Transcript
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Janet Freeman-Daily:
Okay. So there are certain known mutations for which we have approved drugs. Can you talk about those?
Dr. Camidge:
So the—the first example is the EGFR, epidermal growth factor receptor, that was discovered in about 2004. But it didn’t really become truly recognized as a driver that would influence your first-line treatment decision making until about 2009. And then, for a while, that was considered the exception. And strangely enough, the second example, I think, is what helped to really change the field. And the second example was something called ALK, an anaplastic lymphoma kinase gene rearrangement. EGFR mutations are about 10 to 15 percent of lung cancer in the—the west. ALK is about 4 percent.
So they’re little slices of the pie. Each one saying I need a different treatment. And so there are licensed ALK inhibitors. There are licensed EGFR inhibitors. The—the newest kid on the block is what you’ve got. So ROS1, yes, I know, a little shout-out to Janet. So ROS1, gene rearrangements, behave, a little bit like ALK inhibitors. They respond to some of the same drugs, not all of them, but some of them.
And they recently extended the license of crizotinib (Xalkori) to include ROS1. And then, there’s going to be a wave of other little mutations with specific target therapies, which I’m sure we’re going to see licensed in the next year or so.
Janet Freeman-Daily:
So are there any newly approved drugs that you would add to this list besides crizotinib for ROS1?
Dr. Camidge:
I mean, what’s going to—so for those of you that—so, you know, if you’re viewing this at home months later, then, the stuff that’s going to happen is BRAF-V600E mutations, which is probably about 2 percent of adenocarcinoma of the lung is the same mutation that drives a significant proportion of melanoma. So they’ve done the heavy lifting. They’ve already found a combination of something called a BRAF inhibitor and a MEK inhibitor that work very nicely. And that is, almost certainly, going to get licensed probably sometime in 2017 for BRAF-mutant lung cancer.
MET exon 14 skip mutations, which are about 4 percent of adenocarcinoma of the lung, also respond to crizotinib. So crizotinib is the gift that keeps on giving. It keeps finding little niche indications. What else?
Dr. Mohindra:
RET, but they—I don’t think they’ll have an indication. And then, through—like you were saying, acquired resistance. There’s another drug under the epidermal growth factor inhibitors, osimertinib or Tagrisso, that’s already out on the market.
Janet Freeman-Daily:
And—and gets into the brain, as I understand it.
Dr. Mohindra:
It does, it does.
Janet Freeman-Daily:
Yes.
Dr. Camidge:
Well, we can talk about that. So getting into the brain is not an all-or-none phenomenon. And one of the challenges there is how good are we at describing activity in the brain? And I think as we’ve started to recognize, for many of these things, that we’re getting good at controlling disease in the body, recognizing the brain as a relevant battleground has thrown into sharp relief how terrible we have been at describing activity in the brain.
We just didn’t have the tools to capture that information. And so we need to be careful that one scan of somebody with a spot on the brain getting smaller is not proof of brain activity any more than one CT scan of a chest with a module getting smaller is proof of activity. We need to know a denominator that’s one out of one, one out of 100. How long does that control work? So that is still a work in progress.
Published By :
Patient Power
Date :
Nov 23, 2016
