Tehran University Medical Journal

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Background: Endometrial carcinoma is the most common malignancy of the female genital tract. Different molecular alterations have been described in endometrioid endometrial carcinoma that, the most frequently altered gene is mutations of PTEN. Up to 50-83% of endometrioid carcinoma reveal altered PTEN characterized by loss of expression. In endometrial hyperplasia, which are precursors of endometrioid carcinoma, loss of PTEN expression is 30-63%.
Methods: Immunohistochemical staining was performed on 90 cases of endometrial curettage including: 30 proliferative endometrium, 30 hyperplastic endometrium and 30 endometroid carcinoma. Immunohistochemical specimens were graded semiquatitatively by considering the percentage of staining with two cut-point 10% & 50% on the whole section for each specimen.
Results: loss of PTEN expression was observed 0%, 0%, 30% of 51.7% in proliferative, simple hyperplasia, complex hyperplasia and endometrioid carcinoma respectively with cut-point 10% and 0%, 5.3%, 30%, 52.2% in endometrioid carcinoma respectively with cut-point 50%. Also there was no difference in PTEN expression between atypical complex hyperplasia and endometrioid carcinoma but there was significant difference between simple hyperplasia and proliferative with endometrioid carcinoma & atypical complex hyperplasia.
Conclusion: These results show loss of PTEN expression in endmetrioid carcinoma and no differences between endometrioid carcinoma and atypical complex hyperplasia. Therefore, assessment of PTEN expression by negative immunostaining and matched with routine hematoxylin and eosin stained can be a new tool for diagnosis of endometrioid carcinoma.

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Background: Endometrial carcinoma (EC) is the most common gynecologic malignancy however, mechanisms underlying its pathogenesis remain obscure. Endometrial carcinoma has been classified into two major categories: type I (related to estrogen or endometrioid adenocarcinoma) and type II (unrelated to estrogen). Estrogen is the main trigger for the abnormal proliferation in the endometrial epithelium but progesterone can inhibit this process. The aim of this study was to analyze the expression of estrogen and progesterone receptors in all types of endometrial hyperplasia in comparison to endometrioid adenocarcinoma of endometrium.

Methods: Forty-seven specimens including 23 cases of histopathologically confirmed hyperplastic endometrium (12 simple hyperplasia, 5 complex hyperplasia without atypia, and 6 complex hyperplasia with atypia) and 24 cases of endometrial carcinoma were studied. Immunohistochemical staining of estrogen and progesterone receptors was performed in paraffin-embedded blocks and expression of estrogen and progesterone receptors were scored according to the proportion of positive staining cells.

Results: Overexpression of progesterone receptors was seen in 18 (75%) out of 24 cases of endometrial carcinoma and 23 (100%) of all types of endometrial hyperplasia. The aforesaid differences were statistically significant (P=0.023). 70.8% of cases with endometrial carcinoma were 3+ for immunohistochemical staining of progesterone receptors as were 85.7% of the cases with endometrial hyperplasia the difference being also statistically significant (P=0.02).

Conclusion: Considering the increased proportion of progesterone receptor expression in all types of hyperplastic endometrium in comparison to endometrial carcinoma, hormonal therapy by progestinal agents is recommended as a treatment of choice.