Indeed, much research has shown that PR is not only a clinical marker of functional ER expression, but also an important independent """driver of tumor progression"""

The data suggest that phospho-PR may act as a """driver of this transition"" (i.e. tumor progression towards the gain of growth factor-driven pathways that can precede SR loss) as indicated by significant similarity to our uniquely defined PR signatures

However, currently available prognostic signatures fail to link changes in gene expression to the ""molecular drivers ""present in a given tumor

Спасибо!