Replies to post #115114 on Biotech Values

[biomaven0]

There is also a strange wildcard here. Turns out that PSA itself may have substantial impact on bone - at least it does in gene-based in vitro testing. It principally impacts the Wnt pathway, but also appears to down-regulate CTGF, which is very likely a good thing all round. So seeing those improved bone scans all seem to be associated with increases PSA levels, maybe it is actually helping in some way.

(In the papers I have seen, people have tried to make the case that increased PSA might be partly responsible for bone mets, but they were never able to make the case, and it's conceivable that they were on the wrong track).

Peter

[iwfal]

i know it is counterintuitive to think that osteoblast activity decreases during a period of bone formation, but the ratio of osteoclast to osteoblast activity is what is relevant in determining if you have net resorption or formation, and in states of high turnover resorption>formation, and vice versa, so a decline in osteoblast activity ensues when remodeling decreases and you get net new bone laid down because the ratio of clast to blast decreases

I think we are going to have to agree to disagree since somehow you are missing my general point? - when there is bone injury (e.g. break) bone scans are hot for weeks afterward as the bone heals. I can see no reason why injury caused by a tumor should be any different. And clearly a large fraction of PCa patients who are responders to Arbiterone provide even more evidence of this. They get hot spots as the tumor is killed and then it goes dark in the window in which you'd expect healing to be done.