This review paper discusses the main molecular alterations of endometrial carcinoma, the most common cancer of the female genital tract. Two clinicopathological variants are recognized: the oestrogen-related (type I, endometrioid carcinoma) and the non-oestrogen-related (type II, non-endometrioid carcinoma). Whereas type I shows microsatellite instability and mutations in PTEN, PIK3CA, K-RAS and CTNNB1 (beta-catenin), type II exhibits TP53 mutations and chromosomal instability. Recent investigations regarding the role of non-coding RNA have provided important information regarding tumour progression. Understanding pathogenesis at the molecular level is essential for identifying biomarkers of potential use in targeted therapies.
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