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The Expession and Signifieance of CD133and ER in Different Pathological Status of Endometrioid Adenocarcinoma

Author: Chen
Tutor: ZhangMingFang
School: Tianjin Medical University
Course: Pathology and Pathophysiology
Keywords: endometrioid adenocarcinoma cancer stem cells(CSCs) CD133 estrogen receptor(ER) immunohistochemistry
CLC: R737.33
Type: Master's thesis
Year: 2012
Downloads: 36
Quote: 0
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Abstract


ObjectiveThere is a continuous process between endometrial hyperplasia and endometrioid adenocarcinoma. Endometrial hyperplasia includes simple hyperplasia, complex hyperplasia, and atypical hyperplasia, which can develop into endometrioid adenocarcinoma with different percentages. This experiment was to analyze the expression of CD133and estrogen receptor(ER) in different tissues of endometrium, aiming to investigate the possible pathogenesis in endometrioid adenocarcinoma furtherly.Methods135cases of different tissues of endometrium underwent curettage at Tianjin First Ceneral Hospital between2008and2011were retrospectively retrieved, including20cases of normal endometrium,40cases of endometrial hyperplasia and75cases of endometrioid adenocarcinoma. Two-step immunohistochemical staining was used to detect CD133and ER in different tissues of endometrium. Staining was quantified using Image-Pro Plus software, and integrated optical density was measured on each section. All statistical analyses were performed using the statistical package SPSS18.0, including One-Way ANOVA, LSD, Tamhane test and Perarson correlation analysis. P<0.05was considered to have statistic disparity.Results1. In3groups of different endometrium tissues, the positive rates of ER was respectively27.90%,22.04%and11.74%. There was statistical difference between them (P＜0.01). In3groups of different endometrial hyperplasia, the positive rates of ER gradually reduced from simple, complex to atypical hyperplasia, with significant differences in the groups of simple hyperplasia and complex hyperplasia, and also in the groups of simple hyperplasia and atypical hyperplasia(all P<0.01). In75cases of endometrioid adenocarcinoma, ER positive rate was higher in cases with higher pathology grade, with significant differences in the groups of G1and G2, and also in the groups of G1and G3(all P＜0.01).2. In3groups of different endometrium tissues, the positive rates of CD133was respectively0.51%,4.81%and13.43%. There was statistical difference between them (P<0.01). In3groups of different endometrial hyperplasia, the positive rates of CD133gradually raised from simple hyperplasia, complex hyperplasia to atypical hyperplasia, with statistical difference among them (P<0.01). In75cases of endometrioid adenocarcinoma, CD133positive rate was significantly higher in cases with lower pathology grade, and there was statistical difference between different differentiations (P＜0.01).3. In75cases of endometrioid adenocarcinoma, there was a negative correlation between over expression of CD133and low expression of ER (r=-0.551, P<0.01).Conclusions1. The expression of ER was significantly lower in endometrioid adenocarcinoma. As the pathology grade increasing, the expression of ER was decreased. The results implied that ER was a starting factor in the progression of endometrioid adenocarcinoma.2. The expression of CD133was significantly higher in endometrioid adenocarcinoma. CD133may play an important role in endometrioid carcinogenesis and its development.3. The expression of CD133and ER were negativelye correlated, which suggested CD133may replace the proliferation effect of estrogens and made carcinoma developing into the status independent of hormone.

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