The Role of TP53 Gene Codon 72 Polymorphism in Endometrial Hyperplasia

Abstract

Nowadays, endometrial cancer (EC) is the second most common gynecological malignancy worldwide, due to the higher rates of cervical cancer in the developing world [1]. There are several lines of evidence that a diagnosis of endometrial hyperplasia (EH) may precede the development of EC and that the two share common predisposing risk factors. The incidence of EH is three times higher than EC and certain atypical forms of EH are considered to represent direct precursor lesions to EC [2]. The clinical importance of a diagnosis of EH relates to the long-term risk of progression to EC and it is generally accepted that cytological atypia is the principal histological characteristic when assessing EHs for malignant potential [3]. Some genetic deficits may have a role in disease pathogenesis [4]. It is determined that chromosome 17 may be impaired in this disease, because TP53 gene is the most important tumor suppressor gene that is located on the short arm of chromosome 17 [5]. That is why the purpose of the review is to clarify the presence or absence of this correlation, as well as the need for further research in this area.