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Upfront EGFR-Targeted Therapy for NSCLC

Panelists: Mary Jo Fidler, MD, Rush; Roy S. Herbst, MD, PhD, Yale ; Geoffrey R. Oxnard, MD, Harvard; Naiyer Rizvi, MD, Columbia; Mark A. Socinski, MD,
Published: Thursday, Aug 27, 2015

 
Transcript:

Mark A. Socinski, MD: Hello and thank you for joining this OncLive TV Peer Exchange. Modern treatment of advanced lung cancer is based on tumor histology and molecular subtype, with new advances in the field happening at an accelerated pace. This panel discussion will focus on the latest information on advanced lung cancer coming out of ASCO 2015 and will provide important context around the data.
 
My name is Dr. Mark Socinski, and I am the Director of the Lung Cancer Section, Division of Hematology/Oncology and Co-Director of the UPMC Lung Cancer Center of Excellence at the University of Pittsburgh. Participating today on our distinguished panel are: Dr. Mary Jo Fidler, an Associate Professor, and Lead of the Lung Cancer Translational Research Group at Rush University Medical Center; Dr. Roy Herbst, Ensign Professor of Medicine, Chief of Medical Oncology at Smilow Cancer Hospital, Yale Comprehensive Cancer Center, Yale School of Medicine; Dr. Geoffrey Oxnard, an Assistant Professor of Medicine at Harvard Medical School; and Dr. Naiyer Rizvi, Director of Thoracic Oncology and Director of Immunotherapeutics at Columbia University Medical Center in New York. Thank you all again for joining us. Let’s get started.
 
We want to start with the latest news in targeted therapy and that’s the approval of gefitinib for the use in EGFR mutation positive patients, and so Dr. Fidler, could you kind of summarize that data and put your thoughts around it?
 
Mary Jo Fidler, MD: Sure. So the IPASS trial was the first trial that showed the importance of molecularly selecting patients for first-line EGFR tyrosine kinase inhibitor therapy, and that trial showed the progression-free survival benefit that most of us have seen with gefitinib compared with the carboplatin/paclitaxel. And that benefit was repeated in a randomized trial in Japan with gefitinib and carboplatin/paclitaxel. And now we have data from a phase IV trial in Caucasian patients using gefitinib in patients with EGFR activating gene mutations. That trial did have some interesting features. First, the outcomes were what you’d expect with gefitinib in this setting with activating gene mutations, with a favorable response rate and favorable progression-free survival. But, as part of the study, they analyzed patients serum compared with tissue to see if you could detect the EGFR gene mutation with a blood test compared with tissue. And though tissue certainly is more sensitive, the trial showed that you can, in fact, detect the EGFR gene activating mutation in serum which I thought was pretty exciting.
 
Mark A. Socinski, MD: Roy, you’ve had a lot of experience with gefitinib over the years. We obviously have erlotinib and afatinib in this space. How does gefitinib add to that? What are your thoughts? How do you fit it in?
 
Roy S. Herbst, MD, PhD: Well, this is very interesting. We’ve always known this is an active drug. I think we first used this in 1998, and actually, historically, gefitinib was the first EGFR inhibitor approved. Of course, the randomized trial just missed its endpoint because we didn’t know about EGFR mutations back then and that smokers do worse than non-smokers. The drug has been used for many years in Asia and other places, so the fact that these trials now have resulted in its approval I think is a good thing, gives us another alternative to use. You might say, how is it different than erlotinib? It’s not much different, although at the dose that it’s prescribed I think the toxicity is perhaps a little bit better. Many times with erlotinib, you start at 150 mg and you have to dose reduce. I think erlotinib is a great drug, but I think gefitinib at 250 mg might be a very good alternative.
 
Mark A. Socinski, MD: Gefitinib is a nice example of a drug being developed at a biologically effective dose, way before we knew about mutations.
 
Roy S. Herbst, MD, PhD: Exactly. So it’s great to see and now we have multiple choices for these patients. Of course, we’re moving on to the next-generation of drugs and I know that at my center we’re beginning to use it. We talked about it at the conference this morning.
 
Mark A. Socinski, MD: It provides another option for patients with EGFR mutations.
 
Geoffrey R. Oxnard, MD: Mark, some docs like gefitinib because it’s flat dosing. You don’t have to dose adjust. You pick a dose and stick with it versus erlotinib which has some flexibility because you can pick a dose and then have to scale but it is a little more work to find the right dose for the patient.
 
Mark A. Socinski, MD: Roy mentioned gefitinib and erlotinib as first generation drugs, afatinib as second generation drug. We’re now on the brink of third generation drugs coming in.
Transcript Edited For Clarity
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Transcript:

Mark A. Socinski, MD: Hello and thank you for joining this OncLive TV Peer Exchange. Modern treatment of advanced lung cancer is based on tumor histology and molecular subtype, with new advances in the field happening at an accelerated pace. This panel discussion will focus on the latest information on advanced lung cancer coming out of ASCO 2015 and will provide important context around the data.
 
My name is Dr. Mark Socinski, and I am the Director of the Lung Cancer Section, Division of Hematology/Oncology and Co-Director of the UPMC Lung Cancer Center of Excellence at the University of Pittsburgh. Participating today on our distinguished panel are: Dr. Mary Jo Fidler, an Associate Professor, and Lead of the Lung Cancer Translational Research Group at Rush University Medical Center; Dr. Roy Herbst, Ensign Professor of Medicine, Chief of Medical Oncology at Smilow Cancer Hospital, Yale Comprehensive Cancer Center, Yale School of Medicine; Dr. Geoffrey Oxnard, an Assistant Professor of Medicine at Harvard Medical School; and Dr. Naiyer Rizvi, Director of Thoracic Oncology and Director of Immunotherapeutics at Columbia University Medical Center in New York. Thank you all again for joining us. Let’s get started.
 
We want to start with the latest news in targeted therapy and that’s the approval of gefitinib for the use in EGFR mutation positive patients, and so Dr. Fidler, could you kind of summarize that data and put your thoughts around it?
 
Mary Jo Fidler, MD: Sure. So the IPASS trial was the first trial that showed the importance of molecularly selecting patients for first-line EGFR tyrosine kinase inhibitor therapy, and that trial showed the progression-free survival benefit that most of us have seen with gefitinib compared with the carboplatin/paclitaxel. And that benefit was repeated in a randomized trial in Japan with gefitinib and carboplatin/paclitaxel. And now we have data from a phase IV trial in Caucasian patients using gefitinib in patients with EGFR activating gene mutations. That trial did have some interesting features. First, the outcomes were what you’d expect with gefitinib in this setting with activating gene mutations, with a favorable response rate and favorable progression-free survival. But, as part of the study, they analyzed patients serum compared with tissue to see if you could detect the EGFR gene mutation with a blood test compared with tissue. And though tissue certainly is more sensitive, the trial showed that you can, in fact, detect the EGFR gene activating mutation in serum which I thought was pretty exciting.
 
Mark A. Socinski, MD: Roy, you’ve had a lot of experience with gefitinib over the years. We obviously have erlotinib and afatinib in this space. How does gefitinib add to that? What are your thoughts? How do you fit it in?
 
Roy S. Herbst, MD, PhD: Well, this is very interesting. We’ve always known this is an active drug. I think we first used this in 1998, and actually, historically, gefitinib was the first EGFR inhibitor approved. Of course, the randomized trial just missed its endpoint because we didn’t know about EGFR mutations back then and that smokers do worse than non-smokers. The drug has been used for many years in Asia and other places, so the fact that these trials now have resulted in its approval I think is a good thing, gives us another alternative to use. You might say, how is it different than erlotinib? It’s not much different, although at the dose that it’s prescribed I think the toxicity is perhaps a little bit better. Many times with erlotinib, you start at 150 mg and you have to dose reduce. I think erlotinib is a great drug, but I think gefitinib at 250 mg might be a very good alternative.
 
Mark A. Socinski, MD: Gefitinib is a nice example of a drug being developed at a biologically effective dose, way before we knew about mutations.
 
Roy S. Herbst, MD, PhD: Exactly. So it’s great to see and now we have multiple choices for these patients. Of course, we’re moving on to the next-generation of drugs and I know that at my center we’re beginning to use it. We talked about it at the conference this morning.
 
Mark A. Socinski, MD: It provides another option for patients with EGFR mutations.
 
Geoffrey R. Oxnard, MD: Mark, some docs like gefitinib because it’s flat dosing. You don’t have to dose adjust. You pick a dose and stick with it versus erlotinib which has some flexibility because you can pick a dose and then have to scale but it is a little more work to find the right dose for the patient.
 
Mark A. Socinski, MD: Roy mentioned gefitinib and erlotinib as first generation drugs, afatinib as second generation drug. We’re now on the brink of third generation drugs coming in.
Transcript Edited For Clarity
View Conference Coverage
Online CME Activities
TitleExpiration DateCME Credits
Oncology Briefings™: Updates in Novel Therapeutic Options for Lung Neuroendocrine TumorsMay 31, 20181.0
Community Practice Connections™: Working Group to Optimize Outcomes in EGFR-mutated Lung Cancers: Evolving Concepts for Nurses to Facilitate and Improve Patient CareJun 30, 20181.5
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