Research reveals that while mutations are necessary for cancer development, inflammation is the critical factor that allows cancer cells to transform and grow; this discovery opens possibilities for cancer interception using anti-inflammatory drugs, as demonstrated by Novartis's IL-1 beta blocker that unexpectedly reduced lung cancer incidence in cardiovascular trials, with current clinical trials testing this approach to prevent lung cancer before it develops.
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Could a pill prevent the world’s deadliest cancer?Hinzugefügt:
You know, when I was in medical school, we learned that you get cancer because, [music] you know, you're smoking cigarettes, you're going to the beach, and then at the same time you're accumulating all these mutations.
Globally, lung cancer kills more people [music] than breast cancer, prostate cancer, and blood cancers combined.
But research shows that nearly 80% of lung [music] cancer could be avoided.
And this has driven scientists to reanalyze everything they [music] know about the causes of lung cancer. Your body is going to probably develop 100 to 1,000 cancers today, and your [music] immune system is going to immediately eliminate the majority of them. And this we did trigger, you know, this interesting understanding of this mutation really the cause of cancer.
Whilst mutations caused by things like smoking are key drivers of cancer, new research [music] is showing there's another piece to the puzzle.
Inflammation. Inflammation, [music] now we have realized is really a key event in lung cancer initiation.
You can have mutations, [music] and you don't develop cancer. You're only developing cancer in the setting of inflammation. This suggests that we can intervene, right?
We can intersect.
Now, this global team is racing to show that they can [music] use this link with inflammation to stop cancer before it begins.
Stopping mutation is something very difficult. However, we know how to stop inflammation.
So, now we think that [music] this molecule, yes, can prevent lung cancer.
I'm Nolan [music] Harris. I have been coming to the Mount Sinai Cancer Care Center for the last 4 years um, because I had been diagnosed [music] with stage 4 non-small cell lung cancer with a metastasis to the brain in July [music] of '22.
It's a mouthful to get through.
>> [laughter] >> Nolan has been living [music] with her diagnosis for 4 years now.
And she's been treated by Dr. Tom Marron. [music] Nolan is one of the most well-versed patients I've ever had and she's extremely educated and and she came in with a very early stage cancer. [music] >> Initially, the idea was they would just remove that [music] section, about 20% of my lung, and I would also be on this [music] trial therapy to prevent it from appearing anywhere else [music] in the lung.
But as part of that, we always do a screening scan of the brain to make sure that lung cancer [music] hadn't spread to the brain cuz unfortunately that happens sometimes. And when we did a screen of [music] her brain, we did indeed find that she had had cancer that had already spread. Even though her primary cancer was extremely small. It took me on a completely different path, the path that I have today. Nolan's path [music] involved courses of steroids, radio neurosurgery, three-monthly checkups, [music] ongoing targeted therapies, endless scans, and then there's the side effects.
Nail and skin issues, scalp issues, even joint issues that has been addressed pretty successfully with physical therapy. I take calcium supplements, magnesium supplements. I I'm I'm I'm a walking pharmacy.
>> [laughter] >> But I'm walking.
Thanks to Nolan's determination and cutting-edge treatment, she's been doing well for the last 4 years. But that could so easily not have been the case.
Nolan only caught her cancer by chance [music] during a test on her heart. But with hindsight, it surprises her she wasn't considering the possibility [music] of lung cancer from the beginning.
My history with lung cancer is quite accidental.
And to to say it's [music] accidental is a little ironic because I have what is [music] clearly a family history now. A first female cousin and my [music] sister both non-smokers who both succumbed to this disease [music] before the age of 50. And yet it wasn't until her diagnosis that Nolan considered this as a trend.
We have a skyrocketing population of patients that have never smoked before and they're coming to me, you know, on their first diagnosis with brain metastases [music] and and cancer everywhere and most of the cancers that are arising in patients that never smoked they're not very responsive to immunotherapy the way that a smoking related cancer is. And so these patients are inherently incurable right now in 2026. And so we really need to find a way to identify these patients before [music] it's spread to their brain, before it spreads to their lungs.
>> [music] >> Tom wants to find a way to stop cancer before it starts.
This is referred to as cancer [music] interception and it's a relatively new field that's gaining traction in the cancer research community.
Tom works in this lab at Mount Sinai run by Dr. Miriam Merad.
Miriam is placing a laser focus on interception.
Within the 21st century, you know, this is what we should be thinking about, right? How we can prevent diseases as much as can.
Because I think we can.
And to do it, she's reshaping some of the basic approaches [music] to cancer treatment and diagnosis.
>> [music] >> I think our recent realization is that we had focused so long on mutation, you know, the the mutation of cells that contribute to lung cancer. So, for example, we know that we have more cancer with age because we accumulate these mutations. So, the our cells, you know, becomes more damaged and they are more prone to being deregulated.
And and to become cancerous. Until we realized, uh, through, for example, autopsies, that we had lot of mutation in many places in our body. In fact, the first study that suggested it is when we started to biopsy eyelids. And we saw that with age, we accumulated mutation everywhere.
And this really triggered, you know, this interest in understanding, are these mutations really the cause of cancer? Miriam and Thomas' work is contributing to a growing body of research, which suggests that mutation alone is not enough to cause cancer.
There's another factor.
Inflammation. Yes, those mutations absolutely contribute to dysregulation of the cells that will become [music] cancerous, or malignant, but that's not enough. Everybody watching this right now, you your body is going to probably develop 100 to 1,000 cancers today, and your immune system is going to immediately eliminate the majority of them. If you don't have an environment that's also permissive, the cells will not transform. When I say transform, [music] it's that the cells become malignant. The cells become the cancer cell.
So, the realization that [music] somehow inflammation contribute or is necessary, right, for cancer initiation, suggest that we can intervene, right, we can intercept. Stopping mutation is something very difficult. However, we know uh how to stop inflammation. The link Miriam Tom and her collaborators think they've found gives them a new opportunity. Rather than fight a tumor, they could prevent the environment it needs to grow in the first place.
And they hope they can do it using a simple pill. We are very excited by the prospect of of using an immunomodulatory drug to prevent lung [music] cancer. And the reason why we think we are close is that an experiment [music] has been done, in fact, in patients and was successful.
So, many years ago, a company called Novartis was using an immunomodulatory drug to block an inflammatory molecule called IL-1 beta, and they were using it not to stop lung cancer, but to reduce cardiovascular events. And so, they gave these anti-inflammatory drugs to 10,000 individuals, and it did reduce cardiovascular events, but what it did, and which we didn't anticipate at that time, is that it reduced lung cancer incidence. Okay? You know, when something works by serendipity, the one thing they want to do is to test it properly. So, many of us, when we saw this data, we went back to our our animal models, and we started to do the proper experiments. Is it correct? Like, can we stop lung cancer by just modulating this inflammatory molecule?
And indeed, we saw the molecular rationale. In fact, my group saw that we can even block additional one to further reduce that risk. Now, what we have is to go back and test it properly in clinical trial. And those clinical trials are starting now.
We have a trial that is already open um that is accruing patients. So we have I believe 20 to 40 patients are going to be in this first trial. Those are the patients where we're putting on an anti-inflammatory regimen. And we've designed this trial in a [music] in a similar fashion to some of our collaborators where we're going to try many different therapies and try to you know basically pick the best one and then between our institutions we'll do a much larger trial once we see [music] you know a really good clinical signal.
Trials are starting and doctors are hopeful.
>> [music] >> But the treatment is just one part of the puzzle.
Many people will develop what are called pre-cancerous lesions, >> [music] >> but only a small subset of those will ever actually turn into cancer.
So who should doctors target their therapy towards? The challenge starts when we are thinking about pre-cancer [music] lesions.
These pre-cancer lesions that are detectable by imaging, let's say by CT scan, sometimes have different trajectories, right? And some may stay, you know, at the pre-cancer stage for ever. And other will progress. And this is the challenge we have. Which are the one that we need to treat because they are going to progress to lung cancer.
Because if they don't, then we don't want to intervene. We never give a drug to someone that doesn't need it. If right? We don't even take a piece of Advil if it's not [music] necessary, right? And we shouldn't. Even if Miriam and Tom could prevent cancer with a drug, the question remains, who should take it?
And how do [music] you find them?
The Treebed started several years ago with me wanting a way to quiet my mind my my racing mind. [music] Colette Smith is a lung cancer survivor and patient advocate who through her organization Healing the Bronx [music] brings information about cancer treatments, diagnosis, and importantly screening to her community.
And it grew, [music] it blossomed into cancer awareness education beneath the tree [music] beds, subtle signage that said to the community, "Hey, have you checked your colon? Have you checked your lungs?"
When I was told that this might be cancer, I was, "Oh my god, I'm going to die.
How can I live without my lungs? Lung cancer, I'm going to die."
And I thought about my 8-year-old son at the time, and I thought about what it would be like to live without his mom.
And um and it's something that still lives with me.
I feel like in some ways I don't get to breathe, if if you will, like that's a real thing. We hear the sound bites, "Oh, this is the number one cancer killer."
We hear those sound bites so much.
It it it it leaves something that stays with us throughout our lives. Like Nolan, Colette is a non-smoker who is not eligible for screening.
She too caught her cancer during [music] an investigation for an unrelated condition.
But Colette says this is only one of the many reasons why people don't catch their cancers early.
In my opinion, there are several [music] factors. Number one, the stigma.
When I tell anyone that I I have [music] stage four non-small cell lung cancer, the first question is, "Oh, were you a smoker?" [music] And my response is almost immediately, like as they are asking me the question, I'm saying, "No, I never smoked."
[music] Lung cancer is extremely stigmatized. In smokers, that is >> [music] >> a huge barrier to us actually getting the screening to happen. In never smokers, they're not going to get screening to begin with cuz there's no indication for it right now. There's no reason insurance [music] would reimburse that. And so, we really need to focus on getting the message out there that lung cancer screening is not something we should only be doing in smokers, but also that lung cancer is something that [music] exists in non-smokers so that there is less stigmatization around it.
The new realization in lung cancer [music] is that it affects it affects non-smoker potentially more [music] in some country than smokers.
And the question is why wouldn't we screen [music] uh non-smokers? And my answer will be absolutely. [music] We absolutely need to lobby, and I think many of us are trying to lobby for that.
But the collect the problem goes well beyond the stigma of smoking. [music] She says the screening guidelines are fundamentally broken.
The guidelines say number one, you must have been a smoker for X amount of years, and you must be at least 50 years old. What happened to someone who started smoking when they were 10?
And they're now 30, and and they've smoked for 20 years, and they're experiencing symptoms or not experiencing symptoms.
Their life is of value, too. And they 20 years of smoking, that's a lot. The guidelines may have worked in the past, but they certainly don't work now.
We're a educated population, and we demand more.
No one deserves cancer. There have been many calls for better approaches to lung cancer screening.
But what exactly that looks like is less clear. Recent developments in CT scanning, which use lower doses of radiation, have been proposed as one way forwards. But doctors like Tom argue that it may not solve the problem alone.
Low-dose CT is amazing and the the incorporation of low-dose CT into normal screening is really probably saved tens of thousands if not hundreds of thousands of lives already and it's only been, you know, really utilized in the last few years. The issue with low-dose CTs is really twofold. One is it is a little bit of radiation. It's a very low dose of radiation, but, you know, a lot of Americans are going to be doing the screening every year for the rest of their life and Americans are, you know, undoubtedly going to be worried about radiation, but it's also a huge stress on the medical system. Not only do we not have enough radiologists to be reading all these, it's also extremely expensive and we're already sort of railroading towards a lot of problems with expense in in the medical community as is. Obviously, if we detect a cancer before we need to spend, uh, you know, hundreds of thousands of dollars on an immunotherapy cuz we only detected it once it had metastasized, that's a real savings. But, you know, when we're doing these sorts of analyses, you always have to do cost-benefit analyses and obviously our goal is to identify everyone with very early stage cancer, um, but I don't think that low-dose CT is really a viable option for everyone.
But that doesn't mean that Tom and Miriam have given up. They're looking for another solution.
>> [music] >> And yet again, it comes back to inflammation. There is, I believe, a big gap now in clinical practice. You see that we progress tremendously [music] in measuring organ function, you know, when we have all the, you know, our annual wellness visit [music] and where we measure kidney function and liver function and your glucose level, right?
And your cholesterol levels and all these is we [music] are products of of research, right? We, however, do not measure, in any of these [music] wellness visit, never measure the functionality of our immune response or our inflammatory [music] level, inflammation level.
And, um, and yet we know how to measure [music] inflammation. Some of the work that we're doing, you you understanding this inflammation is really looking if we can develop a blood test [music] that is able to identify what who are the patients that are most at risk for eventually developing cancer and who are the folks [music] that we should actually be um doing, you know, annual lung cancer screening on and who can we potentially forego [music] it on. The impact of that of one low-dose CT scan and potentially [music] inflammatory measurement are immense.
And yet, there's still a long way to go.
In medicine, diagnostic tools [music] that use multiple different inputs have a tendency to create false positives.
And so, Miriam and her collaborators around the world are working with huge data sets to try to constrain those predictions.
And she thinks there's reason to be hopeful.
It's an extraordinary time of opportunities and possibilities. [music] Extraordinary development in technology that enables us to measure, you know, the things [music] that were unmeasurable.
Extraordinary development in AI, in our ability to really integrate all these data sets. [music] It is impossible not to be hopeful. If we, collectively, [music] researchers, clinicians, patients, scientists, advocates, the community, if we don't find a way to change those screening guidelines, we're going to have a bigger problem.
>> I'm a phase one doctor, which means I run trials for patients with cancer that have really run out of options. And so, you know, my goal with developing these interception trials is basically to put myself out of business. You know, I want to retire at some point and I'd like for people to stop getting lung cancer.
>> And that's the future [music] I imagine for my niece in the space of 10 years.
I am speaking about having lived with and managed cancer for 4 years now, where >> [music] >> my sister succumbed to it within two.
And so, I I I I can't [music] I can't imagine a better future than one where we have therapies that will just eradicate that possibility from the outset.
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