A progression model for endometrioid carcinoma. Tumor initiation and progression are characterized by acquisition of various molecular alterations. PTEN alterations appear central to the initiation of proliferative lesions that then acquire mutations in other cancer-causing genes (e.g., DNA mismatch repair genes, KRAS, -catenin) in the carcinogensis. An alternative pathway bypasses atypical hyperplasia and low-grade carcinoma to high-grade carcinoma by p53 mutation and HER2/neu amplification. NE, normal endometrium; EH, endometrial hyperplasia without hyperplasia, AH, atypical endometrial hyperplasia; EIC, endometrial intraepithelial carcinoma; LG-ECC, low grade endometrioid endometrial carcinoma; HG-ECC, high grade endometrioid endometrial carcinoma.
