Given that progesterone is the ultimate endometrial tumor suppressor and PR is the key molecule through which it acts, the aims of this study were to 1) understand mechanisms of PR loss with endometrial cancer disease progression by tumor subtype; 2) manipulate and restore functional PR expression; and 3) determine strategies to re-sensitize endometrial cancer cells to progestin-based therapy. Here, PGR is linked to neoplasm.