Lung Cancer Q&A: Any New Research or Treatment for Patients With the TP53 Mutation?

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Topics include: Ask the Expert

Patient Power community member Leo wants to know if there are any research developments for lung cancer patients with the TP53 mutation? Lung cancer experts Dr. Jhanelle Gray and Dr. Theresa Boyle, both from the Moffitt Cancer Center, respond by explaining the course of treatment for patients with genetic mutations and discussing current lung cancer clinical trials with tumor suppressor therapies. Watch now to find out more. 

This is a Patient Empowerment Network program produced by Patient Power, in partnership with Moffitt Cancer Center. We thank AbbVie, Inc., Celgene Corporation, Foundation Medicine, and Novartis for their support.

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Transcript

Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you.

Andrew Schorr:

This one came in from Leo. And Leo says, “Any new research or treatment regarding patients with the TP53 mutation?” So, first of all, Dr. Boyle, what is TP53?

Dr. Boyle:                   

Oh, goodness. I don’t off the top of my head know how that spells out, but it is a tumor suppressor protein. And it’s a gene which we find frequently mutated in all cancer types. And it often causes a worse prognosis. And there are many researchers trying to see if there are better drugs to target therapies. And lung cancer, the clinical trials are pretty early. The highest you get is Phase I and II. So, there has not been a lot of success yet. In leukemia I think there’s more phase two trials. 

We have an excellent researcher here, Elsa Flores, who is looking at animal models in vivostudies to try to understand more. Now, one thing sort of interesting about TP53 is that if you have lung cancer with TP53 and a KRAS mutation, that mutation is gonna be more likely to respond to immunotherapy.

Dr. Gray:                     

KRAS mutation.

Dr. Boyle:                   

There’s a really nice paper out by John Heymach about this if there’s also an STK11 mutation. So, then it’s a lower likelihood of response to immunotherapy.        

So, with more and more research we’re lending some of the nuances of these and we’re hopeful that there’s going to be more that can be done with the TP53 mutations in the future.

Andrew Schorr:          

Okay. So, Dr. Gray. So, you were nodding your head while she explained that?

Dr. Gray:                     

Yeah, yeah. 

Andrew Schorr:          

So, in other words, you’re looking at not just one gene being the bad guy, but this constellation in a given patient.

Dr. Gray:                     

Right.

Andrew Schorr:          

And does that tell you something that you could do in a more refined way for them?

Dr. Gray:                     

Right. I think this is we’re coming into a center where we have this level of expertise and we’re sharing data across the different centers. But exactly what Dr. Boyle noted is that when we look at these genomic reports, right, you’re getting a lot of information coming out back at the medical oncologist. And knowing how to fully understand and interpret that data so you can make the best decisions for the patient is very helpful. 

So, if we see a KRAS mutation, the P53, without an STK11 mutation, certainly that will move immunotherapy up on for the armamentarium for the patient. Now, this is a little bit in experimental mode, but we’ve seen similar data here at Moffitt. And it’s really starting to pick up traction across different cancer centers and lung cancer experts.

Around the specific question of the P53 mutation, we do have a compound that we’re looking at here in collaboration with AstraZeneca. It came from a trial that I had written and am working on that came from work derived here from Moffitt Cancer Center. It’s called AZD1775. But it basically what it is is it’s looking at inhibiting the cell cycle. I’m gonna take us back to biology a little bit. And cells, how they replicate, basically they have to go through mitosis, right? You have to replicate your DNA and then split off and divide. 

And so, what the P53 does is it’s almost—as Dr. Boyle mentioned, it’s a tumor suppressor. What does that mean? It actually puts a stopgap, an intentional stopgap when cells go to replicate. And it makes the cell stop and check and say, “Do I have any mutations? Should I move forward or not?” What cancer cells do is they’ve lost—they mutate the P53. So, they don’t get that stop in place. They just keep replicating. Even though technically these are abnormal cells, they’re damaged cells and they shouldn’t replicate themselves. 

So, what that drug does is it intentionally incorporates—if you have that P53 mutation your cells are not stopping when they’re replicating abnormally. This AZD1775 helps to add that stop so the cells can check themselves and say, “Hey, you know what? We’re really not replicating ourselves properly. We should actually go towards cell death and not cell survival and replication.” So, there are definitely trials that are looking at the P53, to Dr. Boyle’s point, including one that was derived here. And as Ed mentioned, something that you can only find here at Moffitt. And we hope to have that data out maybe later this year or early next year.

Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you.

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Page last updated on September 9, 2019