Isocitrate dehydrogenase 1
12
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7
EPISODES
7
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Search complete. 12 mentions across 7 episodes found for "Isocitrate dehydrogenase 1".
Oct 23, 2026
Amy BrownleeHOST
So this is showing the variety of actionable or therapeutically targetable aberrations that have been found in biliary tract carcinoma.
Amy BrownleeHOST
A lot of these can be readily identified with NGS testing, such as your FGFR rearrangements, IDH1 mutation, and different biliary tracts arising at different portions along the biliary tree have different propensity for these types of aberrations.
Amy BrownleeHOST
Importantly, you'll note that some biliary tract cancers also show ERBB2 amplification, i.e. HER2 positivity.
Amy BrownleeHOST
And so HER2 targeted therapies, again, are an option for patients with biliary tract cancers.
Jay ChaplinHOST
It's less important than the genetics of the cancer.
Jay ChaplinHOST
If someone has a cancer with an IDH1 mutation, That gives certain particular features.
Jay ChaplinHOST
It will do better.
Jay ChaplinHOST
It will grow faster in some people.
Hop Tran CaoGUEST
And I do suspect that there's also patients that we, looking back, will have written off for surgery who, if we had put them through the right sequence of treatment, may ultimately benefit, uh, from surgical exploration.
Hop Tran CaoGUEST
I say this in the sense that it's not uncommon for us, for instance, again, with cer-certain patients with intrahepatic cholangiocarcinoma with favorable quote, unquote, "mutations," IDH1, right, who have metastatic disease to distant nodal stations or distant, you know, peritoneal disease even, who, because the disease can respond well to treatment, ultimately can get surgery to clear that disease, and then they do seem to derive a survival benefit from that clearance of gross disease.
Hop Tran CaoGUEST
So I think there's a lot to learn still.
Hop Tran CaoGUEST
Ultimately, everything that we do and everything we've learned so far reinforces the notion that disease biology drives everything, and, and that's where we still fall well short right now.
Sean GlennGUEST
So what we've been able to do is we've been able to, you know, build all these genes and all these different mutation types into a singular NGS panel.
Sean GlennGUEST
But really where the strength resides is we really needed to be within that less than three-day window because for a lot of NCCN and ELN guidelines, especially around AML, you need to have a FLT3, IDH1, IDH2, MPM1 mutation calling within the first three to five days.
Sean GlennGUEST
And then within the first week, a myriad of other mutations and mutation types for care.
Sean GlennGUEST
And that's in the
AndyHOST
Today we're joined once again by Dave Bolton, a sub 1% survivor of...
Dave BoltonGUEST
A glioblastoma multiforme IDH1 wild type.
Dave BoltonGUEST
You can see why I
AndyHOST
didn't want to say it.
6 MINS LATER
Dave BoltonGUEST
I just moved on to six months.
Dave BoltonGUEST
And when I walked in, it was a scan that changed everything.
Dave BoltonGUEST
So it was a glioblastoma, multiforme, IDH1 wild type.
Dave BoltonGUEST
It is known in the medical world as the Terminator because it is relentless.
Joe AmabileGUEST
Um, so when we went and saw the oncologist at MSK, they looked at it and they're like, "Yep, looks like a low-grade glioma.
Joe AmabileGUEST
Um, my guess is it's IDH mutation." Um, which is what you want.
Kaitlyn BristoweHOST
Okay.
Joe AmabileGUEST
Which is the slowest ty- uh, was, which is the slowest, um, growing tumor you could have.
16 MINS LATER
Joe AmabileGUEST
... yeah, I mean, I would be like, "Is my brain tumor growing?"
Kaitlyn BristoweHOST
Right.
Joe AmabileGUEST
Like, is it, is it, is it growing? Which it wasn't, um, because I, I do have an, like I said, an IDH mutation.
Kaitlyn BristoweHOST
But the brain is so powerful too.
Raj ChakrabortyHOST
So for example, the TP53 mutation, which we all know are very adverse risk, they were seen in about 10.5% in the AZAVEN arm, versus 18.6% in the intensive chemo arm, of course, favoring the Azaven arm.
Raj ChakrabortyHOST
Then the IDH1-2 mutations, which we know as venetoclax sensitizing, it was seen in 31% of the Azaven arm versus about half of that 18.6% in the intensive chemo arm.
Raj ChakrabortyHOST
And the NPM1 mutation was seen in about 12.8% in the Azaven arm versus less than half of that 5.8% in the intensive chemo arm.
Raj ChakrabortyHOST
Curtis, what do you make of these molecular imbalances? Do you think in a small trial like this with 86 patients per arm, these imbalances could have materially influenced outcomes?
Curtis LachowiczGUEST
However, to your point, Raj,
Ashwin KishtagariHOST
you know,
Curtis LachowiczGUEST
TB53 mutations, higher in the IC arm, IDH1 and 2 mutations, which, you know, the data is strongest for IDH2 being more sensitive to HMA-ven, but biologically IDH1 mutations are also sensitive to HMA-ven combinations.
Curtis LachowiczGUEST
And so that's a pretty big imbalance there.