New pancreatic cancer drug might open the door to much longer survival times
economist.com
economist.com
The bigger deal about this is that KRAS was considered an "undruggable" target.
Recent advancements have allowed us to design biologics to do things we previously thought impossible, which broadens the horizons for other treatments in the future.
Baby steps.
I think we should also invest more in better diagnostics and early cancer detection. That could save many lives too.
The issue with non-imaging early cancer detection seems to be false positives.
Afaik, medical regulatory agencies have been... resistant... to allowing marketing of tests.
The thinking seems to be "If people get a positive result, they may opt for interventions that are more harmful than their current disease state."
But, to me, that seems to leave unmentioned the fact that there's a finite "untreatable" cancer progression line, and while that's extending to later disease states, it's still a helluva lot easier to treat earlier.
Complications after his surgery meant he had two more. He is now, three weeks after the first operation learning to walk again. It will be an additional week or two untill he can eat. (Without the complication he would have been walking and eating two weeks after the first operation). Oh and he is a diabetic now, since they removed his pancreas.
Just crossing my fingers that he will get out of the hospital without any more complications, and adapt to the new life.
2. NIH funding notice of awards has slowed to a crawl since Trump did not get his wish to cut Science funding.
3. Putting scientific funding under political control, instructing them to ignore the reviews conducted by peer scientists.
4. Have practically made international collaborations on grants impossible. An expert in Canada or Europe that would be great? Pretty much, too bad.
5. Pushing policies that make grants cancelable at any moment without need to have a justified reason, including potentially for exercising free speech, disagreeing with Administration doctrine, etc, or because you're ugly. This and the funding uncertainty makes planning difficult...just like business, stability/predictability matters.
6. Pushing policies that prevent funds to help cover costs of dissemination, including conference costs.
Is of public knowledge that the National Science Foundation and funds for thousands of scientific projects were gutted by DOGE in 2025.
Each one of the research lines cut needed typically 10 years to grow, so Trump and GOP had destroyed an incredible amount of years of research just on 2025, with consequences probably extending into 2035 or so. Without any visible benefit for Americans, that had still seen their debt sky-rocketing while their taxes are spent in pools and sinks.
Trump has also assured to engrave into the brains of the whole scientific community that US is now an hostile place for students and researchers. The whole planet had seen the main universities attacked by Trump (with Harvard resisting, and Columbia losing their pride), the foreign students targeted by ICE and the department of Education eviscerated
Also the thousands of workers in USAID and Health and Human Services fired for fun. Without mentioning the DOGE mess done at the national nuclear safety administration with 400 essential workers fired and then asked to return to the job ASAP, please, please.
It makes no sense to cut off the hand that saves you even as a rich billionaire who wants to control people in a fascist society.
In reality, mediocre thinkers with inflated egos and little understanding of long-term consequences are pulling the strings almost everywhere.
Actually, I think it's powerful to acknowledge when my beliefs are weak. I still believe it - I think it's true, and I don't have any conflicting beliefs. But still it would not take a lot of evidence to change my mind, and since this is a prediction about the future, I will not be very surprised to find out I was wrong.
Personally, I have epilepsy and am increasingly aware that while some paradigm-shifting treatments are on the horizon, they are a decade or so away and likely won't come to market in time to fully help me (particularly reverse small but accumulating damage caused by seizures). And that's a weird feeling.
Failing a treatment that has held promise for so many others and been heralded as paradigm-shifting is such a weird place to be. There's comfort in knowing others won't suffer, but loneliness is knowing you or a loved one still is.
This subthread there is a fascinating explainer about one user's journey into funding and incentivizing research into their own rare form of blood cancer, and how they are able to push forward the state of the art: https://news.ycombinator.com/item?id=48506997 - something of a modern-day (and more accurate) Lorenzo's Oil!
didnt seem to have lived up to the promise. seemed to have accelerated prostate cancer for my father who passed away in mere three months after first dose.
Immunotherapies on the other hand seems to work wonders for many who respond to it. I regret for not trying it.
Look for how much money the pharmaceutic cartels make annually, that is why these "drugs" aka cure will never ever be released because its side effects are still unknown.
That said, I'll happily take "we discovered a key weakness in 20% of cancers," please and thank you.
One of the most commonly observed broken mechanisms is mutation in the gene KRAS that turns this on/off growth switch into the permanently on position.
This has been known for decades, of course. And there have been huge amounts of effort to try to develop drugs that target KRAS in cancer, but for decades it's always been thought of as 'undruggable' because of the difficulty of finding any molecules that would affect it.
This new drug, that finally treats KRAS mutated cancers, goes about it in a new way. Instead of trying to gum up the works of a single protein by sticking a small chemical in it, it effectively "glues" the KRAS protein to another protein, CypA, which keeps the switch away from reaching the normal areas where it's "on switch" activity works.
So this new drug means two things: 1) a lot of the most difficult to treat cancers are now far more treatable, and in the next 1-5 years clinical trials will tell us which cancers this particular drug works well for, 2) there's an entire new class of drug activity that everybody is chasing at this very moment, so in 5-25 years we'll likely have a huge number more of these sorts of treatments.
Can you help disambiguate this? Are there treatments now, or are there potential treatments with trials in 1-5 years?
https://clinicaltrials.gov/search?intr=daraxonrasib&viewType...
The first two are the trial that just completed and showed success: people that have pancreatic cancer that failed other treatments, then a "trial" that is meant to give quick access to more people now that it's been shown to work.
Then there's a trial for using it as the first-line treatment for pancreatic cancer, one for lung cancer (NSCLC), and also various combinations with other drugs. I expect we'll see a ton of new trials registered in the coming year. Especially something in combination with colon cancer, because a common drug resistance mechanism in colon cancer is to develop KRAS mutation.
The thing is that we don't really know which cancers it will work well in until we try. And there's limited number of people with cancer that enter clinical trials, and we want to give each person their very best chance at survival, and then there's the massive expense of running the clinical trial itself, so learning happens slowly, one month of survival at a time, or one cancer recurrence at a time, or one death at a time. Patients that take part in clinical trials really are the heroes here. (Especially with the side effects of this new drug, which are horrible. It is a revolutionary drug, but we need to learn how to manage the other things it does as well, and that's going to take time.)
> Patients that take part in clinical trials really are the heroes here.
Are they?
To me personally, putting people into a permanent state of requiring drugs to survive, is not really cure. It's just maximizing income for those selling those drugs. And none of those drugs work exceedingly well; people still die, even if to other disease or frailties. I don't understand this hype in general.
> But that's not a cure. If they don't take that drug, assuming it works, they still have the original mutation in the cancer cells.
The person you're replying to called this out specifically:
> and also various combinations with other drugs.
Why do you think they try it in combination with other drugs? You might be right that this drug alone might not be a cure, but if it inhibits cancer growth, then it empowers other drugs to work more effectively.
> people still die
So what... We do nothing, then? This is your complaint? That we can't be immortal, so why bother trying to cure anything?
I don't understand your type in general.
https://usafacts.org/articles/how-have-cancer-rates-changed-...
>However, even though the overall number of cases rises as the population grows, fewer people are getting and dying from cancer. Between 2000 and 2021, the incidence rate — or the rate of new cancer cases per 100,000 people — declined by 5.7%, while the annual mortality rate fell by 27.5%.
Cancer is a broad term encompassing many sorts of malfunction and nearly 40% of Americans will be diagnosed with it at some point because if you survive other hazards and maladies cancer is often what gets you.
If I pulled one person out of a burning building it would be newsworthy. Doctors are and have been pulling train loads every day.
I agree that 6 extra months (on average) means some patients get much more time than that. I agree that a statistically significant improvement on the survival rate for this terrible cancer is a very promising result longer term.
My disagreement was much narrower than that. I disagree that 6 extra months is equivalent to 5 extra years. I disagree that people living an extra 6 months on average is equivalent to one person living 3 extra years and one person living 3 extra days. I think 3 days and 3 years average out to about 1.5 years, not to 6 months.
Think of me as a living fossil who takes it for granted that everyone appreciates how much medicine improves our lives.
The pharmaceutical companies are not the ones making clinical decisions - in this case, it's a shared medical decision between a patient and their oncologist.
Having seen how horrific pancreatic cancer is, how difficult it is to treat, and the decades of slow research done by academic scientists to get to this point, I am elated that we have a tool to give patients more time with their families even if their cancer can't be "cured" with this particular drug.
This may seem unsatisfying, but it's real, measurable progress. KRAS has been known about since the earliest days of cancer research, so it's a true breakthrough to finally have a drug targeting it.
Today, only 4 years later, there are two therapies, one RNA based and one CART that would have been usable in her situation. She’d be alive today most likely.
Frankly, you have no idea what you’re talking about as you spew toxic bullshit. 5 year survival would meant being there for her son through high school. That survival rate was 65% in 2022 and closer to 80% now in recent trials.
Normally I’d scroll on, but in these degenerate days it is important to counter bullshit before it becomes policy.
I know this is a popular "well actually" to do, but it is not always useful in a conversation. Yes, all cancers are different, but yes, cancer is also one thing: unchecked, harmful division of cells.
Bacteria are also all different, but still they are "one thing", and despite their diversity, antibiotics exist that can deal with many species of them at once. It is reasonable to talk about bacteria and antibacterial medications, it is also reasonable to talk about cancer and cancer treatment. I truly hope cancer will meet its "penicillin" one day (yes I know this is unlikely).
> Bacteria are also all different, but still they are "one thing", and despite their diversity, antibiotics exist that can deal with many species of them at once.
Except people don’t ask “what if I get bacteria” the way they ask about cancer. If the story was about a new antibiotic that only affected 20% of common infectious bacteria strains and someone asked “in laypersons terms, how will this help me if I get a bacterial infection”, it would be appropriate to clarify that it only applies to some bacteria.
Yeah, but doctors also don't tell people "you have bacteria" or claim "we found a cure for bacteria". The lack of nuance on average is largely due to a lack of nuance from experts. The media treats cancer as one big thing and bacteria and viruses as separate things. Thus the average joe inherits 'treating cancer as one big thing' from the media.
But yeah, oncologists aren’t telling people “you have cancer” the way they might say “you have MRSA”.
Honestly, I think people probably get false impressions because cancer usually hits old people and old people are, frankly, often not reliable narrators.
Without this understanding it becomes a quick jump from "we're spending all this money on cancer" to "we've made no progress"
An example of the nuance plays out in the common cancers (like breast and prostrate). These have between 90 and 100% 5 year survival rates. Others (like the one in this article, pancreatic) have very poor survivability.
As you note, it's very unlikely that we'll "cure cancer". But we already "cure" (for some definition of cure) some cancers. Progress is slow, methodical, and incremental. It can feel like a lost cause when viewed from afar, but up close very real progress is being made. And that's an important message to pass along.
Like you said, for a lot of common cancers we have multiple treatments. It's usually not just one magic drug, but rather the doctors working with the most effective treatments down to the least effective treatments.
Now, "no, i mean poisons that attack the special chemistry of cancer," oh yes, those we call chemo.
Penicillin works against bacteria, in particular gram-positive bacteria; to a lesser extent gram-negative bacteria too (this depends on the cell membrane structure of bacteria; there are other penicillin derivatives that are also more effective on gram-negative bacteria than penicillin is, but by and large the main target will be gram-positive bacteria). It does not work against human cells. If your comparison is about drugs in general, then of course cytotoxic drugs will have an effect; simplest example I can remember off-hand is colchicin. Of course it should work against cancer cells and non-cancer cells, unless there are some mutations where colchicin could no longer bind to, but that seems very very rare, due to the natural target of colchicin involved in cellular division.
This is false; it does so, but slowly.
https://www.moffitt.org/cancers/squamous-cell-carcinoma/diag...
No, they aren't. Cancer is malignant by definition.
There are benign non-malignant tumors.
"Benign" is any cancer where wait-and-watch is a valid medical approach.
https://jamanetwork.com/journals/jamaoncology/fullarticle/27...
"Malignant tumors are cancerous (ie, they invade other sites)."
https://www.cancer.org/cancer/understanding-cancer/what-is-c...
"Tumors are lumps or masses of abnormal cells (neoplasms) that can be malignant (cancer) or benign (not cancer)."
https://www.merriam-webster.com/dictionary/benign
"of a mild type or character that does not threaten health or life especially : not becoming cancerous"
That cancer is malignant by definition is extremely well known. I won't respond further.
P.S. I looked through your other comments and can highly recommend you to https://www.reddit.com/r/confidentlyincorrect/
A distinction without a difference.
You can label a slow-growing tumor as "not-cancer" if you want, for psychological reasons, I guess; "cancer" just sounds scarier. Some slow-growing "not-cancer" tumors are faster than others. It's a sliding scale, not a dichotomy.
> A distinction without a difference.
What distinction? This is a phrase that this confidently wrong ignoramus apparently doesn't know the meaning of.
Penicillin blocks a specific enzyme (transpeptidase).
https://en.wikipedia.org/wiki/Penicillin-binding_proteins
Cancer cells, by definition, are not a uniform mass. It will depend on the cancer type, which in turn is defined by the properties those cells have. And mutations happen all the time, often more in cancer cells when their repair systems also have mutations, e. g. are less efficient. By that definition alone, there can never be a wonder-cure for all cancer types. At best you can find some proteins more important (p53 for instance) and while more than 50% of cancer cells have some form of mutation in p53, others simply don't. By that definition there will never be a penicillin-equivalent to all cancer types.
However this is just the first version of the drug, it can be combined with other modalities to allow more selective targeting of cancer versus not cancer cells (e.g antibody-drug conjugation). And when used in earlier stage cancers, rather than the advanced cancers in this first clinical trial, there's the possibility of lower dosing that has less strong side effects.
This is just the first attack that has ever broken through to hit a key weakness of some cancers. It's the start of learning, a breakthrough that will launch refinements, enhancements, and a ton of innovation. That sort of innovation is sometimes derided as "me-too" drugs, and not meaningful, but some of the biggest advancements in cancer care have been from taking very hard to tolerate treatments and making them more tolerable and refined and better for patients, allowing longer and more thorough killing of cancer cells. I would expect we will see a lot of that here, as well as work towards combinations with other drugs.
sometimes a cancer can then survive on its own back as a single celled organism
Ways to avoid specific resistance include multiple treatments simultaneously, since the probability of generating resistance to both is the product of the probability of resistance either.
When we first started getting good at sequencing the DNA of tumors, I remember initial reports of taking samples across the 3D space of a tumor and finding great spatial heterogeneity in the tumor genomes.
I'm actually most excited for using this drug in combination with colon cancer, where KRAS mutation is a common drug resistance evolution in response to drugs that target the gene EFGR (though cancer researchers may all have their favorites to go after, colon cancer went after my family especially hard).
It most likely will help if you get pancreatic cancer. It might help if you get one of the other types of cancers with this mutation.
And it will likely lead to new treatments for some of the worst kinds of cancer.
Anyway, since many in my family have died from this horrible cancer, its fantastic news to hear of any improvements there.
That is not true for most cancers, though.
"oncologists went wild over the results of a drug called daraxonrasib."