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Addressing Limitations in EGFR Exon 20-Mutant NSCLC

Insights From: John Heymach, MD, PhD, MD Anderson Cancer Center
Published: Wednesday, Apr 25, 2018



Transcript: 

John Heymach, MD, PhD: The initial study, that we presented, highlights that it is possible to target EGFR exon 20 mutations. Before, there was concern that a tyrosine kinase inhibitor couldn’t be developed for this group because of certain structural constraints that happen when you get these insertions. That’s the good news, that there are certainly drugs that are active. But clearly, additional studies are going to need to firm up what the response rate is overall. And how durable is the benefit? What’s the tolerability look like, over time? Those things are all being looked at in ongoing studies. It’s going to be very important, in the subsequent follow-up phase II study that’s going on across the country, to validate and verify those initial results.

More broadly, I think it’s very exciting that there are other drugs in the pipeline for both EGFR and HER2 exon 20. There’s one, from a company called Ariad, now Takeda, that’s in clinical testing, and there are several others that are out there that are in development or are moving along. So, I think it’s an exciting time. A variety of different drugs may potentially benefit this group of patients. Nationwide, if you look at the different tumors, we estimate that at least 6000 to 9000 lung cancer patients a year could benefit from this. And across all of the different diseases, it may be more than 20,000 people a year—in patients who have exon 20 mutations. When you add up all of those different groups, this is not a miniscule group of patients. Exon 20-mutant diseases, together, would be one of the more common cancer killers. It would a top 10 killer. So, this is really an unmet need. It’s exciting to see that there are some advances being made.

Transcript Edited for Clarity 
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Transcript: 

John Heymach, MD, PhD: The initial study, that we presented, highlights that it is possible to target EGFR exon 20 mutations. Before, there was concern that a tyrosine kinase inhibitor couldn’t be developed for this group because of certain structural constraints that happen when you get these insertions. That’s the good news, that there are certainly drugs that are active. But clearly, additional studies are going to need to firm up what the response rate is overall. And how durable is the benefit? What’s the tolerability look like, over time? Those things are all being looked at in ongoing studies. It’s going to be very important, in the subsequent follow-up phase II study that’s going on across the country, to validate and verify those initial results.

More broadly, I think it’s very exciting that there are other drugs in the pipeline for both EGFR and HER2 exon 20. There’s one, from a company called Ariad, now Takeda, that’s in clinical testing, and there are several others that are out there that are in development or are moving along. So, I think it’s an exciting time. A variety of different drugs may potentially benefit this group of patients. Nationwide, if you look at the different tumors, we estimate that at least 6000 to 9000 lung cancer patients a year could benefit from this. And across all of the different diseases, it may be more than 20,000 people a year—in patients who have exon 20 mutations. When you add up all of those different groups, this is not a miniscule group of patients. Exon 20-mutant diseases, together, would be one of the more common cancer killers. It would a top 10 killer. So, this is really an unmet need. It’s exciting to see that there are some advances being made.

Transcript Edited for Clarity 
View Conference Coverage
Online CME Activities
TitleExpiration DateCME Credits
Community Practice Connections™: Oncology Best Practice™ Decision Points in Advanced NSCLC: Assessing Treatment Options Beyond Disease ProgressionNov 30, 20181.0
Community Practice Connections™: Precision Medicine for Community Oncologists: Assessing the Role of Tumor-Testing Technologies in Cancer CareNov 30, 20181.0
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