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Anderson et al. [30], demonstrated also that DSF increased significantly and recurrence rate decrease with increased BMI. Similar results were published by Everett et al. [31], in whose study, women with BMI>40 had a lower recurrence rate compared with those with BMI[http://www.selleckchem.com/products/BIBW2992.html http://www.selleckchem.com/products/BIBW2992.html] between ERs, COX-2 and aromatase in cancer tissue [11, 16, 18?and?32]. However, there is still controversy in terms of its prognostic significance and whether it is an early or late event in the development of EC [10, 16, 18?and?32]. Interestingly, hormonal control of COX-2 has been described in the literature but not fully explored [18]. Niwa et al. [33], showed that 17-�� estradiol inhibits COX-2 mRNA expression in cell culture and that it is potent as steroids (dexamethasone) in inhibiting both COX-2 mRNA expression and prostaglandins production. However, Zhuo et al. [34] identified an alternative [https://en.wikipedia.org/wiki/PTPRJ PTPRJ] mechanism of hormonal control that is related to the chronically elevated gonadotropin and luteinizing hormone levels that promoted morphologic as well as functional differentiation of endometrial stromal cells into decidua. Our study showed, that human endometrial cancer was characterized by increased expression of COX-2 as compared with normal endometrium. Increased expression of COX-2 in EC is not the case in all studies as some show no change in COX-2 expression in the endometrial cancer or the endometrial hyperplasia [35]. Others detected COX-2 mRNA and protein expression by immunohistochemical analysis in 8 out of 11 endometrial cancers, but found no expression in 3 samples of normal tissues [36]. Fujiwaki et al. [37?and?38] [http://www.selleckchem.com/products/Dasatinib.html selleck] reported increased COX-2 expression in 63 patients with EC (51%). Ferrandina et al. [39] found that COX-2 positivity occurred more often in endometrial cancer with extrauterine involvement and in those with deep myometrial invasion. These findings suggest that COX-2 expression may correlate with tumor aggressiveness [39?and?40]. In our study, we analyzed FIGO I (stage) endometrial cancer, grade: G1, G2, G3 and ER��, ��, COX-2, aromatase expression and there was no statistically association between Ia and Ib stage. However, a trend was noticed for G1 tumors to express higher ER��, ��, COX-2 proteins level than grade 2 and 3 of EC. In accordance, some studies showed elevated expression of ER�� in G1 tumor compared within normal endometrium and higher grade tumors, with a significant negative association between ER�� expression and tumor grade 2 and 3. However, it is not the case in all patients since Pathirage et al.