Resistance is a neat thing.
I remember (and I'm sure someone will reply with a link to it, since I can't find it) reading a story about a fellow with a very seriously antibiotic resistant bacteria infecting his chest. It resisted everything they had. Researchers found a phage that would attack that specific bacteria- but alas, the bacteria became resistant to the phage as well!
Fortunately, the bacteria had limited dimensions in which to change. The changes needed to become resistant to the phage made it no longer resistant to at least one of the antibiotics. It could not have its cake and eat it to. With both attacks against the bacteria ongoing, it was defeated.
What I'm implying with all this is that yes, the cancer may become resistant to this therapy in question but in doing so it may be forced to become less dangerous, or less resistant to other forms of attack. It does not change merely from "not resistant" to "resistant" but from "form A, which is not resistant" to "form B, which is resistant", and "form B" may have a lot of other consequences.
Even more interesting are drug holidays: cancer becomes resistant to drug A by evolving a new clone that uses some other metabolic pathway unaffected by the drug but is less efficient. Stop drug A, the first more efficient clone takes over again. Give drug A again and there is no resistance for a while.
[1] https://www.oncode.nl/news/one-two-punchmethod-published-in-...
> deploying phages can cause the bacteria to evolve in response, and that evolution sometimes involves switching from being antibiotic-resistant to being sensitive to antibiotics.
There's a few big stories like this. Chances are, in the next 25 years you may find yourself being treated with phages.
For that reason it seems wrong to think about cancer as “developing” resistances - I don’t believe that cancer is something that evolves/mutates.
https://en.m.wikipedia.org/wiki/Somatic_evolution_in_cancer#...
It may well be the definition factor, at least some people think so: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3941741/
If I remember their argument correctly, cells that "only" reproduce anarchically present little danger (benign tumor) if they don't also do so at an abnormally fast rate / metabolism.
The cancer I had when I was young, Hodgkin Lymphoma, is one extra rule broken because the lymphatic cells already don't stay in one place and makes extra copies of themselves - which is why it relatively often occurs in young people. One copying error and the "Die when told to" feature breaks in the new copies and now you've got cancer.
In that spirit, subsequent mutations that confer resistance can be seen as a consequence of this abnormally high metabolism rate that overwhelm the system and also cause increasing mutation rates.
In conclusion, while cancer may indeed become a complicated condition to treat, the root cause thus defined is rather simple. Whether this paradigm is valid and useful is an open question, but the article being discussed sure seems to point that way.
Immune cells are already resistant to each other, and especially to stress. Additionally, they have pieces of genetic code that are manipulated during their life and potential to become self-reactive with no activation. If they lose anergy and apoptosis, it can be enough, and there are many paths to activate them into mitosis.
Immune cells can become a cancer just by their number and statistics of error. Just big leukemia is but a symptom but has potential for first stage cancer.
Forgive this (very tortured) analogy, but I think there is a lesson here for would-be extropians who think society will simply tolerate a few vampires here and there.
Specifically: they'd better be living lives of quiet, impoverished contemplation ...
It's randomness. Theoretically speaking every possible combination could happen. So you should be able to have a Cancer cure, a cancer resistant to that, another cure, another cancer, etc.. at least until you cover all of the possibilities.
The goal is to have science become faster than physical mutations. You generate medicines faster than you generate resistant mutations.
Very interesting finding indeed, these T cells seem to (not fully confirmed) target cells with abnormal mrtabolism, which is one of the hallmarks of cancer in general (most cancers at least).
This solves one of the biggest problems with immunotherapy, which is that if a cancer is not different from regular tissue in any fundamental way that the immune system cannot recognize, then it can't fight it. This is why melanoma is the poster child of immunotherapies (skin cells get mutated a ton due to UV so skin cancer has a lot of mutations to differentiate it by). If this cell stands further scrutiny, it could potentially be a very general therapy option indeed.
Potential caveat is that cancers typically find a way to generate resistance, and markers of abnormal metabolism (at least as detected by this MR1 receptor) night be easy to suppress, in which case this might just become one in a line of multiple treatments. That might still be good enough though.