2026-04-17T03:19:47Zhttps://recercat.cat/oai/request

oai:recercat.cat:10459.1/4649412025-09-15T18:05:10Zcom_2072_3622col_2072_479130

00925njm 22002777a 4500 dc Yeramian Hakim, Andree author Moreno Bueno, Gema author Dolcet Roca, Xavier author Catasus, L. author Abal Diaz, Leandro author Colás, Eva author Reventós, Jaume author Palacios, José author Prat, Jaime author Matias-Guiu, Xavier author 2013 In the western world, endometrial carcinoma (EC) is the most common cancer of the female genital tract. The annual incidence has been estimated at 10–20 per 100 000 women. Two clinicopathological variants are recognized: the estrogen related (type I, endometrioid) and the non-estrogen related (type II, non-endometrioid).The clinicopathological differences are paralleled by specific genetic alterations, with type I showing microsatellite instability and mutations in phosphatase and tensin homologue deleted on chromosome 10, PIK3CA, K-RAS and CTNNB1 (β-catenin), and type II exhibiting TP53 mutations and chromosomal instability. Some non-endometrioid carcinomas probably arise from pre-existing endometrioid carcinomas as a result of tumor progression and, not surprisingly, some tumors exhibit combined or mixed features at the clinical, pathological and molecular levels. In EC, apoptosis resistance may have a role in tumor progression. Understanding pathogenesis at the molecular level is essential in identifying biomarkers for successful targeted therapies. In this review, the genetic changes of endometrial carcinogenesis are discussed in the light of the morphological features of the tumors and their precursors. Endometrial carcinoma Genetics Microsatellite instability PTEN PIK3CA K-RAS Beta-catenin Apoptosis Chromosomal instability E-cadherin TP53 Endometrial carcinoma: molecular alterations involved in tumor development and progression