Unless the specificity of an anticancer drug approaches 100%, anything that kills off cancer cells is going to kill off some normal ones as well. This means side effects, often quite nasty.

But what if, instead of killing off cancerous cells, we just shut down their invasive potential?

I’ve been reading up on what differentiates noninvasive cancer cells – carcinoma in situ – against invasive cells. The literature on this has been surprisingly sparse, so either I’m not looking for the right things (quite possible), or this is a very understudied approach. The papers I’ve read have identified a few gene loci and a protein called Twist, but that is as far as I can take my search, lacking the resources to experimentally pursue such lines of study.

My point is this: carcinoma in situ is harmless except in its ability to become invasive cancer. Most of the proteins that seem to cause aberrant behavior in cancer cells seem those that are present during embryonic development (which makes sense in a way, since embryonic development is high-rate controlled, regulated division, whereas carcinogenesis is high-rate uncontrolled, unregulated division), but these proteins are all but absent in adults.

So rather than attempting to kill off the cancer cells, why not attempt to remove their ability to invade (and thus metastasize, destroy tissue, and cause other problems)? Even if the treatment were nonspecific, side effects should be far milder than the “killer” drugs, since normal cells are not known to depend on the function of the identified proteins. And unlike drugs that kill cells, there is little selective pressure against the treatment.

I see so many solutions to this problem. How I wish I could take part…