ADT paradox study.

I found a recent study that challenges the established ADT dogma. I found that the study suggests that androgen levels might have a more nuanced impact on AR signaling than we typically consider. Specifically, it found that low-dose androgens stimulate tumor growth by activating the mTOR pathway through AR monomers, while high-dose androgens suppress growth by forming AR dimers/oligomers, which inhibit c-MYC and promote differentiation.

It seems like this challenges the longstanding dogma that all androgen signalling drives cancer progression, particularly in advanced or resistant cases. In my case, this tumor grew in a naturally low testosterone environment, and my uninformed mind thought that perhaps eliminating testosterone in a naturally low testosterone environment would make the tumor even more aggressive than it already is, therefore accelerating tumor development rather than slowing it.

I was curious about the audience’s perspective on this. How do findings like these fit into our current understanding of androgen deprivation therapy? Do you see any potential for insights like this to guide more personalized approaches in the future?"