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. Author manuscript; available in PMC: 2010 Jan 1.
Published in final edited form as: Annu Rev Pathol. 2009;4:287–313. doi: 10.1146/annurev.pathol.4.110807.092246

Figure 3. Histological and molecular genetic progression of ovarian endometrioid carcinoma.

Figure 3

Low-grade endometrioid carcinomas often arise from endometrioid borderline tumors, which in turn may arise from endometriosis. This step-wise histopathological progression is often accompanied by accumulation of mutations predicted to deregulate canonical Wnt signaling (usually CTNNB1) and/or PI3K/Pten signaling (PTEN, PIK3CA). TP53 mutations are usually observed in high-grade endometrioid carcinomas in the absence of Wnt and PI3K/Pten pathway defects.