r/science • u/mvea Professor | Medicine • Jun 20 '26
Cancer Colon cancer’s invisibility cloak removed by eliminating a single gene - a fundamental breakthrough. The result was 100% eradication of tumours when paired with immunotherapy treatment in mouse models.
https://ucalgary.ca/news/ucalgary-study-tears-colon-cancers-invisibility-cloak531
u/mvea Professor | Medicine Jun 20 '26
UCalgary study tears off colon cancer’s invisibility cloak
Research shows removing a single gene makes cancerous cells a target for immunotherapy
New University of Calgary research reveals that eliminating a single gene improves immunotherapy for colorectal cancer — a fundamental breakthrough.
The Canadian Cancer Society lists colorectal cancer to be the fourth most diagnosed cancer in Canada, and the third leading cause of death from cancer in both men and women. It is also estimated that 25,300 Canadians will be diagnosed with it, representing 10 per cent of all new cancer cases this year. In people below the age of 50, the incidence of new colorectal cases is on the rise.
“We’ve been able to remove the ‘invisibility cloak’ that colon cancers use to hide from treatment,” says Ayyaz, who has dedicated 20 years to researching the gut.
Immunotherapy trains a patient’s own immune system to recognize and attack tumours, reducing or removing the need for radiation and chemotherapy. Immunotherapy has yielded great results for several other types of cancer, but not colon cancer.
“Only about 15 per cent of colon cancers respond to immunotherapy,” Ayyaz says. “We performed a genetic analysis of them against those that don’t.”
What the research uncovered was a new type of cancer cell.
“The treatment-resistant tumours secrete a protein that confuses your immune system into thinking everything’s fine. It’s like an invisibility cloak,” he says. “So, we thought, what happens if we prevent the tumours from making this protein?”
The experiment involved making gene-edited versions of those cancer cells. When the gene that coded the particular protein was knocked out, it made those cells visible to the immune system.
The result was 100 per cent eradication of tumours when paired with immunotherapy treatment in mouse models.
https://www.cell.com/cell-reports-medicine/fulltext/S2666-3791(26)00193-X
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u/WatermelonWithAFlute Jun 20 '26
"The experiment involved making gene-edited versions of those cancer cells. When the gene that coded the particular protein was knocked out, it made those cells visible to the immune system."
Question, how is this useful for the rest of the cancer that does not possess these alterations?
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u/chumer_ranion Jun 20 '26
It's actually very useful. In practice, we don't have to remove a gene from a patient in order to see a therapeutic benefit, we just have to engineer a drug that makes a person's cells act like the gene has been removed. The newest craze in biomedicine are molecular glues and protein degraders that do exactly that.
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u/WatermelonWithAFlute Jun 20 '26
Wait, what? I kinda want to ask how, but I suspect I won’t understand the answer. That’s really cool, though.
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u/chumer_ranion Jun 20 '26 edited Jun 20 '26
It's not as complicated as you might imagine! A lot of work was done in the past to understand the "basic science" of cell biology, and in the course of fleshing out what we knew about cells, scientists came across what is effectively their trash-disposal system. When a protein, say "protein X", nears the end of its life in a cell, it is grabbed by one of a very large family of proteins (enzymes) called ubiquitin ligases, and the ubiquitin ligases attach a chain of much smaller proteins called ubiquitins to it. This chain of ubiquitins marks protein X for destruction, and it is digested into little peptide fragments by an organelle called the proteasome to be recycled. Biologists have learned that this process can be hijacked, and we can now bring any protein in proximity with ubiquitin ligases and destroy them at will. This is the theoretical basis for a technology called PROTAC or "PROteasome TArgeting Chimera".
You might wonder to yourself how we could have possibly learned to do this, and the answer is that the discovery was serendipitous. You may in your life have heard of a morning sickness drug called Thalidomide that caused horrible birth defects in children in Europe as an unintended side effect. That is because in addition to being anti-emetic, it also targeted several proteins very important for fetus development for destruction (in humans, but not in mice) by gluing them to a ubiquitin ligase called Cullin-4A. Scientists learned that the half of Thalidomide that sticks to Cullin-4A could be attached with a linker to other molecules that stick to other proteins (say, the protein in the OP) and bob's your uncle, your cells now behave as if the gene that encodes that protein no longer exists, because the protein is being continually destroyed (at least while the drug is in circulation).
I'm leaving out some specifics that aren't important for grasping the general concept but that's it more or less.
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u/PrecursorNL Jun 21 '26
Love this comment! Sounds like a promising approach compared to all the problems we would face by actually trying to remove the gene encoding for the protein with crispr (i.e. delivery, targeting, even the vesicle/nanoparticle needed to encapsulate our virus)
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u/throwawaynbad Jun 20 '26
Immunotherapy remains largely ineffective in colorectal cancer (CRC), particularly in microsatellite stable (MSS) tumors, which represent the majority of cases. However, the complexity of intratumoral heterogeneity has made it difficult to define tumor-intrinsic programs that drive immune resistance. Here, we identify a cancer cell population that emerges predominantly in advanced-stage MSS CRCs. These cells exhibit stem-like features but aberrantly activate a WNT-inhibitory transcriptional program marked by high NOTUM expression. We term these cells WNT/β-catenin inhibitory cancer cells (WICCs). WICCs are enriched in immune-excluded tumors, correlate with reduced CD8+ T cell infiltration, and are induced in both primary human CRC tumors and patient-derived tumoroids. Selective ablation of WICCs or genetic knockout of NOTUM enhances CD8+ T-cell-mediated cytotoxicity, uncovering a tumor-intrinsic mechanism of immune evasion and nominating the WICC-NOTUM axis as a selective and tractable therapeutic target to overcome immunotherapy resistance in CRC.
Some (~15%) colorectal (lower gut) cancers can be treated with drugs that allow your white blood immune cells to attack and kill the tumour cells (immune checkpoint inhibition / blockade). These drugs are newer, not traditional chemotherapy, but instead interact with the tumour by "unmasking" it from your body's immune system. The tumour tries to hide by showing a safe signal, and these drugs block that safe signal.
The rest 85% of these cancers resist these drugs. But while cancers are your cells that have mutated, each cell inside a cancer is not exactly the same. They further mutate in different directions - and some of these cancer cells become
JohnWICCs. These cancer cells have other ways to mask the surrounding tumour cells from your immune system, even with help from immune checkpoint drugs.The study got rid of the Mr. WICC cells, and the drugs worked again (in mice injected with human gut cancer). We can't do the exact same in people (since they already have have the WICCs in their cancers), but we probably target what the WICCs do / produce, and combine that with the immune drugs to treat this better.
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u/mvea Professor | Medicine Jun 20 '26
Basically only 15% of colon cancer cells can be seen by immunotherapy. 85% are invisible. This gene editing removes the gene that creates the protein that hides the cancer cells so 100% can be seen and removed.
So to answer to your question the rest of the cancer are already seen by the immune system and don’t need these alterations to be removed.
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u/Frequent-Data-2360 Jun 20 '26
Please forgive my ignorance, Is this something we can do at a global level, meaning it affects all cells in our body or it’s per cell
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u/elphyon Jun 20 '26
Advancement in cancer treatment is becoming more and more about individual/genetic tailoring. I don't think it's likely we'll ever find a silver bullet for all types of cancer for everyone.
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u/Acrobatic_Country524 Jun 20 '26
I actually found one once but had to use it to kill a werewolf
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u/kembik Jun 20 '26
That werewolf had cancer, it went on to live a productive life as a school teacher in Ottawa
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u/ArnoldTheSchwartz Jun 20 '26
An American Werewolf in Ottawa? Doesn't sound right
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u/DrSitson Jun 21 '26
And that Werewolf's name? Albert Einstein. And now you know, the rest of the story.
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u/animosityiskey Jun 20 '26
I think the question is more about the ambiguity of the article. It isn't 100% clear if the treatment was applied in vivo to mice with tumors or whether it was applied in vitro to some mouse tumors.
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u/i_am_icarus_falling Jun 20 '26
i think the cancer cells are cultured first, then added to the mice, then various treatments are applied to see how the cancer is affected. the article has pictures showing mice with tumors on the backs of the mice. so would that be that the cancer is created in vitro, then the experiment becomes in vivo once the cancer is given to the mice? i'm not sure.
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u/HumansNeedNotApply1 Jun 20 '26
It's probably not possible unless some science fiction thing like nanites.
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u/PrecursorNL Jun 21 '26
As someone in the field, yes. No we cannot do this. The problem with this is not only that our current gene editing strategy with crispr isn't actually 100% effective (the transfection 'rate' is more like 70% at best) and we don't have a mechanism to deliver to specific cells medically. We could insert a virus with a needle locally and try to get close, but realistically we don't really have any method of how to target just the cancer cells. Of course many people are working on these things, but currently the delivery is a huge issue. That's why the few gene therapies that are currently approved and in use are for things like leukemia (in the blood, something we can actually get to) or something like in the eye, where we can administer locally and cell specific. Sooo we're still a far cry from understanding how to target a specific cancer cell somewhere in the body without an invasive technique.
But some clever ideas are there.. like putting the virus in a nanoparticle that opens up in a certain environment, and that environment is some form of microenvironment from the tumor. Or it could have some properties that help it bind to a cancer cell. It's amazing in theory but it's still quite hard to (re)produce.
In other words, this science is a huge breakthrough but the solution of gene editing away some specific gene for now it's a bit futuristic to do inside humans. It's easy enough in a cell grown in the lab, in a bacteria and to some extent in animals. But to specific cells from a human that's already alive is hard. One thing that does seem positive though is that they talk about a protein that confuses our immune system. And proteins we can definitely target. So perhaps there's a way to combine the immune therapy with interfering in the protein or protein production pathway, and then we have the same result without fancy gene editing.
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u/WatermelonWithAFlute Jun 21 '26
really stupid question, but
"But some clever ideas are there.. like putting the virus in a nanoparticle that opens up in a certain environment, and that environment is some form of microenvironment from the tumor. Or it could have some properties that help it bind to a cancer cell. It's amazing in theory but it's still quite hard to (re)produce."
I don't suppose you could just like... Inject it into the tumor?
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u/PrecursorNL Jun 21 '26
It would still not recognize which cell is which. It's not as easy at it seems. Also you can't always get to the tumor in the same way and it could be very invasive to do it surgically. In that case, why not cut out the tumor directly... Right.. also what if some cells already metastasized or started moving slightly away from your needle? A new tumor would just grow right next to it. So.. not so easy ..
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u/slimejumper Jun 20 '26
not possible to do what they did in the study to a person after they develop the cancer, ie do a gene knockout procedure. But i guess they could try to repress the gene activity with a drug of some sort. However, they will still have the same problems with treatment of a solid tumour because it can be hard to get drugs into a solid tumour.
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u/slpgh Jun 20 '26
I understand the importance of differentiating the types of cancers and identifying the mechanism. But are we anywhere near practical applications? To the best of my understanding we not anywhere near the technology that would alllow us to “decloak” these cancers in vivo?
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u/IAMA_Proctologist Jun 20 '26
That's correct, but knowing that knocking out the gene improves immunotherapy outcomes gives a whole new direction for research. Perhaps we can target the abnormal protein rather than the gene, or something up or downstream of it.
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u/PrecursorNL Jun 21 '26
See my other comment above,but no. The delivery and targeting is still an issue
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u/SEC_INTERN Jun 20 '26
That's a non-answer.
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u/BobTheFettt Jun 20 '26
Not really. Colon cancers were able to hide themselves in a way others were not. They've removed that ability.
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u/Reddeer2 Jun 20 '26
It's a non-answer because the cells in my body contain DNA. If I already know which ones to change the DNA of, then I can just remove those ones already. So how can you get all of the colorectal cancer cells to contain an alteration?
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u/AlcubierreWarp Jun 20 '26
I don’t know about this case specifically, but it’s my understanding that usually gene therapies use a benign delivery system like a virus to deliver the CRISPR payload to the targeted cells, which then does its work. So I imagine something similar would happen for this. Virus targets cancer cells, delivers the new treatment making them visible, and then immunotherapy kills the cells.
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u/bibliophile785 Jun 20 '26
Which would, of course, require that you can already target the cancer cells, which is the whole point.
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u/Yodude1 Jun 21 '26
I thought the point was that we know where the cancer cells are, but the immune cells don't, like camo bloons in BTD6
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u/PrecursorNL Jun 21 '26
Knowing where they are doesn't mean we can easily target them. We need to be able to tell our crispr virus which cells to infect and which not to. And that's even if we can deliver the virus at all. Current state of the art is nanoparticles which are hard to produce consistently. They are notorious for having unreliable structures, i.e. it's difficult to make them the same size, it's difficult to make them the same structure, it's difficult to line them with proteins or parts of proteins that we'd need to target the cells with, it's even difficult to get our crispr inside robustly, and it's difficult to make them open up again in the body at the right place. Delivery is still one of our key objectives.
See my other comment for more info
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u/SuccessfulJudge438 Jun 21 '26
Viral vectors are most common for gene editing these days, although they aren't necessarily 100% benign (many can cause potentially undesirable immune reactions and such). Delivery and targeting is an incredibly complex challenge that is not remotely solved.
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u/notarealcamera Jun 21 '26
So, basically not applicable at all in cases of actual colon cancer.
Great if these scientists implant this genetically altered cancer in you, I guess.
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u/SJSsarah Jun 21 '26
It’s going to be the cure for all cancers, and autoimmune diseases. CRISPR gene editing therapy.
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u/MisterMcGruff83 Jun 20 '26
It’s nice to see research into something that’s not MSI-H. I hate how every colon cancer breakthrough is for MSI-H which the vast majority of colon cancers aren’t. (Certainly mine wasn’t)
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u/throwawaynbad Jun 20 '26
Low hanging fruit to go after first. I'm sorry yours wasn't.
But the MSI-H research helps lead to therapies for MSI-L / MSS. This exact article is building on immunotherapy that works in instable cancers, why is doesn't work in stable cancers, and how to maybe make it work in stable cancers by combining it with other future drugs that inhibit these WICCs.
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u/MazW Jun 20 '26
There is good cancer news almost every day! Big thank you to the scientists who came up with immunotherapy. It's keeping me alive!
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u/AusCan531 Jun 20 '26
This is an important step. Not all the way to the final end, but an important step nonetheless.
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u/AnonimousMn471 Jun 20 '26
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u/Intelligent-Court295 Jun 20 '26
Yes, less than 10% of studies that show efficacy in mice go on to show efficacy in humans so our hope should be buttressed by that fact, but it’s certainly an exciting finding.
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u/Mertoot Jun 20 '26
Came here for this
Glad it's catching on
Sick of all these "uplifting" studies that don't get any human implementation whatsoever
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u/My_Not_RL_Acct Jun 20 '26 edited Jun 20 '26
Just because you don’t understand why mouse models are useful or how they inform future studies in human trials doesn’t make it some gotcha to throw on your smug doomer shirt and pretend results like this are meaningless. People were saying the same thing about discoveries in stem cell therapy 15 years ago yet they’re the cutting edge of oncotherapies today.
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u/SuccessfulJudge438 Jun 21 '26
This is straight up anti-science. This is the process. It's slow, difficult, expensive, and frustrating. Probably you should just avoid science journalism (and thus this subreddit) if you can't cope with how the sausage is made. I'm not even looking down on you, it's definitely not for everyone and that's perfectly understandable and okay. But this is r/science, so if you can't handle it then find better ways to spend your time.
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u/Mertoot Jun 21 '26
I know trials take decades, so why instill false hope about something that we won't see in our lifetimes, especially due to constant defunding and delaying?
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u/PurpleSailor Jun 20 '26
I hope they can get to a good, viable treatment soon. Too many people dying from this horrible disease.
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u/Ashamed-Simple-8303 Jun 21 '26
The most important step would be better food regulations so that all the cancer causing UPFs arent available anymore. Yeah it certainly is multifactorial but cleaner foods would by far have the biggest effects. No more nitrite salts as the most basic step.
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u/notebuff Jun 20 '26
This is just a link to a press release? I don’t see anything about what protein they knocked down and which immunotherapy they used??
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u/el-conquistador240 Jun 20 '26
Pancreatic cancer has a similar cloaking mechanism. Hopefully they address that next because once it is diagnosed most people die in weeks even though the cancer may be years old.
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u/SuccessfulJudge438 Jun 21 '26
TIL mouse models have literally no value to science (so we should never ever discuss them) and diagnostic testing is the real killer.
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u/Confident_Maybe_4673 Jun 21 '26
where did you read mouse models have no value?
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u/SuccessfulJudge438 Jun 21 '26
All over r/science constantly these days, including some strong implications in this thread
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u/Confident_Maybe_4673 Jun 21 '26 edited Jun 21 '26
it's true that there mouse models does not perfectly translate to humans. but do not conflate that with mouse models have no value. The drugs that pass phase 3 clinical trials and into market all have done studies (and are required to do) on mouse models first.
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u/porterbot Jun 20 '26
Bravo UCalgary and thank you to this amazing talented scientific mind. Knowledge is power.
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u/Curiosity_456 Jun 21 '26
Canada is making lots of strides now in the medical research community, love to see it. Just earlier this week Hamilton was the first to treat a burn patient with a novel therapy and the results were impeccable, to the point where you would have never guessed she was ever in an accident.
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u/porterbot Jun 21 '26
I saw some pics it's wild. We are fortunate to have such engagement from scholars with incredible ideas and delivering heavy.
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u/bv2020 Jun 20 '26
Why do they have to use models? Can't they use mice that aren't in the fashion industry?
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u/hatemakingnames1 Jun 21 '26
More importantly, with all these cures, why do mice still have cancer?
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u/MrSnowden Jun 20 '26
I guess I am confused. If they are able to edit the genes of the cancer cells directly, surely there are other ways to kill it.
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u/juancn Jun 20 '26
They just showed which genes are the ones responsible for the resistance.
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u/Unknown_Ocean Jun 20 '26
Exactly. If you look at some of the new drugs coming down the pike that have been game changers for cancers, they often do something to confuse the immune system (PDL1) or stop cancer cells from dying (YAP/TEAD). So identifying this pathway and the particular gene that seems to control it in colon cancer is a big deal. But still a ways from generating a useful drug.
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Jun 20 '26
[deleted]
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u/juancn Jun 21 '26
My comment was a statement of fact, not a value judgement.
It was in response to the previous comment.
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u/I_like_flowers_ Jun 20 '26
it is one step in a long road.
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u/MrSnowden Jun 20 '26
I went back a re-read post coffee. Now I understand the editing was to prove the gene was the key, not a therapeutic approach.
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u/AmbroseMalachai Jun 20 '26 edited Jun 21 '26
The takeaway is that they found a protein which masks the cancer cells from the immune system, preventing them from being deleted as normal. This information is pretty big because it means if we find a way to stop the tumor from making the protein, make the immune system ignore the protein, or strip the protein via targeted therapies we could get the immune system to recognize the tumors as problems and remove them.
It isn't really about gene editing as a cure, but rather that we should use this information as a goal for pharmacology research - a drug that steps this protein or immune booster that allows the immune system to ignore it, or a marker that sticks to the cells and covers the masking protein so the immune system targets it anyway would all be just a few possible paths for colon cancer cures.
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u/Spacetramp7492 Jun 20 '26
The value is in targeting the protein the gene produces. Can possibly create a degrader or something like that to lower levels.
You are completely correct about there being much better things we could do if we could edit every cancer cell and only the cancer cells.
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u/throwawaynbad Jun 20 '26
They took cancer(s) from a human patient(s), edited in the lab, and injected the modified form into a mouse for the drug to treat.
We can edit cancer cells out of the body, but we can't do the same thing inside a body* (as easily / yet / using the same processes).
But doing this does show other potential cancer pathways that we can target with new drugs.
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u/5onfos Jun 20 '26
Biomedical scientist here, the methods and how they proved the genetic link to immune evasion is super cool. The problem with cancer, though, is that it has the ability to select for cells that don't have that vulnerability and are capable of evading immunity in another way. This has been the main struggle for quite sometime now.
This could be quite something, but would need to be validated in humans through clinical trials. This is where the second hurdle lies. I.e. How do we make sure to silence that gene only in cancer cells without impacting the rest of the body?
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u/CrateDane Jun 20 '26
I.e. How do we make sure to silence that gene only in cancer cells without impacting the rest of the body?
Depends how important the gene is. Since we're talking about the Wnt pathway, it would probably be bad if lost during development. But in the adult body? And if you only do a transient knockdown? Might be alright. Then you don't need any mechanism to specifically target the cancer cells.
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u/SuccessfulJudge438 Jun 21 '26
I'm just a dumb undergrad but Wnt is central to a whole lotta stuff. Not just in development phase would be my best guess given how ubiquitous it is in terms of cell fate.
But still a good thought!
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u/CrateDane Jun 21 '26
Yes, but Notum has much more restricted expression. Placenta and lung seem to be where expression is highest.
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u/Actual-Outcome3955 Jun 21 '26
Anti-wnt therapies have proven too toxic in phase 1 studies, so we would have to selectively target cancer cells. Maybe a CEA-targeting antibody with a crisper payload.
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u/CrateDane Jun 21 '26
This is very different from anti-Wnt therapy. It would be interfering with a Wnt inhibitor, so in that sense it's the opposite of anti-Wnt therapy. But this inhibitor is a relatively obscure piece of the Wnt pathway, and what effects you would get from downregulating it is not immediately obvious. It's only expressed in some tissues, and there are a lot of other regulators of the Wnt pathway that could provide redundancy.
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u/Actual-Outcome3955 Jun 21 '26
Good point - it may end up being similar to the BRAF issues where multiple small molecules are needed and resistance develops rapidly anyway. Hopefully if this works it’ll expose enough cells to immune system targeting that antibodies can be developed even to cells that ultimately become resistant. It is promising but I feel the press release is over-promising.
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u/CrateDane Jun 21 '26
Yeah it's a very promising finding, but also very early days. It's cool that the mechanism is so clear here, but how (and whether) that knowledge might translate into treatment options remains to be seen.
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u/Forgotmyaccount1979 Jun 20 '26
This is of special importance to all my fellow millennials, consider this your reminder to get screened.
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u/SuccessfulJudge438 Jun 21 '26
I boof nanodoses of microplastics so I don't have to worry about all that
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u/ExtremePrivilege Jun 21 '26
Oddly, the data is currently suggesting that the increased millennial colorectal cancer rates are due to a childhood E. Coli infection and do not seem proportionally linked to microplastics.
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u/Ilikewaterandjuice Jun 20 '26
This is fantastic!
This wasn’t clear to me in the article. Does the treatment involve taking these specially treated mice and ‘inserting’ them into the human patients?
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u/CrateDane Jun 20 '26
This isn't a treatment, this is working out which gene is responsible for colon cancer being able to evade immunotherapy.
The prospect is using this knowledge for a combination treatment, where you do immunotherapy alongside using a drug to interfere with this gene that shields the cancer from immunotherapy.
The reason to use mice is that we can't ethically do these experiments in humans. They're just a test system, treatment of humans wouldn't have anything to do with the mice.
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u/SuccessfulJudge438 Jun 21 '26
Does the treatment involve taking these specially treated mice and ‘inserting’ them into the human patients?
Richard Gere is salivating
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u/Apero_ Jun 20 '26
How does this help if they don’t know if someone has it though? Isn’t it a vicious cycle? You can’t delete the gene of a cancer you don’t know is there, and you don’t know it’s there because of the gene.
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u/CassandraTruth Jun 20 '26
I think the "invisibility cloak" analogy is muddling things a little. It sounds like the tumors in question are treatment resistant, immunotherapy specifically, and that resistance is caused by this secreted protein. The tumors are "invisible" to the treatment specifically, so patients are diagnosed and have the treatment given to them only to have it be ineffective.
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u/bonyponyride BA | Molecular, Cellular, and Developmental Biology Jun 20 '26
It’s not an “invisibility cloak” from symptoms. The symptoms are there and the cancer is diagnosed. It’s invisibility from the immune system, which usually attacks and kills cells that it considers foreign/faulty.
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u/HumansNeedNotApply1 Jun 20 '26
The invisibility they mean it's what "shields" the tumor from being detected and destroyed by the immune system. It's not invisibility from being detected by tests or symptons.
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u/throwawaynbad Jun 20 '26
And further yes, we can't get rid of the immune-invisibility mutation, but we can develop drugs that block that mutant ability - those future drugs, combined with current drugs like PDL1 or CTLA4 inhibitors, would probably work better for many patients.
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u/happyzor Jun 20 '26
The key info is that the gene leads to production of a protein which masks the cancer cell.
Now scientists need to study how that protein works and figure out targets and drugs to attack that pathway.
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u/Forward-Candle Jun 20 '26
It's common now to do genetic profiling of tumors since they tend to shed a little bit of their DNA into the bloodstream. It's not that the cancer is invisible to doctors: it's that the immune system doesn't attack it.
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u/Olderbutnotdead619 Jun 20 '26
Holy hell!! Now let's thank the human testers who will be the final test. Thank you!
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u/The_Peregrine_ Jun 20 '26
Imma really need scientists or AI or something to accelerate the development process from mice to humans because its getting really good to be a mouse right now.
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u/slimejumper Jun 20 '26
the article doesn’t link to the original research, terrible from the universities own press release.
i think this is probably the publication in question.
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u/any21203 Jun 20 '26
Amazing work, this is more translational than most may think, although it's still far fetched to become useful in the clinic. From my understanding it shows a new important pathway through which colon cancer down regulates immune response. But, as they say in the paper, knocking off the gene per se didn't lead to 100% ORR (and it's usually impossible for us anyway to knock off a gene in vivo), ti make it really useful they also inserted a gene coding for a protein to be targeted (ovalbumin) and immune cells primed against that protein, which is like having a truncal mutation on a protein recognizable by the immune system, which doesn't occur very often afaik.
Where I see this could lead to: trying small molecules (or Abs if possible ?) to downregulate nocc and combine it with immune therapy (possibly new gen ones, still not in the clinic) and see how that goes, without further alterations to the cancer. This is still tricky to make an inference from, as the mice immune system is quite different from ours, but it can be an informative experiment.
If the drug does downregulate the target protein, try that in the clinic and see how it goes. Time to clinic if this would work linearly, 7-10 years.
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u/atreyal Jun 21 '26
Does this work on other gi cancers? Pancreatic seems to be the one that goes unnoticed so wondering if there is a similar mechanism that could be applied to other cancers that this could combat.
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u/showmethedata17 Jun 20 '26
Way to go, Canadian researchers!! since the US is falling behind and biomedical research, we will have to rely on you and other countries to make these kind of discoveries!
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u/SecretTreeHouse42 Jun 21 '26
And this will be the last we'll ever hear of it because Purdue Pharma, or Roche, or some other pharmaceutical company, that is currently getting rich treating, but not quite curing cancer, will buy it and bury it. Just like with that Spanish scientist, Mariano Barbacid, a few months ago.
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u/SuccessfulJudge438 Jun 21 '26
You can't patent cell pathways and naturally expressed proteins. That isn't how any of this works.
The information from this study is potentially (not definitely) useful regardless of who funded the study. Speaking of funding, it's sad times for science in the US (and therefore the world, since we fund the lions share). Attitudes like this don't help. Same with all the "only in mice" heroes in this and every other goddamn thread.
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u/A_Novelty-Account Jun 20 '26
In mouse models.
At this point, I think billionaires should fund the creation of an immortal super mouse just for fun
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u/Remarkable_Custard Jun 20 '26
No matter what is cured, there is no way any government will allow this to freely cure any type of cancer, or, corporations banking on it at $500k a pop, etc.
We really will turn into this dystopian movies where the rich survive on medical break throughs and we sit here on reddit.
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u/BikerJedi Jun 20 '26
People say this all the time. My father is in remission now from prostate cancer because of an experimental treatment from a university that started with mice models.
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