Yes, in addition to what others have mentioned the other way to do it is to make a virus that can *only* replicate in cancer cells.

So the cancer cells aren't being directly targeted, but the mutant virus can't replicate in normal cells. Presumably when the virus enters non-cancerous cells it just gets quietly degraded during general protein and nucleic acid turn-over

This may sound weird at first. However, There is some overlap with the way some cancer cells and some viruses need to be able to disrupt the cell to replicate effectively.

Most cells in an adult are senescent or dividing very slowly, so all the machinery for DNA replication and spare bases are are at low levels.

Cancer cells divide by definition, and viruses tend to evolve to sort of force cells into dividing or dividing faster, so that they will then be able to replicate faster.

If these things get "turned on" when they shouldn't most cells will commit suicide (apoptosis) with the help of "checkpoint proteins" and other mechanisms. Cancer cells tend to have mutation in these checkpoints (which is why they don't commit suicide).

So one can imagine a scenario where you have a cancer with a known checkpoint mutation, and a virus that targets the same checkpoint protein (with one of the viruses numerous genes/proteins).

If you remove or mutate the gene in the virus that targets that checkpoint, the virus will only be able to replicate in cells that have a defective checkpoint.

I saw talks back in the late 90s where they had a few great results with inoperative head and neck tumors, but there were too many complications and deaths.