I know a lot of people here are tired of these teaser headlines and don't want to be told anything until there's an actual cure. But here me out - I'm old enough to have lost several friends and family to cancer. Along the way there have always been headlines like this where it seems that a breakthrough is imminent, and you know what? We are much better at preventing, detecting, and treating cancer than we were 40 years ago!
I personally know several people who have gotten breast cancer and survived! I remember when that was practically a death sentence. Ditto for colon cancer. Even your prospects for lung cancer have improved dramatically.
What has made this progress possible is this relentless research. Research that leads to reports being published. Promising leads being discussed. A huge portion of this research leads to dead ends - BUT - some leads to real progress and has in turn lead to real lives being saved. So I say continue with the research and continue publishing and sharing the research results.
zug_zug · 1h ago
Yes that's true, but I think a lot of the knee-jerk reaction isn't intended to communicate "Stop researching cancer" it's more intended to communicate "Stop linkbaiting us."
If the title said "Might someday" then that would probably be a more accurate picture of where something at this stage of research is at.
Obviously some people here want to know all up-and-coming possibilities, clinical trials, or longshots because we're nerds about it. But others of us only care about the ones that are already succeeding in people. Having titles differentiate the two can avoid the frustration.
hughw · 49m ago
Ok but after the first 1500 articles you’ve read about cancer breakthroughs, you understand that you’re going to read about a very early phase research project. You’re no longer sucked in by the baity headlines, are you? Do you really click it and then be totally surprised it says “in mice” in the text?
zug_zug · 30m ago
So it sounds like you're arguing linkbait is fine because we all have internalized some general skepticism to fight it. But actually I don't think that's the best approach. For one it takes more cognitive overhead to scan through 40 links and then play the mental "what will I actually get if I click this link?" 40 times.
For the most part HN is great about not having linkbait. But when I do see something that sounds improbably good I just go straight to the comments and see if other people find the article legit (as is the case here).
phtrivier · 1h ago
Of course, and I'm glad for you and loved ones (and so sorry for your losses)
That being said, would any of this incremental research have been slower, or canceled, or derailed, if the HN articles about intermediate reports of lab experiment on mice had the word "on mice" in the title ?
That's literally all I'm asking for here.
asdff · 4h ago
Basically, seed tumors with IFN-1 using targeted RNA nanomolecules (that accumulated in the lungs in this case where they modeled lung cancers). This converts the tumor microenvironment from one hostile to immune cells to one where immune cells are now active and on the hunt for tumor specific neoantigens.
The one open question I wish they would get at is the exact sentization mechanism behind the PD-L1 inhibitor and IFN-1 response. The idea is that cancer cells have selective pressure to hide from the immune system and one way of doing that is presenting this PD-1 receptor to the PD-L1 ligand on the immune cell, an interaction that keeps the cancer cell from being killed and one that PD-L1 inhibitor drugs target to enable tumor cells to now be visible to the immune system (as they output a lot of screwed up things that are otherwise visible to the immune system as "not self").
They tested tumors that aren't sensitive to pd-l1 inhibition so presumably evading immune surveillance another way instead of presenting PD-1, and then found them to then be sensitive to PD-L1.
It could be that within a tumor there are subclonal cells that do express PD-1 but are otherwise protected from PD-L1 inhibitiion having any effect from the hostile tumor microenvironment keeping immune surveillance from operating normally anyhow. Induce the immune response, now the T cell is in the area for PD-L1 inhibition to work. Another possibility is that the IFN-1 induction leads to PD-1 now being expressed by cells that didn't do it previously.
Authors didn't explore this though. Probably would take more experiments and mice are expensive and time consuming. It could be answered by single cell RNA sequencing of these unresponsive tumors and seeing if there is some subset of cryptic tumor cells that do express PD-1 already before IFN-1 induction. As well as measuring expression after IFN-1 induction (maybe several timepoints to measure change in gene expression profile in the tumor population, if any)
rpdillon · 4h ago
This seems so cool that I was immediately suspicious, but this isn't my area of expertise, so it's hard for me to understand the original paper:
This is the abstract, though, which suggests the need for a standard "in mice" disclaimer:
> The success of cancer immunotherapies is predicated on the targeting of highly expressed neoepitopes, which preferentially favours malignancies with high mutational burden. Here we show that early responses by type-I interferons mediate the success of immune checkpoint inhibitors as well as epitope spreading in poorly immunogenic tumours and that these interferon responses can be enhanced via systemic administration of lipid particles loaded with RNA coding for tumour-unspecific antigens. In mice, the immune responses of tumours sensitive to checkpoint inhibitors were transferable to resistant tumours and resulted in heightened immunity with antigenic spreading that protected the animals from tumour rechallenge. Our findings show that the resistance of tumours to immunotherapy is dictated by the absence of a damage response, which can be restored by boosting early type-I interferon responses to enable epitope spreading and self-amplifying responses in treatment-refractory tumours.
karaterobot · 4h ago
The linked article said the vaccine was still in pre-clinical trials, which means it hasn't been tested on humans yet. Mouse models are a stepping stone toward that. When you hear 'pre-clinical' think 'alpha testing', or 'proof of concept' stage.
_Microft · 4h ago
The submitted article mentions that it was a study conducted on mice though?
[0] "In this study on mice with melanoma, the vaccine was able to clear existing tumors that had proven drug-resistant."
its not just, put it in a mouse, then guess about what happens to humans.
slater · 4h ago
It's common for medical articles posted here to have a great-sounding breakthrough in their title, and you then have to read the article to find out it's only been done in mice. "en-mice'd/en-micing" is a term for mods editing titles, here :D
asdff · 4h ago
Lay people act like this is a trump card but this is just how science is done. You can't really perform this in humans without having some data that it may very well work. Mice have been pretty good models for cancer biology. Nature Biotechnology is also a good and selective journal.
CoastalCoder · 3h ago
Out of curiosity, are there examples of drug development that did poorly in animal models, but then did much better in human trials?
I'm guessing this is rarely tested since animal modeling is usually a gating factor for human testing?
mrosett · 3h ago
Checkpoint inhibitors (which are the primary driver of improved cancer treatment over the last 15 years and generate > $50B/year in sales) generally don't look very good preclinically. Even their clinical data can be hard to interpret prior to a large scale trial, which led to them almost being shelved.
The catch here is that only two targets (PD(L)-1 and CTLA-4) turned out to work well in humans. All of the other immunotherapies that looked mediocre preclinically turned out to also be mediocre or entirely ineffective in humans.
slater · 4h ago
I agree, I'm just mentioning it re: clickbait titles (not calling anyone out) vs. "oh, [xyz] hasn't been cured, there's just some promising results in mice"
hughw · 2h ago
I miss the old @justsaysinmice twitter (account deleted)
Something that "essentially tells the body to ... stimulate the immune system" usually would cause high fever? I didn't see this mentioned so wondering if it is or isn't a complication with this.
rolph · 4h ago
its a function, not a bug.
Fever and the thermal regulation of immunity: the immune system feels the heat
mRNA research. Something which the current government just cut funding across the board.
SoftTalker · 3h ago
If they smell a "universal cancer cure" the big pharmas will fund it themselves. It would be a license to print money.
chasil · 3h ago
It is just a vaccine that expresses common cancer epitopes.
phtrivier · 2h ago
I still hate those articles title with all my heart.
Is there a way to ban lies about cancer vaccines, fusion reactors, and infinite battery storage ?
Sure, okay, people are working on that, and they're making small incremental improvements and that's good for them ; and unfortunately they need to advertise to secure more funding for the later incremental stage of their research. I understand that.
But please stop with the nonsensical "cancer vaccine", "miracle cancer treatment", "cancer breakthrough" etc... This is an insult to everyone who lost a loved one to cancer.
Cause I'll be _really_ happy when a _real_ cure happens (as in, when anyone can go the their doctor, for real, and get a real "cure", and they have no cancer after that, and it's a simple as getting a cure for, well, you know, the diseases that we "cure", and that are definitely not cancer ?)
But this is not today. Today we "deal" with cancer, we "spare" people some time, we squash it a bit and maybe save a couple of years if you have the "lucky" kind of cancer - and that's great, and let's continue doing that.
But enough with the headlines.
Play it like Apple, please.
Tell me about it when I can buy it.
hughw · 2h ago
But we know how to read critically, don't we? When I read it, I searched for and noticed "mice" and "proof of concept" in the text, and understood the limited claims they're making. I'm glad to learn about this incremental progress because cancer immunotherapy seems a promising avenue.
phtrivier · 1h ago
Our ability to "read critically" is not incompatible with the expectation that other people will "write honestly". If it's incremental and a promising lead and it works only in mice, there are an infinite number of titles that are closer to the truth than "universal cancer vaccine".
Otherwise, I'm going to start posting things about that "AGI" that I was able to train, and that can think () !!! Trust me, it's in Rust !!
() : at the same level as a single cell organism in a simulated environment
amelius · 2h ago
> Tell me about it when I can buy it.
Sorry if this comes across as snarky but perhaps you should not read posts on a hacker forum, and instead limit yourself to reading advertisements?
0xbadc0de5 · 4h ago
... in mice.
Don't get me wrong, it's encouraging to see research in this field progressing. But there is a long list of treatments that work in mice that do not work in humans.
I'll temper my enthusiasm with a healthy dose of pragmatism.
amelius · 3h ago
Of course it is in mice. If they were in the human testing phase, you would have read about it long before on HN!
phtrivier · 2h ago
But the title "inadvertently" forgets to mention that the "universal cancer vaccine" is not universal, not a vaccine, and does not cure cancer unless you're a rodent.
So, of course it gets to the HN front page, because the title is so catchy !
I guess the only way to make it go to the front page faster would have be to label the article : "MIT alumni-founded, Standford-based, YC-funded startup creates universal cancer vaccine with AI, in Rust"
suzzer99 · 3h ago
Isn't this literally the plot of I Am Legend? And we also have scientists thawing out 2.5 million year old ice, just to see what happens. smh
chasil · 3h ago
Did this film address ribosomes?
If not, no.
Nasrudith · 2h ago
It seems that people's separation of reality and fiction has gotten downright dismal. I would blame LLMs but I have seen far too many peope unironically cite "Elysium" as "evidence of what the rich are planning" well before LLMs went mainstream.
I personally know several people who have gotten breast cancer and survived! I remember when that was practically a death sentence. Ditto for colon cancer. Even your prospects for lung cancer have improved dramatically.
What has made this progress possible is this relentless research. Research that leads to reports being published. Promising leads being discussed. A huge portion of this research leads to dead ends - BUT - some leads to real progress and has in turn lead to real lives being saved. So I say continue with the research and continue publishing and sharing the research results.
If the title said "Might someday" then that would probably be a more accurate picture of where something at this stage of research is at.
Obviously some people here want to know all up-and-coming possibilities, clinical trials, or longshots because we're nerds about it. But others of us only care about the ones that are already succeeding in people. Having titles differentiate the two can avoid the frustration.
For the most part HN is great about not having linkbait. But when I do see something that sounds improbably good I just go straight to the comments and see if other people find the article legit (as is the case here).
That being said, would any of this incremental research have been slower, or canceled, or derailed, if the HN articles about intermediate reports of lab experiment on mice had the word "on mice" in the title ?
That's literally all I'm asking for here.
The one open question I wish they would get at is the exact sentization mechanism behind the PD-L1 inhibitor and IFN-1 response. The idea is that cancer cells have selective pressure to hide from the immune system and one way of doing that is presenting this PD-1 receptor to the PD-L1 ligand on the immune cell, an interaction that keeps the cancer cell from being killed and one that PD-L1 inhibitor drugs target to enable tumor cells to now be visible to the immune system (as they output a lot of screwed up things that are otherwise visible to the immune system as "not self").
They tested tumors that aren't sensitive to pd-l1 inhibition so presumably evading immune surveillance another way instead of presenting PD-1, and then found them to then be sensitive to PD-L1.
It could be that within a tumor there are subclonal cells that do express PD-1 but are otherwise protected from PD-L1 inhibitiion having any effect from the hostile tumor microenvironment keeping immune surveillance from operating normally anyhow. Induce the immune response, now the T cell is in the area for PD-L1 inhibition to work. Another possibility is that the IFN-1 induction leads to PD-1 now being expressed by cells that didn't do it previously.
Authors didn't explore this though. Probably would take more experiments and mice are expensive and time consuming. It could be answered by single cell RNA sequencing of these unresponsive tumors and seeing if there is some subset of cryptic tumor cells that do express PD-1 already before IFN-1 induction. As well as measuring expression after IFN-1 induction (maybe several timepoints to measure change in gene expression profile in the tumor population, if any)
https://www.nature.com/articles/s41551-025-01380-1
This is the abstract, though, which suggests the need for a standard "in mice" disclaimer:
> The success of cancer immunotherapies is predicated on the targeting of highly expressed neoepitopes, which preferentially favours malignancies with high mutational burden. Here we show that early responses by type-I interferons mediate the success of immune checkpoint inhibitors as well as epitope spreading in poorly immunogenic tumours and that these interferon responses can be enhanced via systemic administration of lipid particles loaded with RNA coding for tumour-unspecific antigens. In mice, the immune responses of tumours sensitive to checkpoint inhibitors were transferable to resistant tumours and resulted in heightened immunity with antigenic spreading that protected the animals from tumour rechallenge. Our findings show that the resistance of tumours to immunotherapy is dictated by the absence of a damage response, which can be restored by boosting early type-I interferon responses to enable epitope spreading and self-amplifying responses in treatment-refractory tumours.
[0] "In this study on mice with melanoma, the vaccine was able to clear existing tumors that had proven drug-resistant."
https://www.nature.com/articles/s41590-019-0416-z
https://news.uthscsa.edu/scientists-create-first-mouse-model...
https://www.nature.com/articles/s41571-022-00721-2
its not just, put it in a mouse, then guess about what happens to humans.
I'm guessing this is rarely tested since animal modeling is usually a gating factor for human testing?
The catch here is that only two targets (PD(L)-1 and CTLA-4) turned out to work well in humans. All of the other immunotherapies that looked mediocre preclinically turned out to also be mediocre or entirely ineffective in humans.
https://www.statnews.com/2019/04/15/in-mice-twitter-account-...
Fever and the thermal regulation of immunity: the immune system feels the heat
https://pmc.ncbi.nlm.nih.gov/articles/PMC4786079/
Is there a way to ban lies about cancer vaccines, fusion reactors, and infinite battery storage ?
Sure, okay, people are working on that, and they're making small incremental improvements and that's good for them ; and unfortunately they need to advertise to secure more funding for the later incremental stage of their research. I understand that.
But please stop with the nonsensical "cancer vaccine", "miracle cancer treatment", "cancer breakthrough" etc... This is an insult to everyone who lost a loved one to cancer.
Cause I'll be _really_ happy when a _real_ cure happens (as in, when anyone can go the their doctor, for real, and get a real "cure", and they have no cancer after that, and it's a simple as getting a cure for, well, you know, the diseases that we "cure", and that are definitely not cancer ?)
But this is not today. Today we "deal" with cancer, we "spare" people some time, we squash it a bit and maybe save a couple of years if you have the "lucky" kind of cancer - and that's great, and let's continue doing that.
But enough with the headlines.
Play it like Apple, please.
Tell me about it when I can buy it.
Otherwise, I'm going to start posting things about that "AGI" that I was able to train, and that can think () !!! Trust me, it's in Rust !!
() : at the same level as a single cell organism in a simulated environment
Sorry if this comes across as snarky but perhaps you should not read posts on a hacker forum, and instead limit yourself to reading advertisements?
Don't get me wrong, it's encouraging to see research in this field progressing. But there is a long list of treatments that work in mice that do not work in humans.
I'll temper my enthusiasm with a healthy dose of pragmatism.
So, of course it gets to the HN front page, because the title is so catchy !
I guess the only way to make it go to the front page faster would have be to label the article : "MIT alumni-founded, Standford-based, YC-funded startup creates universal cancer vaccine with AI, in Rust"
If not, no.