I don’t know enough biology to know how feasible these ideas are (how I wish I could find training), but here goes anyway:

I had previously come up with an idea involving selecting out the cells believed to be most sensitive to chemotherapy or other treatments and strategically placing them in the center of existing tumors (in the hopes that the chemosensitive cells would displace the more resistant ones), then delivering a high dose of chemotherapy (or whatever treatment is being used). I have no idea whether this will actually work, but from what little I know of cancer biology, this seems reasonable. Unfortunately, it wouldn’t be completely effective because it depends on infiltration of specific tumors, which could also be removed surgically, for that matter (this is less invasive, however).

I just thought of a particularly nasty extension that we may or may not have the technology for today.

Here’s the basic premise: anything that outright kills cancer cells or prevents them from dividing is going to have a hard time succeeding because it’s fighting evolution (even the most effective treatment, surgical excision, does not outright kill cancer cells; it merely removes them from the body). This is presumably why tumors become resistant to chemotherapy following treatment.

First, the plausible idea: what if we could “tag” the cells we extracted with antigens before placing them? (Is this how traditional immunotherapy works? I was under the impression it relied more on chemical signals such as IL2). We could then insert them into tumors, perhaps in conjunction with IL2 to stimulate the immune system, and let it learn that the cells are not to be tolerated.

Ideally, this could be made genetic and the patient’s immune system could be suppressed for a time, to allow the tagged cell to infiltrate the tumor. Then the immunosuppressants would be withdrawn. Same principle as the first idea, except we’re actually inducing a weakness.

Next, the less plausible but seemingly more promising idea: what if we could infect the specific cells with a lysogenic virus that targets cancer cells? This will cause the cell to silently continue replicating, but with a viral plasmid. Using a lysogenic virus would be helpful here because there would be no chance for the other cells to adapt to counter it; upon initiation of the lytic cycle of the virus, the tumor would be inundated from its own infected cells, “taken by surprise”. Moreover, this need not be left to chance; we can manually initiate lytic cycles when most convenient (say, as a neoadjuvent therapy). This should theoretically cause a substantive die-off of the tumor, while preserving normal cells if the virus were specific enough.