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SciShow Explains Cardiff’s Potential Universal Cancer Treatment

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Three weeks ago, Nextbigfuture covered the cancer treatment breakthrough made by researchers at the University of Cardiff.

Now SciShow has a video that explains how this discovery was made and why it is so promising.

The researchers took a range of killer t-cells from the body and tested them against cancer. One of the killer t-cells was very effective and killed all of cancer cells and not just the ones with bacteria inside them. They tested it against other types of cancer and it was effective against all of the different cancers.

This was done in mice.

They hope to have human clinical trials in a few years and they are trying to understand the exact mechanism being used to identify cancer cells while differentiating from healthy cells.

31 thoughts on “SciShow Explains Cardiff’s Potential Universal Cancer Treatment”

  1. I wonder how much of that is due to:
    A. Earlier detection
    B. People being enabled to survive brutal treatments that used to just kill them; i.e. being able to survive the treatments, not the disease.
    Perhaps I am a little bitter, having lost both parents to cancer; the first to secondary infection when her immune system was knocked out due to chemo. And the second because of a series of missteps and failures when my father’s PCP retired and the net PCP failed to detect the cancer in time to do anything about it. These are real world “complications” too, and complicate straight line lab result improvements.

  2. there are plenty of terminally ill who are experimental guinea pigs. But that isn’t what the meds and treatments are meant for that are being tested. It’s like throwing a bucket of sand on a house that is ablaze, while the same bucket could potentially put out a small fire in the kitchen (or you need water, or CO2, or Halon), not to mention fire prevention to start with. Besides, many of these experimental treatments kill the patient not because the meds may have worked, but because the rest of the body (immune system, metastasized tumors, organ failure etc) is in such bad shape it is very hard to determine whether the meds would have worked (on someone not terminal). Risk of overwhelming false positives.

    Unfortunately, too many get false hopes, but it’s human nature to want to live.

  3. Do read up on immunotherapy. Cures. Ipilimumab. Dr Allison (of Nobel prize fame) discovered this in 1994-6. By 2001 it underwent clinical trials and FDA approved 2011. About 16 years from basic research trial and error to approval. Can this process be faster-tracked? Absolutely. Spend MORE time on the basic research (though in this case Allison is a genius and very quickly discovered the recipe), and “get it right”. Data and molecular modeling and AI can help a lot. Then, shorten the clinical trial phases, also with better data.

    The biggest problem with the long approval time frames are the localized small data samples in each country’s jurisdiction and process. To make the faster process work it needs global coordination in parallel testing streams.

  4. I think he was referring to the high mutation rate in cancer cells which causes the cells with the most resistance to a particular treatment to survive and thus the causing the cancer to change it’s characteristics with times.

  5. All the building blocks are falling into place for a complete panacea cure for cancer.

    My best friend recently received a diagnosis that he had a deadly leukemia – and 5 months to live.

    Then he went to a research facility and received TCAR therapy and was COMPLETELY CURED! They even changed his blood type in the process. Who knew they could do that?

    Lives are at stake and they must be careful, but we’re getting there!

    Thanks for the great article Brian!!

    JD

  6. cancer still can evolve inside a single patient. And it does all the time to avoid immune system’s response. However, the real important question is what is the off-site damage. It is pretty easy to kill cancer cells. Killing them while keeping the body alive is much harder, though. So here we have a therapy that looks promising but will not be a silver bullet, yet still can save millions of lives. Probably some cancers will respond very well, some not at all. We will know in some 10 years

  9. It’s also market failure. Regulators have no incentive to allow trails will realistic risks of death or injury, because they get blammed by politicians when some people die on one. Big pharm companies actually prefer the high cost of trials as it acts as a barrier to entry for smaller biotechs. Currently biotechs often sell/partner their molecules at stage 2-3 with big pharma who have the financial resourses and clinician networks to run stage 3 trials.

    One way out of this mess may be clinical trials on dogs, as they are often much better models of human disease than mice, particularly if they have naturally arising cancers rather than transplanted cancers as in mice. People are now more willing to pay for expensive treatments such as CAR T therapy for their dog, giving a financial incentive to pay for trials in dogs. As people are less outraged when a bunch of dogs die in a trial, clever politicians may spot a chance to get out of the circular log jam of regulators and politicians both seaking to avoid getting the blame for a run of patient deaths on a trial.

  11. Apparently all, or just about all, normal human body cells display MR1. There’s something different about what cancer cells display in concert with MR1 which the researchers don’t understand yet.

    But yes, there’s a fair likelihood that some type of healthy tissue or another (maybe just rapidly dividing stem cells) has a similar MR1 profile. The clinical trials will be important.

  12. The cure rates for cancer have been improving steadily for decades now. Often very dramatically.

    It’s just not true to say that the cure rates haven’t gone up.

  13. Please Google t cells killing cancer. This field isn’t entirely new and many people have been cured using early methods of this treatment.

  14. In the paper, they tested normal cells which have MR1. They also tested cells presenting bacterial products in MR1. Neither of these could activate the tumor-specific cells. Selection for MR1 negative tumor cells could be a problem but this could be compensated with other treatments like CAR or checkpoint inhibitors.

  16. Most likely there are non-cancerous cells in the human body that also display MR1 on their surface. So T cells will kill the cancer cell and … will kill human cells that are critical to the body’s survivor. (Unlike in the mouse body.)

  17. And if this could be used as a broad prophylactic, it could knock down cancerous cells before they can divide much and have the opportunity to mutate in a way that is immune to this treatment.

  18. That’s unlikely. Cancer is not a lifeform. They do not spread to other people. Each cancer is contained in a single patient.

    “Superbugs” are dangerous because they are not contained to a single patient. So you have millions taking antibiotics. In one patient a bacteria has a mutation that makes it immune. That bacteria will spread to other people.

    In cancer, if someone s cancer develops immunity, that person will either die or the cancer will have to be removed by other means. Either way it won’t spread to other people. The chances that cancer’s in everyone will develop immunities are pretty slim.

    Even if the person had children, the children will not acquire that cancer with immunity

  19. Most people skip over words like “potential cure” in popsci write ups and other caveats in the source literature, if they even bother to dig that deep.
    Just because some treatment works in a pitrie dish, a mouse or a dog etc, that does not mean it will be a viable treatment in humans.
    Take care not to conflate what the research is actually saying and what you or the popsci write up is hoping it could mean/lead.
    I’m not saying hope or speculation is bad, you just cant forget that your hopes and speculations my not pan out.

  20. What you say is mostly correct, however many cancer cells evolve also gaining functions and not only simplifying their genome. As every cell contains all the genes of the organisms cancer cells that reactivate pathways to induce better blood flow (to gain nutrients), to reorganize their cellular skeleton (becoming more flexible and mobile), and to evade immune response and programmed cell death, all have significant advantages.
    The same is true for telomerase reactivation.
    Here on NBF we always read about age reversal but tissue ageing is what mainly prevents (or at least decreases) the incidence of tumors.

    Regards

  21. well, cure rate has already significantly increased (obviously there is always space for improvement).
    Adjusted for demographic changes the age-standardized death rate from cancer has fallen by 15% since 1990 worldwide. In the US and Germany the age-standardized cancer death rate has fallen by 20%; in France by 25%; and in Italy by 28%.

    Source ourworldindata dot org

    Regards

  22. You can deal with this by using an AND logic function. Give a T cell two receptors. If it has a common surface protein AND does not have MR1 on its surface then kill the cell. Your regular T Cells already do this for MHC (receptors that present cut up bits of protein from within every cell).

  24. Well… technically there ARE cancers that expand beyond a single patient.

    Tasmanian devil facial tumour disease

    Canine transmissible venereal tumors

    But yes, 99.999% of cancers are restricted to one individual.

  25. There is a new “cure” for cancer in some science blog like this one about every week, and a big breakthrough like this every few months. Yet, it’s still Cut, Poison, Burn (CPB) pretty much as it has been for the last 50 years. Doctors are able to discover cancers earlier, are able to bring more patients to the edge of death and back again to kill their cancer – often with a lifetime of debilitating effects – but really haven’t upped their cure rate much, especially for the major types of cancers.
    If someone could find a cure for why such promising treatments fail to get to market, we’d be cancer free by now. Instead cancer remains the 2nd highest cause of death.
    Here’s hoping it’ll be very different this time. I am running out of time due to age.

  26. So how many people need to die of cancer before they do human clinical trials on people. We certainly would not want to endanger those people with 6 months to live, while they are at the same time being in great pain!

  29. Cancers do evolve, but only within the one patient. They have a very high mutation rate and generally a high clonal expansion rate so they effectively evolve like asexual single celled organisms.

    Unlike other single celled organisms though, they start with a very high complexity – way more genes than is needed for their simplified life. So they typically evolve by losing unnecessary genes, not by recombining new ones. A cancer might lose the MR1 gene, or another gene involved in what it presents on the surface, but it won’t develop a sophisticated method of hiding it or altering it.

    That said, you can kill a cancer before it evolves by hitting it hard enough. And if this works so well on so many different cancers, then perhaps there is some reason why they really need their MR1 to thrive and can’t lose it.

  30. This is very promising. I hope they continue to follow up both lines of inquiry. We still need stuff to kill bacteria and viruses, as well as cancer.

  31. Seems likely that cancer would evolve to not present MR1 on the cell surface, thus rendering the therapy ineffective.

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