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. Author manuscript; available in PMC: 2020 Aug 25.
Published in final edited form as: Nat Rev Cancer. 2019 Aug 6;19(9):510–521. doi: 10.1038/s41568-019-0177-x

Figure 1. Overview of endometrial carcinoma origin, development, and molecular classification.

Figure 1.

(a) The image in this panel was deleted to comply with Nature Reviews Cancer policy on self-archiving. Schematic depiction of the initiation and progression of endometrioid (B) and serous (C) endometrial carcinomas (ECs) from the normal and atrophic endometrial glandular epithelium, via precursor lesions (CAH and SEIC). Columnar epithelial cells that have acquired somatic mutations are colored; intratumoral heterogeneity is depicted by differentially colored epithelial cells. PTEN mutation and TP53 mutation are, respectively, early events in the etiology of many endometrioid and serous endometrial carcinomas. In some instances, carcinomas, particularly high-grade carcinomas, undergo an epithelial to mesenchymal transition to give rise to uterine carcinosarcomas, which are biphasic tumors consisting of epithelial carcinoma cells and sarcoma cells (blue). (D) Pie charts showing the distribution (% of tumors) of low grade (grade 1 and grade 2) endometrioid EC, high grade (grade 3) endometrioid EC, and serous EC among the four molecular subgroups delineated in The Cancer Genome Atlas15.