A couple of things –
- When you say “they test for the amount of inductivity in the cells during and after culture”, I think that’s not exactly what they’re testing for during culture. Actually, they’re testing for the presence of activated genes which are ASSOCIATED with inductivity. This is correlation by association, but it is not a direct test of inductivity.
So what they’re doing is, they look at what genes are activated, and what genes are inactivated, in fully inductive cells. Then they look at what genes are activated and inactivated in cells cultured in different ways. The more concordance they see (matches in genes being active or inactive), the more they will ascribe inductivity to the cultured cells. The goal is go keep refining culturing techniques until the gene profile (active vs. inactive genes) of the cultured cells is as close to, or identical with, the gene profile of the fully-inductive (non-cultured) cells.
This is a good method, but has the potential for error, because one can’t assume that EVERYTHING in the genetic profile of the fully inductive cells is a contributor to their inductivity. Also, there’s potential for other problems. For instance, what if doing one thing to the culture improves the concordance of one gene, but eliminates the concordance of another gene? So, the process is almost like flying blind. It’s a good process when you don’t know that much about what each gene actually does, but there are a lot of variables and unpredictable things that can happen.
- The issue of the “therapeutic area” you discussed – I agree with your description of that, but the problem may even be deeper than that. In order for the injections to work well, a few things have to happen: (A) lots of the cells, per injection, have to land at the therapeutic area; (B) they have to actually stay there; © they have to PENETRATE the epithelium around the follicle, which is almost like a capsule. They have to make their way past several layers or stacks of cells; and (D) they have to be integrated into the tissue of the dermal papilla.
Even if you can get a lot of cells to land at the therapeutic area (A), what guarantee is there they will stay there? What’s holding them there? I would argue not much. THEN, they have to penetrate obstacles – the outer epithelium of the follicle (B). How do they do this? Does the follicle suck the cells inside? I doubt it. There is no magical force pulling the injected cells into the dermal papilla. And if they do get past all this, how are they integrated into the dermal papilla?
The last step might be the easiest, but in order for the last step to occur, steps A, B and C have to work just right.
What percentage of the injected cells do you think are fortunate enough to make it past all that? I would guess it’s quite a low percentage.
This explanation might also answer the question of why injecting cells seems to work “just a bit” – enough to keep researchers interested – but never good enough to say, “OK, success! Now we can turn this into a commercial therapy.”
Maybe what we are seeing is just the “tip fo the iceberg” – the 1% or fewer cells that manage to integrate into follicles. This would explain the technique working just a little bit – having a very low (but, as Dr. Kemp said, “importantly not zero”) success rate.
A technique where only a very small percentage of cells succeed in inducing regrowth, and that works irregularly, and with a low success rate, but still works enough to keep researchers interested, would demonstrate exactly this kind of experimental profile, I think.