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We Finally Have a Weapon Against the Deadliest Cancer
We Finally Have a Weapon Against the Deadliest Cancer
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Subtitles (260)
0:00
Pancreatic cancer isn’t a silent disease you can catch early. It’s
0:04
stealth. It slips past the body’s early warning signs, so by the time something
0:08
feels wrong, it’s often already advanced. Over the years, survival has barely moved. Only
0:13
a handful of patients out of every hundred ever make it through. Statistically, it’s like playing
0:17
Russian roulette with 5 chambers loaded out of 6. But after decades of failure, researchers have
0:22
started breaking through pancreatic cancer’s defenses. They’ve turned it from untouchable
0:27
into something they can go after. And what they’ve discovered inside
0:30
that “stealth” system changes everything. Pancreatic cancer is one of the most lethal
0:34
diseases around. While modern medicine has made huge headway combating viruses and
0:39
improving cancer survival rates, pancreatic cancer has remained an unsolved mystery. A
0:44
fortress that’s been impossible for doctors to penetrate with drugs.
0:48
Even with modern medical developments, the overall survival rate for pancreatic cancer is low.
0:53
Very low. Today, it sits at only 13%.
0:56
It’s the lowest of all major cancers. In rich countries, the average 5 year-survival rate for
1:02
all cancers diagnosed in 2017 was 70%. And it gets worse.
1:07
Because most pancreatic cancers don’t get identified until it’s too late. They’ve already
1:12
metastasized to stage IV. In fact, over 4 out of 5 pancreatic cancers get diagnosed at this stage.
1:18
The survival rate for metastatic pancreatic cancer? In five years,
1:22
only 3% of patients are still alive.
1:25
What makes it so lethal?
1:27
The way pancreatic cancer works. It’s a perfect storm of location, immune response,
1:31
and presentation. Pancreatic tumors rarely cause noticeable symptoms, partly because
1:36
of their location deep inside the body. They don’t become physically visible, and they don’t
1:41
cause symptoms a patient can feel until they’ve spread to other organs and parts of the body.
1:46
There are no screening tests to catch the disease early as it builds up quickly
1:50
and quietly. Usually, patients only notice the first symptoms - jaundice,
1:54
abdominal pain - once the cancer has already spread.
1:57
By then, the chances of survival are next to nothing.
2:00
Pancreatic cancer suppresses the body’s early warning systems because of its own structure,
2:04
making it virtually treatment-proof.
2:06
Until now.
2:07
Doctors were always puzzled at the body's response to pancreatic cancer,
2:11
because in most patients, there was almost none. They couldn’t figure out
2:15
why patients’ immune systems never seemed to come online. Cancer cells would grow
2:19
and multiply throughout the body without T-cells putting any kind of stop to it.
2:24
Then researchers discovered what was actually going on.
2:26
Pancreatic tumors cloak themselves with glycoproteins to mimic healthy cells.
2:31
This sugar coating signals the immune system to “stand down”, allowing the tumor cells to
2:36
hide in plain sight. The most common form of pancreatic cancer - PDAC - may trigger some
2:42
kind of immune response. But the T cells still can’t infiltrate the tumor. There’s something in
2:47
the design of pancreatic cancer cells that stops the one thing that could fight them in its tracks.
2:53
But there’s a new development on the horizon. Because the untreatable,
2:56
“undruggable” code… has just been broken.
2:59
To outsmart pancreatic cancer, scientists had to find a way to permeate the concrete
3:04
bunker the cancer creates. A bunker known as the “desmoplastic stroma”. A
3:08
fortified wall scientists thought was almost impossible to break through.
3:12
As pancreatic cancer grows, it hijacks the cells around it.
3:15
The mutated cancer cells in turn damage the tissue around them. As a result,
3:20
the body’s wound-healing mode is activated, creating scar tissue around the tumor.
3:25
PDAC uses this tissue as a shield. Called a stroma, it’s much denser than the tissue that
3:31
surrounds most other cancers. For some reason, PDAC creates an incredibly fibrous tissue barrier
3:36
that stops most cancer treatments from even reaching the cells they’re supposed to fight.
3:41
Besides working as the worst kind of high-security fence,
3:44
the desmoplastic stroma creates another problem.
3:47
Internal fluid pressure.
3:49
Tumor cells create a highly hydrophilic sugar that attracts and absorbs water,
3:54
causing parts of the tumor to swell. But the tumor can’t drain or expand outwards because the
3:59
dense stroma is blocking it. It’s like filling a balloon with water inside a concrete shell.
4:04
There’s nowhere for it to expand, resulting in internal pressure on cells and blood vessels.
4:09
Even if doctors could find a way around the barrier, the pressure the stroma creates
4:13
physically squeezes shut the blood vessels that would deliver medicine. At that point,
4:18
chemotherapy becomes a losing battle. Throwing drugs at a pancreatic tumor
4:21
becomes akin to throwing spaghetti at a wall and expecting it to pass through.
4:26
All of this made traditional therapies against pancreatic cancer painful,
4:30
and mostly useless. The medical world had to come up with something else. Something better.
4:35
Enter NALIRIFOX.
4:36
Traditional chemotherapy doesn’t target cancer cells. It targets everything.
4:41
Chemo is the equivalent of biological carpet bombing.
4:44
Used against a disease it can’t reach, it basically ends up killing a lot of
4:48
functional parts of the bodies while leaving the pancreatic tumor untreated. One oncologist,
4:53
Dr. Sameek Roychowdhury, said, “even with our best chemotherapies,
4:57
the average benefit is around 6 months, sometimes as little
5:00
as weeks or months….It’s barely enough time for families to grasp the situation”
5:04
But NALIRIFOX uses a smarter approach. A targeted one.
5:08
The drug uses the cancer’s stealth against itself. It slips past healthy tissue,
5:12
breaks through the tumor’s defenses, and only releases its full payload once it’s inside.
5:17
A study called the NAPOLI-3 trial was conducted across 18 countries to see how effective the
5:22
new medication was. 770 patients who had been diagnosed with metastatic pancreatic
5:27
cancer - the deadliest kind - were selected to take part in the trial in 2020 and 2021.
5:32
About half of them were given NALIRIFOX, while the other half was given the normal
5:36
first-line chemotherapy treatment for metastatic pancreatic cancer.
5:40
Those who were given the standard chemotherapy treatment had a median
5:43
survival rate of 9.2 months. Those who had been treated with NALIRIFOX? Had
5:48
an extended median survival rate of 11.1 months.
5:52
While that may not seem like much to the average person,
5:55
it’s a major victory for oncology. That translates to a 20% improvement
6:00
in survival for what was considered an almost certainly terminal disease.
6:04
In the world of cancer that’s a generational leap forward.
6:07
In addition, patients took NALIRIFOX for 6 weeks more, on average, than the standard
6:12
chemotherapy treatment, which allowed the drug itself to be more effective.
6:16
Due to these incredible results, the FDA made reviewing NALIRIFOX
6:19
a top priority. In February 2024, the drug got official FDA approval,
6:24
making it more easily accessible to patients who needed it, as well as, possibly,
6:28
affordable. Though the FDA doesn’t directly control what insurance can and can’t cover,
6:33
when a drug is FDA approved, it usually translates to being covered by Medicare and Medicaid.
6:38
But NALIRIFOX is just step one.
6:41
Because once doctors got inside the tumor, they still had to
6:44
deal with a dangerous enemy…one they couldn’t physically touch. A genetic
6:48
villain that had made pancreatic cancer a death sentence for most.
6:51
The structure of the mutation that caused the cancer itself.
6:55
Approximately 90-95% of pancreatic cancers are driven by the KRAS mutation. Science had
7:02
famously labeled it “untouchable” for 40 years.
7:05
The KRAS gene works like an on/off switch,
7:08
controlling how cells grow in the body. In most pancreatic cancers,
7:12
the KRAS has somehow been flipped into the on position and becomes permanently stuck there.
7:17
Scientists had figured out the exact mutation
7:19
they needed to target. The problem? They had no way of going about it.
7:23
Drugs usually work by latching onto a protein’s surface. But the KRAS mutation was incredibly
7:29
smooth. So smooth scientists called it “The Greased Ball”. Nothing could latch on. Medicines
7:34
couldn’t bind to it, and as long as they couldn’t bind to it, they couldn’t work against it.
7:39
Until scientists realized they were going about it all wrong.
7:43
Billions were spent trying to find a way to grip the surface of the
7:46
protein. Decades of experimental drugs and clinical trials turned
7:50
out to be complete flops. But there was a hidden flaw in the armor all along.
7:55
One that could be used to go after the heart of the tumor.
7:58
Because the protein may not have had a crevice for drugs to latch
8:02
onto…but scientists realized that, using the right methods, they could force one to open.
8:06
The problem was never what it appeared to be in the first place. The funding for the
8:10
war on cancer hadn’t been wasted. Scientists put a lot of effort into discovering exactly
8:15
the chemicals needed to kill the cancer cells. The only problem was that the KRAS
8:19
protein seemingly had no pocket for the drugs to sit in and deliver the fatal chemical dose.
8:24
In 2013 Kevan Shokat, a biochemist at University of California, San Francisco, focused on a
8:30
specific KRAS mutation called G12C. In simple terms, this mutation turns glycine into a highly
8:37
reactive residue. Scientists designed a bunch of molecules that would glue themselves onto it.
8:42
And when they did, something interesting happened.
8:45
The gluing action forced the protein to shift, revealing a small, hidden cavity
8:49
within it. Scientists called this discovery the “Switch II” pocket.
8:53
Shokat’s breakthrough only applied to a tiny fraction of pancreatic cancers, less than 1%. But
8:58
it proved something many researchers had doubted for decades: KRAS could be targeted. Finding the
9:04
right chemicals that would take advantage of this backdoor for most other types of pancreatic cancer
9:09
took much longer. Ones that could be used not to attack the protein…but to take it offline
9:15
altogether. Over 480 potential compounds were screened for bonding to the Switch II pocket.
9:20
Until they found the chemicals that would turn the KRAS “switch” back to the “off” position.
9:25
Forever.
9:26
Scientists had unlocked a perfect drug delivery system. Now they just needed
9:31
to develop a highly specific weapon to exploit it. But there was a problem. The compounds were
9:36
almost too precise. They only worked against that specific mutation. Change the mutation,
9:41
and the drugs lost their target, becoming virtually useless against the cancer.
9:45
After years of research and experimentation, it appears scientists have the answer they want.
9:50
Their own personal assassin, lethal against the world’s deadliest cancer: Daraxonrasib.
9:56
And it could be the “Holy Grail” of oncology.
9:59
Researchers had already come up with some targeted KRAS G12C inhibitors,
10:04
but they were a little too targeted. They weren’t as effective against pancreatic
10:08
tumors as doctors would like it to be. If the protein mutated further,
10:12
or became drug resistant, these drugs’ effectiveness went down to almost nothing.
10:16
Daraxonrasib is more broad-spectrum and it shows potential to overcome
10:21
drug resistance to first generation inhibitors.
10:23
The drug works by recruiting a helper molecule called cyclophilin A. Acting
10:28
like a kind of molecular glue, it creates a connection that lets the
10:32
drug lock onto KRAS and shut down the signals driving the cancer's growth.
10:36
So the drug rips through the body, finds the mutated KRAS proteins,
10:41
and latches onto them like a magnet. Where chemotherapy is a full-body carpet bombing,
10:45
Daraxonrasib functions as a targeted assassination.
10:49
The results were outstanding. In a series of drug trials,
10:52
500 patients were selected to either receive chemotherapy or treatment with Daraxonrasib.
10:57
Almost 92% of them had RAS G12 mutations.
11:01
The average survival rate for chemotherapy was 6.7 months. For those treated with Daraxonrasib
11:07
it increased to 13.2 months. Individual patient reports also showed that for most,
11:13
Daraxonrasib was much less toxic than chemotherapy. Patients experienced fewer and
11:18
less severe side effects overall. And way fewer decided to stop the treatment because of them.
11:23
It only gets better.
11:24
Because KRAS mutations don’t just drive pancreatic cancer. They trigger a whole lot of tumors,
11:30
including lung, colorectal, ovarian, endometrial and some of the other most common and deadly
11:35
cancers around. Over 5.1 million people are diagnosed with one of those 4 cancers every
11:41
year. In addition to the over 500,000 people that will receive a diagnosis of pancreatic cancer.
11:47
A drug that went after the KRAS mutations that caused the cancer could give a whole new hope,
11:52
and be the literal difference between life and death, for 5.6 million people annually. In fact,
11:58
just lung, pancreatic, and colon cancers alone are the 3 leading causes of cancer deaths.
12:04
Cracking the KRAS G12D mystery doesn’t just provide hope for pancreatic cancer patients;
12:09
but for all patients suffering from KRAS-driven cancers.
12:13
While this new miracle drug starts taking out current tumor targets, there’s an even
12:18
brighter future on the horizon. Scientists are on the brink of another incredible development:
12:22
a technology that doesn’t just target cancer, but ensures that the tumor never returns.
12:27
A cancer vaccine.
12:29
While Daraxonrasib is a near-miraculous development, it’s not the end of the
12:33
story for pancreatic cancer patients. Because for most people, Daraxonrasib
12:37
stops working after a while. Their tumor becomes drug-resistant. Despite an extended lifespan,
12:42
they are left once again facing their worst fear: the return of their cancer.
12:46
One company is using mRNA technology - like the kind used in the vaccine that
12:50
ended the COVID-19 pandemic - to change this narrative. Their hope is to use modern medicine
12:55
not just to treat pancreatic cancer, but to stop it from ever coming back again.
13:00
The BioNTech customizable mRNA vaccine is currently in its Phase 1 trial. So far,
13:06
the results look promising.
13:07
The vaccine is custom-made for each patient based on their unique tumor DNA. To better
13:12
target the cancerous cells it needs to eradicate, which differ from patient to
13:16
patient. In the BioNTech trial, vaccines were given to 16 patients after pancreatic
13:21
cancer surgery. The treatment was paired with chemotherapy and immunotherapy drugs.
13:26
In half of the patients, the vaccine activated tumor-specific immune cells. The mRNA shot
13:31
specifically trained these soldier cells to recognize the tumor’s unique signature,
13:36
and wipe out the cancerous cells. They teamed up with the body’s own
13:39
immune system to train it to identify and fight the pancreatic invader.
13:43
And how effective is this current “search and destroy” vaccine for pancreatic cancer?
13:48
Of the 8 patients whose immune systems the vaccine activated,
13:52
7 of them were still alive 4 to 6 years after surgery. That’s an almost 90% survival
13:58
rate. Much higher than the 13% currently attributed to pancreatic cancer patients.
14:03
Oncologists were stunned at the results.
14:05
One doctor at Memorial Sloan Kettering Cancer Center said of the new vaccine:
14:09
it “has the potential to make a difference for one of the deadliest cancers”.
14:13
Researchers still need to figure out why some patients’ immune systems respond
14:17
to the vaccine while others don’t. Even for those who might respond well to the vaccine,
14:22
there’s a huge question of if they can get it in the first place.
14:25
Because the cost of survival is shockingly high.
14:28
NALIRIFOX, Daraxonrasib, personalized mRNA vaccines…all of them represent
14:34
giant technological, scientific, and medical leaps forward. Unfortunately,
14:38
all of them are currently out of reach for all but the wealthiest of patients. Each
14:43
of these drugs costs tens of thousands of dollars per cycle. And the cycles
14:47
needed to keep someone in remission over a lifetime can add up to astronomical costs.
14:52
NALIRIFOX costs an average of $7,800 per cycle. For the multiple cycles of treatment required,
14:58
this can easily add up to between $150,000 and $200,000 in lifetime costs. That’s enough to
15:04
cover a 4-year-degree at a private university, or even a starter home in a cheaper area.
15:09
Paying it for one drug alone would throw most people into bankruptcy.
15:13
And in combination with the other drugs on this list? It would be prohibitively expensive.
15:18
Daraxonrasib is not yet commercially available. But an analysis of Revolution
15:23
Medicines’ potential profits revealed how much the company expects to charge patients for it.
15:28
A monthly course would be priced between $30,500 and $37,300. The
15:33
per-patient revenue this adds up to an average of $250,000.
15:38
Taking these two drugs together would already put the average
15:40
pancreatic cancer patient half a million in the hole. That’s before they’ve even
15:45
considered a custom-made mRNA vaccine. The cost for that? BioNTech has stated,
15:50
after years of work, they can probably get it down to under an eye-watering $100,000 per dose.
15:56
Will access to potentially life-saving medicine be given to all patients? Or
16:00
will it represent yet another “Healthcare Divide”? One where the elite get the most
16:05
effective drugs and best chances of survival, while everyone else
16:08
defaults to paying exorbitant amounts for chemo and hoping for the best?
16:12
The good news is the FDA has approved expanded access to Daraxonrasib based on its early,
16:17
promising results. And now that researchers have shown KRAS can be beaten, pharmaceutical
16:22
companies are racing to develop their own drugs to exploit the crack in its armor.
16:26
As of June 2026, Johnson & Johnson has spent $1 billion to enter the race for KRAS-related cancer
16:33
treatments. Theoretically, competition between the major pharmaceutical companies should drive
16:38
drug prices down. But given the fact that in countries like the U.S., many drugs remain
16:43
distressingly out of reach for the average citizen due to cost, even with competition in the mix,
16:48
the political and social reality of these medical leaps forward in the future remains to be seen.
16:53
But does this all mean that we’re at the end of the cancer death sentence?
16:57
One thing is certain. We have entered a new scientific reality. A “God Mode”
17:02
era of oncology. One in which no mutation is off limits, where “undruggable” conditions
17:07
don’t make diseases untreatable; they just present another challenge to be solved.
17:11
The new methods developed to treat KRAS mutations can be applied to a whole lot
17:15
of formerly undefeatable mutations and proteins.
17:18
The only thing that’s doomed is pancreatic cancer’s horrific 13% survival rates. Based
17:24
on the trials, patients treated with these new medical miracles had their lifespans
17:28
almost double after being diagnosed with pancreatic cancer. Even patients
17:32
with metastatic pancreatic cancer saw their risk of death reduced by 60%.
17:37
Better yet, the actual quality of patients’ lives went up as well.
17:41
The milder side effects of Daraxonrasib meant these patients gained more than
17:45
extra months. They gained quality of life and more time with loved ones.
17:49
And the only thing they need to do? Take 3 pills once a day.
17:53
Families that in the past only wished for, at best,
17:56
a few more months with loved ones through painful,
17:59
excruciating rounds of chemotherapy now have new hope. The hope that they could get anywhere
18:04
from over a year to several years with their relatives after a pancreatic cancer diagnosis.
18:10
Even the hope that one day, their loved one could be completely cancer free.
18:14
The medical community has come together to - quite literally - give people new life. And
18:18
the dream is that these breakthroughs won’t just stop at pancreatic cancer.
18:22
Cracking the “undruggable” code could be the first step in treating some of
18:25
the deadliest cancers the world has ever seen. The new medicines being developed
18:29
today could save enough people to fill up an entire major city. Every single year.
18:34
And who knows what other miracles the future of medicine could bring…
18:38
Breakthroughs like this can buy time. But they can’t stop the inevitable. And those
18:42
who see it every day have learned some surprising lessons. Find out
18:45
more in “What Doctors Wish Their Patients Knew About Death.” Or watch this video.
