Abstract
BackgroundDifferent molecular alterations have been described in endometrioid endometrial carcinoma (EECA). Among them the most frequently altered is loss of the PTEN protein, a tumor suppressor gene. The purpose of this study was to evaluate the expression pattern of PTEN gene in normal, hyperplastic and neoplastic endometrium.MethodsIn a study in a referral gynecologic hospital in Tehran, Iran, immunohistochemical (IHC) evaluation of PTEN was performed on 87 consecutive specimens to the following three groups; group A- normal proliferative endometrium(n = 29); group B- hyperplastic endometrium [including simple hyperplasia without atypia(n = 21) and complex hyperplasia with atypia (n = 8)] and group C- EECA(n = 29). Immunostaining of cells was analyzed by arbitrary quantitative methods according to both slide's area staining and intensity of color reaction.ResultsPTEN immunoreactivity was present in all normal proliferative endometrium, all simple hyperplasia, 75% of atypical complex hyperplasia and in 48% of EECA (P < 0.001). The intensity of PTEN reaction was significantly higher in group with proliferative endometrium than hyperplastic endometrium and EECA (P < 0.001).ConclusionPTEN expression was significantly higher in cyclical endometrium than in atypical hyperplasia and endometrioid carcinoma.
Highlights
Different molecular alterations have been described in endometrioid endometrial carcinoma (EECA)
PTEN expression was significantly higher in cyclical endometrium than in atypical hyperplasia and endometrioid carcinoma
Endometrioid endometrial carcinoma (EECA) accounts for three fourths of endometrial cancers and are thought to develop following a continuum of premalignant lesions ranging from endometrial hyperplasia without atypia, to hyperplasia with atypia and to well differentiated carcinoma[1,2]
Summary
Different molecular alterations have been described in endometrioid endometrial carcinoma (EECA). Diagnostic Pathology 2009, 4:41 http://www.diagnosticpathology.org/content/4/1/41 endometrial hyperplasia), have poor reproducibility [1,3] Solving these problems needs new insights into the morphology of biologically defined premalignant lesion of endometrium [1]. EECA has a variety of genetic alternations, including microsatellite instability (MI) and mutations of PTEN, k-ras, and β-catenin genes [5,6] These molecular genetic alternations have been described in atypical endometrial hyperplasia [5]. The hypothesis that loss of PTEN expression could be assessed by immunohistochemical method has led to the suggestion that PTEN immunostaining may be a new and effective tool for screening of malignant and premalignant endometrial lesions [11,23]
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