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The authors declare that they have no competing interests. Authors’ contribution FS and FP were the main authors of the manuscript; SB and FP collected and studied the bibliography; DS, MB, GT, AOM and BV participated in the sequence alignment and drafted the manuscript; FS corrected the language form; MA and GP carried out immunohistochemical MRT67307 ic50 studies; FS drafted the article and revised it critically for important intellectual content. All authors read and approved the final manuscript.”
“Introduction Endometrial cancer is one of the most common gynecologic cancers in developed

countries [1, 2]. Although its incidence rates are up to ten times higher in industrialized countries when compared to Asia or Africa, its prevalence has also been increasing in developing countries during the last decades [2]. As with all solid tumors, endometrial cancer is a heterogeneous disease with complex genetic and environmental influences. It has been suggested that environmental risk factors such as obesity Carnitine palmitoyltransferase II and overexposure to endogenous Go6983 or exogenous hormones may be involved in the pathogenesis of endometrial cancer [3, 4]. In addition, predisposition to endometrial cancer is mediated by genetic factors including both germinal and somatic alterations as well as genetic polymorphisms [5, 6]. The murine double minute-2 (MDM2) is a key negative regulator of the P53 tumor suppressor pathway which has been suggested to be implicated in a variety of cancers [7]. Evidence shows that MDM2 can bind directly to P53 protein and inhibit

its activity, thus resulting in its degradation via the ubiquitination pathway [8]. A single nucleotide polymorphism (SNP) in the promoter region of MDM2, SNP T309G (rs2279744), has been identified and was demonstrated to up-regulate the expression of MDM2 via a greater affinity for the SP1 transcription factor. Consequently, individuals carrying the GG genotype of the MDM2 SNP309 polymorphism were found to have higher MDM2 levels, which led to attenuation of the TP53 pathway and acceleration of tumor formation in humans [9]. It was reported that the increase in MDM2 results in direct inhibition of p53 transcriptional activity, enabling damaged cells to escape the cell-cycle checkpoint and become carcinogenic [10]. Hence, it is biologically reasonable to hypothesize a potential relationship between the MDM2 SNP309 polymorphism and endometrial cancer risk.