VISIT US IN CHICAGO JUNE 2-4 AT BOOTH 2073!

Select Topic:
Browse by Series:

Final Thoughts on Squamous NSCLC Research

Panelists: Mark A. Socinski, MD, Florida Hospital Cancer Institute; Tracey L. Evans, MD, University of Pennsylvania; David M. Jackman, MD, Dana-Farber Cancer Institute; Edward S. Kim, MD, Levine Cancer Institute; Jared Weiss, MD, UNC Lineberger Comprehensive Cancer Center
Published: Thursday, Mar 30, 2017



Transcript:

Mark A. Socinski, MD:
David, are there any hot, new ideas drug-wise in squamous disease?

David M. Jackman, MD: Absolutely. Obviously, we’ve talked a lot about immunotherapy alone, or potentially, in combination. That will remain, I think, the most exciting potential area for squamous patients. But beyond that, I think we back up a little to some of the seminal work of Peter Hammerman, when he was at Dana-Farber Cancer Institute, and Paul Paik of Memorial Sloan Kettering Cancer Center, where they had published information looking at the squamous genome. We talked about how we don’t see targetable mutations in squamous disease. And I think that’s something we’re trying to crack at. We see that squamous patients can have PIK3CA mutations, PTEN loss, and FGFR mutations.

Now we’ve moved forward and we look at the Lung-MAP study that is trying to study squamous patients’ tumors, and then, depending on what we find, putting them on a sub-study arm—if we find an FGFR mutation, we’re putting them on treatment with a FGFR inhibitor. We are looking at patients with CDK inhibitors, and we are looking at patients with PIK3CA mutations getting specific drugs. I think, ultimately, we’re going to try to figure out if these are mutations that we’re seeing, are they druggable? Does drugging them potentially alter the course of these tumors, or is it just that these are not a strong enough driver of disease?

Mark A. Socinski, MD: And having said that, the Lung-MAP trial, if our audience has the ability to accrue to it, that’s an important trial for us to do.

David M. Jackman, MD: Absolutely.

Mark A. Socinski, MD: I want to thank you guys. This has been extremely informative. Before we get to the end of this discussion, I’d like to get your final thoughts. I’ll start with you, Tracey.

Tracey L. Evans, MD: I think we’ve got a lot of new hope for this patient population, but we need to remember that a lot of these agents won’t work for people. I used to be a big erlotinib fan, before anyone died of their non–small cell lung cancer, because it had that small survival benefit. I don’t think that way anymore, in part because there are so many other options. I’m not tolerating these drugs that don’t work well. And also, I think it gets in the way of the important work that all of our patients have to do, and that is, facing the fact that they have a terminal illness. It’s wonderful when these drugs work, but we need to remember to support our patients when they don’t.

Mark A. Socinski, MD: David?

David M. Jackman, MD: I hope that, for our squamous cell patients, we learned lessons from what we’ve done in nonsquamous patients. We need to get adequate biopsies so that we can do these tests, so that we can check PD-L1, and so we can potentially enroll them on the Lung-MAP trial. For all of our squamous cell patients, I hope that we’re getting adequate biopsies so we can inform our treatment decisions.

Mark A. Socinski, MD: Ed?

Edward S. Kim, MD: What a cool time to be in lung cancer! You have people, now, who are actively seeking, who want to be thoracic oncologists because of all the stuff that’s happening—EGFR mutations, ALK translocations, ROS1, and now PD-L1. It’s phenomenal stuff. I think, again, to the community oncologists out there—I deal with many of them in our system, you deal with them now—you have to test for biomarkers. Please test for biomarkers.

Mark A. Socinski, MD: Jared?

Jared Weiss, MD: I think historically, in squamous lung cancer, every time we had an advance that we thought was “it,” it turned out to be incremental. And I think many who have been around this field for some time are afraid we’re going to do the same here. I’d like to sound a note of hope in a prediction that I don’t think that the checkpoint inhibitors are going to be a one-off incremental advance. I think they’re the beginnings of something much larger, that legitimately is going to translate to some cure or something cure-like—durable control in a larger percentage of patients than even our greatest optimists are imaging right now.

Mark A. Socinski, MD: Well, I’m the senior member of this panel, and I will tell you that I trained at a time in lung cancer where we argued whether or not lung cancer could be treated at all. And that wasn’t that long ago. This has been wonderful. I want to thank you all for your contributions to this discussion. On behalf of our panel, we thank you for joining us, and we hope you found this Peer Exchange® discussion to be useful and informative.

Transcript Edited for Clarity

Slider Left
Slider Right


Transcript:

Mark A. Socinski, MD:
David, are there any hot, new ideas drug-wise in squamous disease?

David M. Jackman, MD: Absolutely. Obviously, we’ve talked a lot about immunotherapy alone, or potentially, in combination. That will remain, I think, the most exciting potential area for squamous patients. But beyond that, I think we back up a little to some of the seminal work of Peter Hammerman, when he was at Dana-Farber Cancer Institute, and Paul Paik of Memorial Sloan Kettering Cancer Center, where they had published information looking at the squamous genome. We talked about how we don’t see targetable mutations in squamous disease. And I think that’s something we’re trying to crack at. We see that squamous patients can have PIK3CA mutations, PTEN loss, and FGFR mutations.

Now we’ve moved forward and we look at the Lung-MAP study that is trying to study squamous patients’ tumors, and then, depending on what we find, putting them on a sub-study arm—if we find an FGFR mutation, we’re putting them on treatment with a FGFR inhibitor. We are looking at patients with CDK inhibitors, and we are looking at patients with PIK3CA mutations getting specific drugs. I think, ultimately, we’re going to try to figure out if these are mutations that we’re seeing, are they druggable? Does drugging them potentially alter the course of these tumors, or is it just that these are not a strong enough driver of disease?

Mark A. Socinski, MD: And having said that, the Lung-MAP trial, if our audience has the ability to accrue to it, that’s an important trial for us to do.

David M. Jackman, MD: Absolutely.

Mark A. Socinski, MD: I want to thank you guys. This has been extremely informative. Before we get to the end of this discussion, I’d like to get your final thoughts. I’ll start with you, Tracey.

Tracey L. Evans, MD: I think we’ve got a lot of new hope for this patient population, but we need to remember that a lot of these agents won’t work for people. I used to be a big erlotinib fan, before anyone died of their non–small cell lung cancer, because it had that small survival benefit. I don’t think that way anymore, in part because there are so many other options. I’m not tolerating these drugs that don’t work well. And also, I think it gets in the way of the important work that all of our patients have to do, and that is, facing the fact that they have a terminal illness. It’s wonderful when these drugs work, but we need to remember to support our patients when they don’t.

Mark A. Socinski, MD: David?

David M. Jackman, MD: I hope that, for our squamous cell patients, we learned lessons from what we’ve done in nonsquamous patients. We need to get adequate biopsies so that we can do these tests, so that we can check PD-L1, and so we can potentially enroll them on the Lung-MAP trial. For all of our squamous cell patients, I hope that we’re getting adequate biopsies so we can inform our treatment decisions.

Mark A. Socinski, MD: Ed?

Edward S. Kim, MD: What a cool time to be in lung cancer! You have people, now, who are actively seeking, who want to be thoracic oncologists because of all the stuff that’s happening—EGFR mutations, ALK translocations, ROS1, and now PD-L1. It’s phenomenal stuff. I think, again, to the community oncologists out there—I deal with many of them in our system, you deal with them now—you have to test for biomarkers. Please test for biomarkers.

Mark A. Socinski, MD: Jared?

Jared Weiss, MD: I think historically, in squamous lung cancer, every time we had an advance that we thought was “it,” it turned out to be incremental. And I think many who have been around this field for some time are afraid we’re going to do the same here. I’d like to sound a note of hope in a prediction that I don’t think that the checkpoint inhibitors are going to be a one-off incremental advance. I think they’re the beginnings of something much larger, that legitimately is going to translate to some cure or something cure-like—durable control in a larger percentage of patients than even our greatest optimists are imaging right now.

Mark A. Socinski, MD: Well, I’m the senior member of this panel, and I will tell you that I trained at a time in lung cancer where we argued whether or not lung cancer could be treated at all. And that wasn’t that long ago. This has been wonderful. I want to thank you all for your contributions to this discussion. On behalf of our panel, we thank you for joining us, and we hope you found this Peer Exchange® discussion to be useful and informative.

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
Publication Bottom Border
Border Publication
x