It’s good progress but I want to say it’s still not a magical cure - the fundamental idea is flawed - the tumor can and likely will in many patients just mutate the immunogenic epitope.
I guess for the treatment to be most effective you need to target some of the earlier mutations, rather than a small clone.
From my perspective, and not having read the paper, I thought the technology to predict what TCR would bind a particular peptide on a particular MHC-1 was not there yet.
Could you elaborate? I'd like to understand what you mean, as I don't work on onc. Aren't recurring mutations in response to treatment in f.e EGFR is the reason we keep developing multiple generations of small molecule therapies for it?
Novel epitopes should be high copy number - and driver mutations will be present in 80-100% of the cancer cells. It depends how many cancer cells you get in your biopsy that you sequence I guess.
It is easier for a cancer cell to mutate or remove a cell surface protein than to mutate the same mutation targeted, but you are right - that can happen and I'm sure will be a form of treatment resistance for these types of treatment in the future.
https://www.sciencedirect.com/science/article/pii/S155608642...