: All of your patients need to have comprehensive genetic testing on their tumors. That’s the most important thing I can say. It’s important not only for 

 exon 20 mutations, but also important for all the other targets we now have. You’re not going to find it if you don’t look, so make sure you’re doing comprehensive NGS [next-generation sequencing] testing for all of your patients.

 I see the future for studying mutations in non–small cell lung cancer to be very bright because we now have the ability to perform molecular tests on patients as soon as non–small cell lung cancer is diagnosed, especially in early stage. This has opened an important door in non–small cell lung cancer: discoveries of new mutations, sensitizing mutations to treatment, and a possible biomarker for response. The most important effort that oncologists can make is NGS profiling of our patients with non–small cell lung cancer so that we can understand more and more about this cancer.

Using these, not only EGFR tyrosine kinase inhibitors [TKIs], but also in other types of molecular alterations, early in non–small cell lung cancer is a key component. Very often patients with non–small cell lung cancer who have driver mutations, even if they present at an early stage, they have a pretty high tendency to metastasize, especially to the brain, which is the site of 40% of recurrences in 

 mutated non–small cell lung cancer. I think the money should really be put toward molecular profiling in non–small cell lung cancer and then treating these patients with a more tailored approach. A non–small cell lung cancer with a driver mutation is a very different type of cancer from a nondriver mutation altered non–small cell lung cancer that arises in a prior smoker, and will most likely do well on immunotherapy. I think the most important thing we can improve is the rate of molecular profiling for non–small cell lung cancer, which unfortunately is still suboptimum in the United States, especially in community type or small practices.

 exon 20 is a real morale boost for all of us. It’s exciting for the patients, and it’s exciting for the investigators because we’re finding that these targets that were once considered undruggable are now druggable. It’s the same thing for 

 mutations, it’s exciting for us. It shows that the research that we do matters, and it shows that we’re able to make a difference by finding the right key to the right lock. Being able to then bring that to the patient level and see a patient respond is so gratifying.

Other interesting things that we’re looking at with amivantamab are CNS [central nervous system] penetration, and how we can improve responses. There’s a CHRYSALIS-2 trial going on that’s looking at amivantamab in addition to a tyrosine kinase inhibitor, a third-generation TKI called lazertinib. The thought of combining the 2 is important because lazertinib has CNS penetration. For amivantamab, we’re not really sure about its CNS penetration yet. But we know that brain metastasis is often a big problem for these patients, so can we combine these 2 drugs to provide better responses and provide better coverage in the CNS? Also, if that combination works well, how does it compare to first-line osimertinib? There’s an ongoing trial called MARIPOSA that’s randomizing patients to first-line osimertinib vs amivantamab plus lazertinib.

I think there are a lot of exciting things to look forward to. We’re all building on great research from all of these scientists and physicians before us. I feel really lucky to do this work because it is really cool.

Videos

Before closing out their discussion on EGFR exon 20 insertion mutations in NSCLC, experts share their thoughts on the future treatment landscape and potential unmet needs. 

NSCLC: Future Treatment Landscape of EGFR Exon 20 Insertion Mutations

: Experts briefly review a number of other agents in NSCLC that target 

 exon 20 insertion mutations around the same time mobocertinib and amivantamab were being studied. I think it’s a less exciting drug for 

 exon 20 insertions. It’s probably going to be more exciting for patients with HER2 exon 20. The FDA has granted fast track designation to poziotinib for HER2 exon 20 in non–small cell lung cancer.

 exon 20 insertion mutations, the response rates were quite low. Poziotinib demonstrated response rates around 14.8%, and the rates of treatment-related grade 3 and above rash and diarrhea were also quite high at 28% and 26%. I think that poziotinib is probably going to be more for the HER2 patients.

 Patients with exon 20 insertion are looking for ways to improve their treatment, and there are other options. One is a higher dose of osimertinib. It was previously tested and the results were presented at ASCO [American Society of Clinical Oncology annual meeting] in 2020. This was a cooperative group trial of 21 patients treated with a higher dose of osimertinib. The dose was double what we currently give to patients with 

 sensitizing mutations at 160 mg vs 80 mg.

This dose was continued daily until intolerable toxicity or withdrawal. One line of therapy was required as eligibility criteria, and stable asymptomatic brain metastases were allowed. Six patients remained on treatment at the time of the analysis, which was generated in 2020. Among the 20 eligible patients, the best response was a partial response [PR] in 4 patients and 1 complete response. Therefore, the response rate was 25%. Twelve patients, or 60% of them, had stable disease. The median progression-free survival was 9.7 months, and the median duration of response was 5.7 months. It was very well tolerated. The only higher than grade 3 treatment-related adverse events [AEs] observed in patients were anemia, fatigue, and prolonged QT interval. So this is an option for patients who have exon 20 insertion mutations.

Other possibilities are in clinical trials. There is no other specific FDA-approved inhibitor. But I want to mention one trial. It’s the MARIPOSA trial, in which they are seeking to randomize 1000 patients to lazertinib, which is a new EGFR tyrosine kinase inhibitor, plus either amivantamab or placebo, versus osimertinib plus placebo. This is being studied as first-line therapy for patients with locally advanced or metastatic non–small cell lung cancer with 

There is also the possibility of having additional cohorts in the CHRYSALIS-2 trial. There were some cohorts looking at patients with exon 20 insertion and uncommon 

 alterations such as S768 or L861Q and G719X. So I think the possibility of combining lazertinib and amivantamab also could be explored in 

 The other exciting exon 20 insertion trial is CLN-081. Preliminary findings were presented at ASCO by [Zofia] Piotrowska, [MD,] and among 25 response-evaluable patients 10, or 40%, had a PR, and 14, or 56%, had stable disease. The AEs we saw were rash in about 49% and diarrhea in 24%. But again, these are known EGFR toxicities. This drug seems to have efficacy in both heavily pretreated patients and also in treatment-naive patients, so I think that’s an exciting trial to keep an eye on. I have patients who have progressed on amivantamab, and they’re like, “What’s next?” One patient has tried mobocertinib and amivantamab and had responses to both, but now is looking for something else. It’s good that we have new things coming out.

Experts briefly review a number of other agents in NSCLC that target EGFR exon 20 insertion mutations.

Other Agents Targeting EGFR Exon 20 Insertion Mutations in NSCLC

: One important difference is that amivantamab is given intravenously, and mobocertinib is given by mouth. Depending on the patient population, there could be some preference for either IV [intravenous]or oral medication. The other important thing we need to consider as medical oncologists is the toxicity profile, so we do tailor therapy according to the patient’s preexisting conditions and other comorbidities. There are at least 2 options now to choose between, but the major differences are in the toxicity profile and administration.

: Mobocertinib is an oral pill, so that may make a difference for some patients. Amivantamab is given via IV, and it’s given on day 1 and day 2. It’s given weekly for the first cycle, so for the first few weeks, and then after that it’s given every other week. That can be more taxing for patients who have to come into an infusion center.

Mobocertinib is an oral pill. The ORR [overall response rate] seen with mobocertinib was a bit lower. It was 28% vs 40% with amivantamab. The median duration of response with mobocertinib was 17.5 months. In terms of toxicity, for mobocertinib, treatment-related AEs [adverse events] that were grade 3 and above were 46%.The majority of patients, 90%, had diarrhea, and I think 21% were grade 3 to grade 4. So there can be significant diarrhea, and rash in about 45% of the patients.

There are some differences in the toxicity profile, and amivantamab has that infusion-related reaction that we had discussed. But the grade 3 and above AEs were a little bit lower at 35%. I think both drugs provide our patients with great options we didn’t previously have. I think it’s exciting to have 2 things for these patients now.

Shared insight on the differences between amivantamab and mobocertinib and when they may be appropriately used in patients with NSCLC.

Key Differences Between Amivantamab and Mobocertinib in NSCLC

The mechanism of action of mobocertinib [Exkivity] is an irreversible 

 tyrosine kinase inhibitor. However, it differs from osimertinib [Tagrisso], which is currently approved for exon 19 and21 mutations. There is a significant overlap between the exon 20 insertion mutation wild type defined by the ATP [adenosine triphosphate] binding pocket. But this renders osimertinib not very effective in the binding of the pocket for the activity of this compound and it’s against the 

exon 20 insertion mutation. The amino acid insertion in the exon 20 is located at the C –helix or the P-loop [phosphate-binding loop] of the 

 kinases and pushes the C-helix into a permanent active confirmation that is distant from the ATP binding site.


Mobocertinib was designed in selectivity by targeting proteins in the vicinity of the alpha C-helix, a binding site not exploded by osimertinib. More specifically, osimertinib was not able to bind the exon 20 insertion mutations and mobocertinib is able to bind this pocket that is created in the confirmation of this mutated 


The data that led to the accelerated approval of mobocertinib was presented at ASCO [American Society of Clinical Oncology] 2021 by Dr [INAUDIBLE]. The data was from 2 different cohorts. One was with platinum-pretreated patients’, which included 100 first time patients. The other one was the original phase 1 cohort that included 96 patients from the EXCLAIM safety cohort.


The data cutoff was in November 2020. The median age of the 115 patients within the platinum-pretreated patients cohort was 60 years old—it was 66% female, 60% Asian, and 59% had at least 2 or more prior systemic anticancer treatments. The objective response rate by the independent investigative review committee was 28%. It included 1 complete response in which the rate was 78%, and the median duration of response was 17.5 months.


The EXCLAIM cohort included 96 patients with a median age of 59 years. The cohort was 65% female, 69% Asian, and 49% had at least 2 or more prior lines of therapy. The confirmed objective response rate was 25% with 1 complete response. The disease rate was 76% and the median duration of response was not reached at the time of analysis. In EXCLAIM, the baseline brain metastasis was present in 33 out of 96 patients, so 34%. The first site of disease progression was in the brain among 40% of all patients and 73% of patients had a baseline with brain metastasis. The confirmed responses were seen in both groups, in the platinum previously treated patients, and the EXCLAIM cohort. The treatment-related adverse events in the platinum-pretreated cohort were 91% of patients had diarrhea, 45% had a rash, and 38% experienced paronychia. There was also decreased appetite, nausea, dry skin, and vomiting. The grade 3 or higher incidents which led to discontinuation, were about 2% diarrhea and 4% nausea. The most important and frequent toxicity for mobocertinib was diarrhea.



Mobocertinib was FDA [Food and Drug Administration] approved in September for patients with 

exon 20 insertion mutations after progression of platinum based first-line therapy. These patients are in the metastatic incurable setting. This patient population already had the recent approval of amivantamab [Rybrevant]. Mobocertinib offers these patients another treatment. Current clinical trials are testing both drugs, amivantamab and mobocertinib in mutations not treated before, for metastatic incurable non-small cell lung cancer. The clinical trials are especially testing mobocertinib because it is an oral EGFR tyrosine kinase inhibitor. Mobocertinib is a significant option that could increase survival for these patients that [they] otherwise did not have until a few months ago.

Considerations for the FDA approval and practical use of mobocertinib in patients with EGFR exon 20 insertion mutations in NSCLC. 

NSCLC: Mobocertinib for Patients With EGFR Exon 20 Insertion Mutations

[epidermal growth factor receptor-mesenchymal-epithelial transition] bispecific antibody with immune cell directing activities. It’s different from your traditional TKI [tyrosine kinase inhibitor] and has a completely different mechanism of action. It binds at the extracellular domain, or the top, as opposed to diffusing through the membrane. Amivantamab can therefore inhibit ligand binding. It can also promote receptor antibody complex on endocytosis and degradation. It can induce trogocytosis by macrophages and ADCC [antibody-dependent cell-mediated cytotoxicity] by natural killer cells. It has a whole triple or quadruple prong approach.

 exon 20 insertions, it alters the active site that then causes steric hindrance to prevent the TKI from binding. But that’s all inside the cell so, if you think about it, the mechanism of action of amivantamab is great because it’s extracellular so all of that stuff that’s happening inside the cell is irrelevant to it.


CHRYSALIS was the first in human phase 1 dose-escalation and dose-expansion trial. I was very fortunate to be one of the first investigators on this amazing trial. It had several different cohorts. Some cohorts are still ongoing, but cohort D in particular was for patients with 

The primary endpoint was objective response rate and limiting the incidences of toxicity because remember this was a phase 1 trial, first in humans. The pivotal efficacy population included 81 patients with 

exon 20 insertions who had progressed on platinum-based chemotherapy. The safety profile included rash, paronychia, stomatitis, and most importantly, this infusion-related reaction that occurred in about two-thirds of the patients but almost exclusively on cycle day 1.

As we treated more patients on amivantamab we learned more and more about this infusion-related reaction. It is seen mainly on day 1. We’re able to pre-medicate with steroids and Benadryl and Tylenol and such to lower the incidents. And then if you stop the infusion and then just slow it down most patients are able to continue and complete that first day. The first infusion is split up between day 1 and day 2 and that way the patient gets a little taste of it on day 1 and then they get the rest of it on day 2. With all of those precautions, the infusion-related reactions have been very manageable. This paper was published in the 

 and the important takeaway numbers are the ORR [overall response rate] was 40%, which is quite good in a post-platinum population. The median PFS [progression-free survival] was 8.3 months and the median duration of response was 11.1 months.

The FDA [Food and Drug Administration] approved amivantamab on May 21, 2021, for patients who had progressed on or after platinum-based chemotherapy. Your patients would have had to receive a platinum-based doublet first and after that, they could go on to amivantamab. The NCCN [National Comprehensive Cancer Network] also updated the exon 20 insertions as a new targetable mutation and amivantamab is a treatment option there.

The approval of amivantamab for patients with 

 exon 20 insertions is huge. These patients didn’t have any targetable options previously and now you’re giving them new hope with new drugs. It’s a really exciting time for them.

Considerations for the FDA approval and practical use of amivantamab in patients with EGFR exon 20 insertion mutations in non-small cell lung cancer. 

NSCLC: Amivantamab for Patients With EGFR Exon 20 Insertion Mutations

 In the past, prior to our new FDA approvals, I was giving my EGFR exon 20 insertion patients chemotherapy. That was typically carboplatin and pemetrexed. Sometimes I would add bevacizumab. I don’t use immunotherapy with them. They tend to be on the nonsmoker spectrum, so immunotherapy is less exciting for them. Also, you don’t want to use immunotherapy in these EGFR patients who may go on to a tyrosine kinase inhibitor because there can be some adverse effects seen with the 2, 1 after the other.

In general, I’ve been using chemotherapy. I’ve also had patients come to me from their oncologist who didn’t realize that this was a special type of 

 mutation—they thought this was a typical 

 mutation—and just started them on osimertinib. When they came to me, I explained that this was an EGFR exon 20 insertion, which is different from the traditional 

 mutation. I probably wouldn’t start them on osimertinib. I’ve definitely switched some of those people to chemotherapy.

Nowadays, we’re lucky to have the new FDA approval of several agents for EGFR exon 20 insertion patients. If my patient progressed on platinum, I’m now putting them on amivantamab, which is the new Janssen EGFR-MET bispecific antibody. I’ve had very nice results with that drug. That’s where I am in the second line after platinum.

 My standard treatment for patients with exon 20 insertion mutations in the first line—outside clinical trials, because at our institution [City of Hope] we do have many clinical trials—in non–small cell lung cancer has been with chemotherapy plus or minus immunotherapy. I also use the 4-drug approach, which is platinum, Taxol, osimertinib, and amivantamab. However, there are more and more data showing that exon 20 insertion mutations don’t respond well to immunotherapy. Even if a patient has a high PD-L1, I wouldn’t advise immunotherapy alone as first-line treatment. I would treat the patient with chemotherapy and then eventually add immunotherapy. That’s my first-line approach.

After progression of first line, we have many clinical trials. We participated in several that led to the approval of amivantamab and mobocertinib, and we have more ongoing trials.

Current standard-of-care approaches toward the management of patients with non–small cell lung cancer with EGFR exon 20 insertion mutations.

NSCLC: Standard Treatment Approaches for EGFR Exon 20 Insertion Mutations

 Exon 20 is an interesting part of the EGFR story. The EGFR story has historically been about L858R and the exon 19 deletion. Those are historically the targetable 

 mutations. Those are the ones in which we’re using osimertinib. If you think about EGFR as a whole, it’s 10% to 15% of nonsquamous non–small cell lung cancers, but maybe 4% to 5% of them have an EGFR exon 20 insertion. It’s a small but definite population. And those have a low response rate with the currently approved tyrosine kinase inhibitors like osimertinib. EGFR exon 20 is characterized by either in-frame insertions or duplications near the C-helix of the EGFR kinase domain. It’s a very heterogeneous mutation. It’s not the same with every patient, which is the way L858R looks. With the EGFR exon 20 insertion, the active site is altered. It’s like the steric hindrance that prevents TKI [tyrosine kinase inhibitors] binding, and therefore TKIs have very low response rates with EGFR exon 20 insertions.

 In my practice, our institution [City of Hope] has PS65 molecular tests available. If a patient comes undiagnosed, we’ll do the molecular test. It’s an NGS platform, so it includes mutation analysis and fusions, and we also have some research background data. My advice is to do a broad molecular test like NGS in the metastatic incurable setting. You can also have liquid biopsies. If there’s a very small amount of tissue, I usually do liquid biopsy and NGS because at least you’ll have data in about 2 weeks. If liquid biopsies come out negative and there’s the option to do a tissue biopsy without delaying the care of the patient, I encourage that.

On the other side, if you have a positive liquid biopsy, you can proceed with treatment recommendations. The exon 20 insertion mutations are detected by NGS testing as well as liquid biopsies. However, with positive liquid biopsies, tumor burden contributes to cancer cells shedding into the blood steam. For patients with small tumor burden or only malignant pleural effusions, the liquid biopsy might be negative. Therefore, for malignant pleural effusions, we’re very successful obtaining tumor blocks to test for NGS.

 exon 20 insertion mutation significantly impacted the patient care because they aren’t very sensitive to the FDA-approved EGFR tyrosine kinase inhibitors, including osimertinib. Therefore, now that we have FDA approval, it’s definitely improved the care for these patients.

In the setting of non–small cell lung cancer, experts consider the importance of EGFR exon 20 insertion mutations as a therapeutic target. 

EGFR Exon 20 Insertion Mutations as a Therapeutic Target in NSCLC

The current gap in molecular testing is related to 2 large categories of reasons. One is insufficient tissue because, unfortunately, metastatic non–small cell lung cancer is found by small biopsies. Very frequently they’re found only with FNAs [fine needle aspiration biopsies], which are taken during bronchoscopies. Therefore, there isn’t enough material to conduct molecular testing, especially on the ones that come back in a stepwise-type of testing. This means there are some institutions, providers, and pathologists that will go first with 

-mutation testing. If those are negative, then they’ll then go with some sequence testing.

Unfortunately, stepwise testing requires many unstained slides. The majority of non–small cell lung cancers aren’t found from biopsy alone. The tumor isn’t very abundant. I advise to do NGS [next-generation sequencing], which is comprehensive genomic sequencing. With NGS, you save material from the comprehensive landscape of what the cancer in that moment is expressing.

You can find both mutations and no mutations, which will be handy in the future.

Ten years ago, we didn’t know about intrafusions or 

 mutations. For many decades, we were unable to target these mutations. More recently, with FDA approval, we can target the kinase G12 specific inhibitor. NGS testing on a patient is like gold at the moment. I encourage my colleagues to order NGS as early as possible so mutations are still in the early stage of small cell lung cancer. If we do the test broadly, we can find many other mutations that could potentially help these patients not only in the future but also in the immediate future, because we have many ongoing clinical trials open in adjuvant setting.

The other thing providing some barriers to molecular testing is that PD-L1 tests are easily accessible because they’re done by immunohistochemistry and require only a few slides of the tumor block. Therefore, if a provider does PD-L1 testing without doing any NGS molecular testing, and the PD-L1 is high, the patient might be treated with immunotherapy. For patients with 

 and other types of mutations, that’s not the best way to start treatment in metastatic noncurable settings.

I encourage requesting molecular testing on tissue biopsies. If molecular testing isn’t available, there’s also the option of liquid biopsies, which is approved by the majority of insurance carriers in the metastatic noncurable setting. For early stage, we can do molecular testing on either the surgical resection or on the biopsy that’s done for diagnosis if surgical resection isn’t available.

Erminia Massarelli, MD, MS, PhD, shares insight on potential barriers to appropriate molecular testing in patients with non–small cell lung cancer.

NSCLC: Overcoming Barriers to Testing and Molecular Profiling

 The field of lung cancer has changed greatly in the last 20 years. We’ve really learned how to treat the disease, not as just 1 disease, like lung cancer, but as many separate diseases. The first type of personalized cancer treatment was when we separated the lung cancers into different histologies: small cell lung cancer and non–small cell lung cancer. Then under non–small cell lung cancer, it was squamous cell carcinoma and adenocarcinoma. Later, when we started to genetically profile the adenocarcinomas, we found out there were more targets that are important. Adenocarcinomas then became 

-mutant lung cancers. As the years have gone on, we’ve found more targets. Now we have things like ALKrearrangements, ROS1, BRAF, RET. Even for KRAS, we have the targeted agent. The field has changed so much in the last few years. We have not only particular molecular genotyping but also drugs that target those particular mutations. It’s a cool time to be in.

 The molecular background starts in the early 2000s, when the first trials were done with gefitiniband erlotinib, which found that a proportion of patients were having higher responses to EGFR tyrosine kinase inhibitors. At that time patients weren’t included based on the molecular test because the 

 mutations weren’t known. Then in 2005 there was a discovery of the 

-sensitizing mutations. In the last 16 years, there have been a lot of discoveries about what the responsible driver mutations for non–small cell lung cancer are. More recently we have multiple tyrosine kinase inhibitors and other kinds of molecular inhibitors. 

 mutations represent 10% to 20% of tumors, and non–small cell lung cancer tumors have 

 mutations. These are the data for Caucasian ethnicity. If we look at data for Asian ethnicity, the 

 mutations are about 50% of non–small cell lung cancers. We’re talking about a significant number of patients, especially of Asian ethnicity. Among all these 

 mutations that don’t have significant response to the appropriate EGFR tyrosine kinase inhibitors. Of these, the most frequent nonresponsive 

 mutations are the exon 20 insertion mutations, which are present in 2% to 3% of 

 Comprehensive genomic profiling in non–small cell lung cancer has changed the landscape of lung cancer. That means treating a patient with lung cancer today is so different from treating a patient with lung cancer 20 years ago, when you were just giving chemotherapy. In my clinical practice, every adenocarcinoma gets reflexive NGS [next-generation sequencing] testing. That’s just the way Columbia [University Herbert Irving Comprehensive Cancer Center] works. It’s not just stage IV; we do it for every lung adenocarcinoma. It’s reflexively tested, and if we want to do additional testing for squamous cell carcinomas, I send that out as a separate test.

I test every adenocarcinoma that comes through my clinic. They all get a reflexive next-generation sequencing lung cancer panel. I also test every never-smoker. Even if a never-smoker has a squamous cell carcinoma, I do NGS profiling because sometimes the cancer is heterogeneous, and maybe you’re not catching an important mutation. I try to dig deep for my never-smokers. I test at progression, especially for patients with 

 or other mutations where we might be able to find some actionable acquired resistance mutation.

The advent of liquid-based assays or blood-based assays has been huge. In the past, we only had tissue, which takes a long time. For tissue, you have to get the biopsy, and then you have to send it to do the NGS panel. This probably takes 2 to 3 weeks. With some blood-based assays you’re able to get results in as few as 7 days, which is amazing. I try on all my new metastatic diagnoses to do an additional blood-based assay. You still need the tissue. The tissue is always important. Tissue is the gold standard. You need tissue for a diagnosis. I do the tissue, but at the same time, I’ll also send off for a blood-based assay, because if it comes back with an 

 mutation, then you’re able to start them on treatment right away. It’s important to do that. Sometimes, before the patient even sees me, I’ll ask my office staff to draw a liquid biopsy, so that when I see them I’ll at least have the results of that.

Experts take a broad look at how molecular profiling has impacted the treatment landscape of non–small cell lung cancer.

The Evolving Landscape of Molecular Testing for NSCLC

Erminia Massarelli, MD, PhD, MS, associate clinical professor, Department of Medical Oncology and Therapeutics Research, City of Hope, discusses the adoption of alectinib (Alecensa) as the first-line therapy in the treatment of patients with 

-positive non—small cell lung cancer (NSCLC).

The new standard first-line therapy for patients with 

-positive NSCLC is alectinib (Alecensa). It has proven to be particularly effective in treating patients who have brain metastases. In one clinical trial, there was a head-to-head comparison between alectinib and crizotinib (Xalkori). The patients who received alectinib had better progression-free survival (PFS) and less development of brain metastases than the patients on crizotinib.

The side effect profile is also better in alectinib in comparison with crizotinib and ceritinib (Zykadia). Overall, alectinib is an easier drug to manage in patients and facilitates less breaks in therapy, Massarelli concludes.

Erminia Massarelli, MD, PhD, MS, associate clinical professor, Department of Medical Oncology and Therapeutics Research, City of Hope, discusses the adoption of alectinib (Alecensa) as the first-line therapy in the treatment of patients with ALK-positive non–small cell lung cancer (NSCLC).

Erminia Massarelli, MD, PhD

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