Experiencing cancer in my family I can tell for sure all of that buzz is quite exciting, but in the last 5 years there haven't been breakthroughs that would significantly improve outcomes for an average patient.
We don’t have 5 year survival rates for people diagnosed less than 5 years ago. That doesn’t mean things have stopped improving, we just don’t have the data yet.
Average person with cancer does better when any individuals cancer treatment improves and there have been improvement. This doesn’t mean everyone with cancer gets a slight improvement, often it’s specific types or stages that improve without impacting others. Where general progress comes from is it’s not the same improvements year after year.
I agree, or at least I would stress that people should be allowed to consent to that.
I don't know what the prevailing medical ethics of doing that kind of thing in consenting patients
in that state, but my uninformed intuition is I would disagree with it.
Though one thing that I might think researchers might not want is people may be too sick to recover even if their cancer disappeared tomorrow.
In the US, the FDA has a Compassionate Use exemption to clinical trials for exactly this circumstance!
There must be informed consent, no reasonable alternatives (which, in cases we deem terminal, is often the case), and some evidence pointing to the treatment possibly being helpful. It's an excellent ethical program that gives patients a choice and advances science.
In my experience most biotech companies working on promising drugs and therapies don’t want to touch the exemption with a 30 foot pole. Since they raise most of their money from the public to fund clinical trials, a single bad reaction could generate enough bad PR to derail fundraising and kill the drug. Sticking to clinical trials allows them to control that blast radius so even though the FDA approves >95% of applications, in practice very few drugs are available that way.
Both patient participation in clinical trials and compassionate use of experimental treatments are fairly common for cancer patients, with various accessibility barriers. (One issue with the latter, for example, is that the incentives aren't lined up for companies to provide unapproved drugs to dying patients, you're way more likely to get a horrible complication that leads to bad press than a miraculous recovery).
Actually, when in the lifecycle of developing a treatment does anyone have a real idea of what cost will be? Can anyone know this yet?
In terms of where _prices_ are set, that negotiation is a function of efficacy relative to other things in the market right? If it ends up treating cancers that each already have a reasonably effective treatment, maybe the pricing isn't that high -- but if it is effective in cases where currently there are no options, the price should be high?
But for something that potentially works against a range of cancers, should we expect to see a sequence of more specific trials (i.e. one phase 1 for basic safety, a bunch of phase 2s for efficacy on specific cancer types, a sequence of phase 3s in descending order of estimated market value? And in 10 years, Alice and Bob with different cancers will pay radically different amounts for almost exactly the same treatment but with small variations in some aspect of the formulation so they can be treated as distinct products?
Does the cost matter? Many countries subsidize healthcare, so there's either no charge or a token payment which doesn't even pretend to cover the cost of treatment.
Other countries use insurance, so once again the end cost is essentially irrelevant.
"When we systemically administered our nanoagent in mice bearing human breast cancer cells, it efficiently accumulated in tumors, robustly generated reactive oxygen species and completely eradicated the cancer without adverse effects ..."
So it kills human cancer and doesn't harm the mouse in the process.
Xenografted human tumors in mice != human cancer. The support structure of the tumor (tumor microenvironment) differs between model mice and humans, cells derived from human cancer that can be cultivated in a lab and xenografted differ from typical human cancer cells, and xenografting requires immunodeficient mice, just to name a few factors that affect treatment response.
Mice models of cancer are useful, but you should never be too surprised when something that works in mice doesn't work in the clinic, xenografting or no. Cancer is complicated.
Literally reactive oxygen species targets cancer cell DNA. We are taking advantage of the unique chemical environment of the inside of a cancer cell and using it to generate oxygen in a double-whammy to destroy itself.
This is perhaps the best targeted method devised as it seems to collect basically entirely in tumors. Chemo and Radio therapy just aren't that targeted.
Sounds promising, as always fingers crossed these sorts of new techniques produce positive results.
However, here are the problems that Gemini 3.1 pro identified:
1. The Scale of the Human Body: A mouse is tiny, meaning nanoparticles injected into its bloodstream circulate quickly and have a high chance of hitting the tumor. In a human, the circulatory system is vast. The human liver, spleen, and kidneys act as massive, highly efficient filters (the reticuloendothelial system) that often trap and clear metal-organic frameworks (MOFs) out of the body long before they ever reach the tumor.
2. Tumor Architecture: The mouse models used in these studies are usually "xenografts"—tumors grown rapidly over a few weeks under the skin. Human tumors develop over years, building dense, fibrous, scar-like tissue (stroma) and highly pressurized cores. Even if the nanoparticles reach the outside of a human tumor, they often cannot physically penetrate deep enough into the dense human tissue to eradicate the whole mass.
3. Immune System Differences: To grow human tumors in mice for testing, scientists often have to use immunocompromised mice (mice bred without an immune system so they don't reject the tumor). When you inject foreign iron-based nanomaterials into a human with an intact, highly aggressive immune system, the body may attack the particles, causing severe systemic inflammation or immune toxicity.
A great deal of effort and money is spent running studies. I'm inclined to assume the experts in the field are more aware of the tradeoffs of that decision and how to mitigate the downsides than probably all, but certainly the overwhelming majority, of people commenting on this thread.
Someone who needs to ask an LLM will not be helpful in trying to point out something they missed.
They're not pointing out something the researchers missed, they're pointing out something the people in this thread confidently hyping the results are missing. I'm certain the researchers are familiar with the limitations of the models they used (is it bad that the incentives of science and science journalism leads to overoptimistic coverage that hint at groundbreaking implications without explaining to lay readers what the unknowns are? Probably, but that's not these researchers' faults).
The average person in this thread, however, would probably be better informed by asking an LLM for context. They'd be even better informed by taking a few weeks to work through a textbook on cancer biology, but realistically they won't.
My horse in the race is that I'm annoyed by overenthusiastic comments that display a lack of understanding of the history of cancer treatment, and I'm going to be even more annoyed in a few months when the rounds of "haven't we had 1000 cures to cancer posted to HN??? why aren't we using any of them???" start showing up again. I'd rather encourage informed, skeptical optimism.
No, they aren't: the second is irrelevant and unphysical. Highly-pressurised cores? Really? "Dense", I could buy, but:
• If there's blood supply, then (A) it can't be a much higher pressure than the blood pressure (unless there's some Rube Goldberg machine involving active transport), and (B) the tumour is reachable by treatments like this;
• And if there isn't blood supply, then the tumour's core is necrotic, and a treatment to kill the dead cells wouldn't do anything anyway. (Sure, killing the tissue that isolates a lump of necrotic flesh from the rest of the body might cause new and exciting problems, but somehow I think those might be preferable to incurable breast cancer.)
The second is just not a relevant criticism. The third, if it's an actual issue, can probably be worked around by tweaking the molecule slightly – and if not, suppressing the immune system isn't that difficult (it's a known side-effect of many chemotherapies). The first, if it's an issue, can be avoided by injecting the medicine near the target site.
I agree that this treatment might not work in humans, but all the AI's done is taken a generic list of potential concerns, and inserted technobabble to try to make it match the scenario. If you want generic criticism, see https://news.ycombinator.com/item?id=47209076: at least that's true.
Targeted delivery of anti cancer methods is hard. Weather it is multiple radiation beams or anti-body cross linked chemo agents it’s never easy. Chemotherapy poisons the entire body but the cancer cells die faster. A generally administered compound that only affects cancer would be huge.
This is kind of true but misses the bigger picture. We have developed many drug options more targeted than traditional chemotherapy, famously Gleevec for example. The question isn't whether we've found one that could work at all, but how well does it work, what types of cancer it works for, and what the side effects are.
I lost my brother yesterday to cancer. I hope one day this can save lives. Go Beavs.
I'm sorry you have to go through that. Speaking from experience.
<3 awful buddy
me too
Experiencing cancer in my family I can tell for sure all of that buzz is quite exciting, but in the last 5 years there haven't been breakthroughs that would significantly improve outcomes for an average patient.
We don’t have 5 year survival rates for people diagnosed less than 5 years ago. That doesn’t mean things have stopped improving, we just don’t have the data yet.
Average person with cancer does better when any individuals cancer treatment improves and there have been improvement. This doesn’t mean everyone with cancer gets a slight improvement, often it’s specific types or stages that improve without impacting others. Where general progress comes from is it’s not the same improvements year after year.
They should give it to some people with fatal stages of cancer.
I agree, or at least I would stress that people should be allowed to consent to that. I don't know what the prevailing medical ethics of doing that kind of thing in consenting patients in that state, but my uninformed intuition is I would disagree with it.
Though one thing that I might think researchers might not want is people may be too sick to recover even if their cancer disappeared tomorrow.
In the US, the FDA has a Compassionate Use exemption to clinical trials for exactly this circumstance!
There must be informed consent, no reasonable alternatives (which, in cases we deem terminal, is often the case), and some evidence pointing to the treatment possibly being helpful. It's an excellent ethical program that gives patients a choice and advances science.
In my experience most biotech companies working on promising drugs and therapies don’t want to touch the exemption with a 30 foot pole. Since they raise most of their money from the public to fund clinical trials, a single bad reaction could generate enough bad PR to derail fundraising and kill the drug. Sticking to clinical trials allows them to control that blast radius so even though the FDA approves >95% of applications, in practice very few drugs are available that way.
Both patient participation in clinical trials and compassionate use of experimental treatments are fairly common for cancer patients, with various accessibility barriers. (One issue with the latter, for example, is that the incentives aren't lined up for companies to provide unapproved drugs to dying patients, you're way more likely to get a horrible complication that leads to bad press than a miraculous recovery).
Here's an insightful blog series about Jake Seliger's experience participating in clinical trials. He was a regular HackerNews user who passed away in 2024: https://bessstillman.substack.com/p/please-be-dying-but-not-...
If it worked, how much might it roughly cost per treatment, at scale?
Actually, when in the lifecycle of developing a treatment does anyone have a real idea of what cost will be? Can anyone know this yet?
In terms of where _prices_ are set, that negotiation is a function of efficacy relative to other things in the market right? If it ends up treating cancers that each already have a reasonably effective treatment, maybe the pricing isn't that high -- but if it is effective in cases where currently there are no options, the price should be high?
But for something that potentially works against a range of cancers, should we expect to see a sequence of more specific trials (i.e. one phase 1 for basic safety, a bunch of phase 2s for efficacy on specific cancer types, a sequence of phase 3s in descending order of estimated market value? And in 10 years, Alice and Bob with different cancers will pay radically different amounts for almost exactly the same treatment but with small variations in some aspect of the formulation so they can be treated as distinct products?
Does the cost matter? Many countries subsidize healthcare, so there's either no charge or a token payment which doesn't even pretend to cover the cost of treatment.
Other countries use insurance, so once again the end cost is essentially irrelevant.
Yes? Countries that subsidize healthcare don't calculate infinite value per person.
Of course it does. Countries have budgets. Expensive drugs aren't doled out like candy; they require screening, waits, connections, and even bribes.
As far as nanomaterial assembly goes MOF syntheis is pretty scalable
in mice?
Yes, in mice, but human cancer cells:
"When we systemically administered our nanoagent in mice bearing human breast cancer cells, it efficiently accumulated in tumors, robustly generated reactive oxygen species and completely eradicated the cancer without adverse effects ..."
So it kills human cancer and doesn't harm the mouse in the process.
Xenografted human tumors in mice != human cancer. The support structure of the tumor (tumor microenvironment) differs between model mice and humans, cells derived from human cancer that can be cultivated in a lab and xenografted differ from typical human cancer cells, and xenografting requires immunodeficient mice, just to name a few factors that affect treatment response.
Mice models of cancer are useful, but you should never be too surprised when something that works in mice doesn't work in the clinic, xenografting or no. Cancer is complicated.
Doesn't harm the mouse. But would it harm the normal human cells?
Human breast cancer, in mice.
Anything that doesn’t genetically target cancer cells is just not the solution long term. Any progress is good though.
Literally reactive oxygen species targets cancer cell DNA. We are taking advantage of the unique chemical environment of the inside of a cancer cell and using it to generate oxygen in a double-whammy to destroy itself.
This is perhaps the best targeted method devised as it seems to collect basically entirely in tumors. Chemo and Radio therapy just aren't that targeted.
Sounds promising, as always fingers crossed these sorts of new techniques produce positive results.
However, here are the problems that Gemini 3.1 pro identified:
1. The Scale of the Human Body: A mouse is tiny, meaning nanoparticles injected into its bloodstream circulate quickly and have a high chance of hitting the tumor. In a human, the circulatory system is vast. The human liver, spleen, and kidneys act as massive, highly efficient filters (the reticuloendothelial system) that often trap and clear metal-organic frameworks (MOFs) out of the body long before they ever reach the tumor.
2. Tumor Architecture: The mouse models used in these studies are usually "xenografts"—tumors grown rapidly over a few weeks under the skin. Human tumors develop over years, building dense, fibrous, scar-like tissue (stroma) and highly pressurized cores. Even if the nanoparticles reach the outside of a human tumor, they often cannot physically penetrate deep enough into the dense human tissue to eradicate the whole mass.
3. Immune System Differences: To grow human tumors in mice for testing, scientists often have to use immunocompromised mice (mice bred without an immune system so they don't reject the tumor). When you inject foreign iron-based nanomaterials into a human with an intact, highly aggressive immune system, the body may attack the particles, causing severe systemic inflammation or immune toxicity.
The people that want to prompt an LLM will do it.
These are all correct observations about the limitations of xenografted mouse models.
A great deal of effort and money is spent running studies. I'm inclined to assume the experts in the field are more aware of the tradeoffs of that decision and how to mitigate the downsides than probably all, but certainly the overwhelming majority, of people commenting on this thread.
Someone who needs to ask an LLM will not be helpful in trying to point out something they missed.
They're not pointing out something the researchers missed, they're pointing out something the people in this thread confidently hyping the results are missing. I'm certain the researchers are familiar with the limitations of the models they used (is it bad that the incentives of science and science journalism leads to overoptimistic coverage that hint at groundbreaking implications without explaining to lay readers what the unknowns are? Probably, but that's not these researchers' faults).
The average person in this thread, however, would probably be better informed by asking an LLM for context. They'd be even better informed by taking a few weeks to work through a textbook on cancer biology, but realistically they won't.
My horse in the race is that I'm annoyed by overenthusiastic comments that display a lack of understanding of the history of cancer treatment, and I'm going to be even more annoyed in a few months when the rounds of "haven't we had 1000 cures to cancer posted to HN??? why aren't we using any of them???" start showing up again. I'd rather encourage informed, skeptical optimism.
No, they aren't: the second is irrelevant and unphysical. Highly-pressurised cores? Really? "Dense", I could buy, but:
• If there's blood supply, then (A) it can't be a much higher pressure than the blood pressure (unless there's some Rube Goldberg machine involving active transport), and (B) the tumour is reachable by treatments like this;
• And if there isn't blood supply, then the tumour's core is necrotic, and a treatment to kill the dead cells wouldn't do anything anyway. (Sure, killing the tissue that isolates a lump of necrotic flesh from the rest of the body might cause new and exciting problems, but somehow I think those might be preferable to incurable breast cancer.)
The second is just not a relevant criticism. The third, if it's an actual issue, can probably be worked around by tweaking the molecule slightly – and if not, suppressing the immune system isn't that difficult (it's a known side-effect of many chemotherapies). The first, if it's an issue, can be avoided by injecting the medicine near the target site.
I agree that this treatment might not work in humans, but all the AI's done is taken a generic list of potential concerns, and inserted technobabble to try to make it match the scenario. If you want generic criticism, see https://news.ycombinator.com/item?id=47209076: at least that's true.
Targeted delivery of anti cancer methods is hard. Weather it is multiple radiation beams or anti-body cross linked chemo agents it’s never easy. Chemotherapy poisons the entire body but the cancer cells die faster. A generally administered compound that only affects cancer would be huge.
This is kind of true but misses the bigger picture. We have developed many drug options more targeted than traditional chemotherapy, famously Gleevec for example. The question isn't whether we've found one that could work at all, but how well does it work, what types of cancer it works for, and what the side effects are.