Johns Hopkins Kimmel Cancer Center Podcasts
Oct 8, 2026 · 17 min · 7 segments
Dr Bill Nelson speaks with Dr Neeha Zaidi about the progress being made against pancreatic cancer and the promise on the horizon from the development of pancreatic cancer vaccines.
Neeha ZaidiGuest
Bill NelsonHost
Now we get down to business, if you will, where you and others are really trying to focus some efforts, is, you know, all cancers are fundamentally disorders of acquired defects in genes and gene function.

But pancreatic cancers are incredibly tightly associated with acquired defects in the KRAS gene, which is basically the mutation's effectively converted into an on switch, which is driving uncontrolled growth and other bad behaviors, um, that, that, that are unchecked.

But now, of course, immunotherapists and people trying to build drugs have those set of mutant, those defective proteins firmly in their sights.

And so we have a drug, which you can tell us a little bit about, diraxunrasib, just out treating pancreas cancer.

And of course, then we'll get to what you're doing, which is trying to target it for immunotherapy.

That's super exciting and really, really a game changer in the way that we're gonna treat, uh, that we are actually and currently treating pancreas cancer, and is gonna really transform the way, continue to transform the way we treat pancreas cancer.

So as you mentioned, mutations in this gene called KRAS occur very early on in the majority of precursor lesions.

So I always say that this may be actually the model cancer to go after in terms of treatment, and also as we'll talk about in the prevention setting, because we do know that there's the singular target that drives the growth of this cancer.

The one I'll talk- About first is the mechanism that diraxantrasib is using, which is to actually inhibit that pathway using a small molecule inhibitor.

And so that really shuts down the growth of the cancer for a much longer time than we had seen before.

So the recent trial that got a lot of attention was actually looking at patients who had gotten chemotherapy versus patients who were getting diraxantrasib in a randomized fashion.

So patients either got chemotherapy or diraxantrasib, which is the inhibitor of KRAS, and the patients who got diraxantrasib lived for twice as long.

Obviously, all these pills are, have some side effects, but most of the time can be managed.

So the fact that we're seeing an oral pill actually work in patients in doubling overall survival is super exciting.

And, you know, looking back as a fellow now 10 years ago, I never thought this day would come, and it really has, and it's, it's amazing.

So that's one approach, is to use small molecule inhibitors to actually target mut- mutations in KRAS.

Now we get down to business, if you will, where you and others are really trying to focus some efforts, is, you know, all cancers are fundamentally disorders of acquired defects in genes and gene function.

But pancreatic cancers are incredibly tightly associated with acquired defects in the KRAS gene, which is basically the mutation's effectively converted into an on switch, which is driving uncontrolled growth and other bad behaviors, um, that, that, that are unchecked.

But now, of course, immunotherapists and people trying to build drugs have those set of mutant, those defective proteins firmly in their sights.

And so we have a drug, which you can tell us a little bit about, diraxunrasib, just out treating pancreas cancer.

And of course, then we'll get to what you're doing, which is trying to target it for immunotherapy.

That's super exciting and really, really a game changer in the way that we're gonna treat, uh, that we are actually and currently treating pancreas cancer, and is gonna really transform the way, continue to transform the way we treat pancreas cancer.

So as you mentioned, mutations in this gene called KRAS occur very early on in the majority of precursor lesions.

So I always say that this may be actually the model cancer to go after in terms of treatment, and also as we'll talk about in the prevention setting, because we do know that there's the singular target that drives the growth of this cancer.

The one I'll talk- About first is the mechanism that diraxantrasib is using, which is to actually inhibit that pathway using a small molecule inhibitor.

And so that really shuts down the growth of the cancer for a much longer time than we had seen before.

So the recent trial that got a lot of attention was actually looking at patients who had gotten chemotherapy versus patients who were getting diraxantrasib in a randomized fashion.

So patients either got chemotherapy or diraxantrasib, which is the inhibitor of KRAS, and the patients who got diraxantrasib lived for twice as long.

Obviously, all these pills are, have some side effects, but most of the time can be managed.

So the fact that we're seeing an oral pill actually work in patients in doubling overall survival is super exciting.

And, you know, looking back as a fellow now 10 years ago, I never thought this day would come, and it really has, and it's, it's amazing.

So that's one approach, is to use small molecule inhibitors to actually target mut- mutations in KRAS.
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