Hormonal multi-resistance – A potentially self-sustaining system

Many hormones, cytokines and other signaling molecules stimulate PGE2 production. PGE2 can in turn modulate their production, secretion or signaling. We hypothesize that excessive PGE2 activity may impair the signaling of substances that normally stimulate PGE2, leading to compensatory upregulation and further PGE2 production.

→ PGE2 antagonizes other agents

→ PGE2-mediated antagonism and hormonal resistance, interrelated?

→ A Hypothetical Model of “Hormonal multi-resistance”

→ “Hormonal multi-resistance” as a context-dependent survival mechanism?