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Let's say a human cell mutates cancerously, we identify the mutated gene sequence and use CRISPR to mutate the patient's cells to include some variation of the cas genes and spacer sequences matching the mutated cancerous sequence.

Then design a virus to "infect" cells (cancerous and healthy) with this cas gene sequence and spacer sequences.

The infected cells would then produce a specific cas9-like protein targeting the mutated cancerous gene sequence in the patient. As the modified protein producing cells multiplied to replace the old ones, the custom cas9-like protein would detect and remove the targeted cancerous sequence.

More elaborately the approach could be used to inject a large library of known cancerous sequences as cas spacers in reproductive cells to start developing a species-wide defense against a significant range of cancerous mutations.

What primary obstacles would be in the way? I suspect research has been done on this.

My knowledge so far:

  • Basic understanding of virotherapy - I'd like to clarify my question is asking about something beyond research I've seen on anti-cancer oncolytic viruses which target cancer cells. My question is about repairing the cells rather than killing them.
  • A big picture of how CRISPR functions and how it can be modified to achieve specific gene editing functions. Spacer DNA sequences matching targeted gene sequences (usually threats such as bacteriophages) are used by the cas genes to produce proteins called cas9 (or some variation) which couple with crRNA and tracrRNA to match and slice targeted DNA sequences.
  • a closer look at the specifics of cas9 and its behavior.

Potential problems I considered but couldn't find specific studies on:

  • Whether the viral delivery of the modified dna would be prevented by the immune system before all the cancer cells could be "infected".

  • Whether human DNA's size (roughly 1000x the size of some bacteria DNA) might be too "large of a search space" for the cas9 or cas9-like proteins to "find" the targeted sequence.

  • Whether customization of cas9 into some more specialized / effective variant would overcome any obstacles to this approach.

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  • $\begingroup$ I don't have time for a real answer with citations, but briefly - by the time a cell becomes cancerous, it has already suffered at least two major mutations, and in reality tumors have many more. Genome instability is a hallmark of cancer. So, your targeted CRISPR/cas9 may have some effect in, say, repairing a major tumor driver, just like an antibody therapy, eventually the tumor is going to mutate around it and keep growing through some other mechanism. $\endgroup$ – MattDMo Jan 3 at 17:56

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