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Comment by cyberax | Hacker News Reader

There are some ideas about making it triggerable. So first you load the cells with a protein that is ready to start shredding but is inactive. Then you trigger it with a second compound.

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This would shorten the timeframe for cells to mutate and acquire resistance mechanisms, but would not address the issue of cells with preexisting (epi)genetic resistance mechanisms that would then be promptly selected for.

Yes, and if you shorten the timeframe enough, there's a chance that it can clear all the cancerous cells. You also ideally would use multiple variations of the therapy to further reduce the chance of a pre-existing escape mutation.

That's how we deal with HIV. No single HIV therapy (so far) is effective enough to suppress the virus all by itself, but a combination of them provides a barrier that is too high for mutations to jump.

Agreed. Assuming it's ultimately proven to work in vivo, I think the endgame of this therapy is multiple guides targeting multiple mutations along with multiple delivery mechanisms (a formulation-diverse cocktail of LNPs + eVLPs [0]?). Sure, tech like [0] is futuristic and fanciful, but so is the tech of the OP, and both will probably reach in vivo maturity around the same time.

[0] https://pmc.ncbi.nlm.nih.gov/articles/PMC8809250/

This will also cause problems because too many cells die at once. See the comments in other threads; killing the entire cancer at once is very hard on the body.

Tumor lysis syndrome is a thing, but it can be managed. It's far better than the alternative.

The new therapies will also likely be applied after surgical resection and/or classic therapies to reduce the bulk of the cancer.

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