J Gynecol Oncol | Volume 4, Issue 5 | Review Article | Open Access
Angel Octavio MG1,2, Norma EHG1* and José Damián GA3,4
1Laboratory of Molecular Oncology, National Polytechnic Institute, Mexico
2Laboratory of Immunology, Iztacala UNAM Faculty of Higher Studies, Mexico
3Department of the Gynecologic and Obstetric, Medical Center “La Raza”, Mexico
4Laboratory of Cellular and Molecular Morphophysiology, Mexico
*Correspondance to: Norma E Herrera-González
Fulltext PDFEndometrial Carcinoma (EC) is the abnormal proliferation of endometrial tissue and constitutes more than half of all gynecological cancer diagnosis in USA. In Mexico, is also the second most common carcinoma? Pathological classification is a relevant element of disease management. EC is classified into two types: Type I, is known as endometrioid carcinoma and comprise 90% of adenocarcinomas. Type II, known as non endometrioid carcinoma, conforms 10% of the adenocarcinomas and is poorly differentiated. Objective: The purpose of this review is to introduce the role of genetics in this type of adenocarcinomas, as well as update the current information regarding EC. In Type I, the most relevant genetic alterations are the inactivation of PTEN gene, the altered expression of PAX-2, the mutation in β-catenin/CTNNB1 and the microsatellites instability. Due to the fact that Type I adenocarcinoma is the most frequent type of endometrial carcinoma, we focus on the genetic alterations on PTEN and PAX-2. Methods: To make this review, we used the research engines PubMed, OVID, MEDLINE and SciELO with the following keywords: Endometrial carcinoma, genetics, molecular classification, PTEN, PAX2, P53 and mutations.
Endometrial carcinoma; Genetics; PTEN; PAX2; P53
Angel Octavio MG, Norma EHG, José Damián GA. Endometrial Adenocarcinoma: A Genetic Focus Review. J Gynecol Oncol. 2021; 4(5): 1070.