However, type II endometrial cancers are believed to develop through molecular pathways involving p53 mutations, which more closely resemble high-grade serous ovarian tumors in molecular alterations and morphology and commonly do not express either ER or PR [2, 44], suggesting that estrogen (or its inhibition) should have no effect on the growth of such tumors. The gene discussed is PGR; the disease is ovarian serous tumor.