great, they have no side effects, and it's working. If they have stage 4 lung cancer, there's no evidence of cancer right now, and we're at 2 years, they ask why they would stop. It's hard for me to argue with that. When we look at the 5-year data from KEYNOTE-24 and KEYNOTE-189, while patients who make it 2 years do very, very well, there are late recurrences after 2 years. I don't know if continuing therapy more than 2 years would have prevented a recurrence if it was manifest destiny that it was going to happen regardless or if we could have avoided it. We know there's a response rate when you rechallenge after stopping, but the response rate is not 100%. It's more like 50/50. I have a shared decision-making model in that setting. At 2 years, we have a discussion, and in the studies, we stopped at 2 years. I'm very comfortable stopping at 2 years. Then we monitor the patients closely. But if patients feel like they're going to be very anxious and not able to sleep after stopping at 2 years, and they feel very strongly about continuing, I also think it's reasonable to continue until intolerance or progression.
Sands: This is another great setting for some kind of biomarker or a minimal residual disease blood-based test if a patient's cancer has cleared by the time of 1 year and they're still having an ongoing response at 2 years. Two years is the more natural and obvious timepoint for testing. It feels like in the next 3-5 years ahead, we're primed for a biomarker revolution with increasing technology to better assess some of the different subgroups you've described in our discussion today.
Liu: I think that's where we have to go. And you know, Jacob, I'm looking to you to lead those studies.
Sands: Well, there are a lot of people smarter than me who are working on some of this. This has been an absolutely wonderful discussion and I really appreciate Dr Stephen Liu joining us today for a discussion about immunotherapy for non–small cell lung cancer. Thank you for tuning in. If you haven't done so already, take a moment to download the Medscape app to listen and subscribe to this podcast series on lung cancer. This is Dr Jacob Sands for InDiscussion.
Listen to additional seasons of this podcast.
Resources
Update 2020: Management of Non-Small Cell Lung Cancer
Targeted Drug Therapy for Non-Small Cell Lung Cancer
Pembrolizumab Versus Chemotherapy for PD-L1-Positive Non-Small-Cell Lung Cancer
The Current Lung Cancer Neoantigen Landscape and Implications for Therapy
Pembrolizumab Plus Chemotherapy for Squamous Non-Small-Cell Lung Cancer
Nanoparticle Albumin-Bound Paclitaxel: A Novel Cremphor-EL®-Free Formulation of Paclitaxel
Pembrolizumab Plus Chemotherapy in Metastatic Non-Small-Cell Lung Cancer
First-line Treatment With Ipilimumab Plus Nivolumab for NSCLC
Nivolumab Plus Ipilimumab in Advanced Non-Small-Cell Lung Cancer
Identifying New Biomarkers to Detect Lung Cancer Earlier
The importance of STK11/LKB1 Assessment in Non-Small Cell Lung Carcinomas
STK11/LKB1 Mutations and PD-1 Inhibitor Resistance in KRAS-Mutant Lung Adenocarcinoma
Atezolizumab for First-line Treatment of PD-L1-Selected Patients With NSCLC
Atezolizumab for First-line Treatment of Metastatic Nonsquamous NSCLC
Paclitaxel-Carboplatin Alone or With Bevacizumab for Non-Small-Cell Lung Cancer
Advanced Non-Small-Cell Lung Cancer With Epidermal Growth Factor Receptor Mutations
Next Generation Sequencing Technology in Lung Cancer Diagnosis
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Cite this: Immunotherapy, Next-Generation Sequencing, and Shared Decision-Making in the Treatment of Non–Small Cell Lung Cancer - Medscape - May 17, 2023.
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