Tehran University Medical Journal

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Background: Cervical cancer is the second leading cause of cancer death among women. In this cancer, the effects of prevention, early diagnosis and treatment more than other cancers decrease the mortality rate. In 1970 human papilloma virus (HPV) was introduction as major etiologic factor of cervical cancer. Different studies throughout the world revealed strong correlation between HPV and cancerous & precancerous changes in epithelial cells. Since cell culture and serological methods can not recognize the virus and its subtypes, the importance of the molecular methods including polymerase chain reaction (PCR) in early and definite diagnosis of virus is obvious.

Methods: In this study, after patient selection using the related protocol and completion of the questionnaires, 100 samples from cancer lesions of cervix selected. Then DNA extraction from paraffin blocks performed using standard method. Multiplex PCR with two pairs of primer (one as internal control) performed and the PCR product run on 8% polyacrylamid gel.

Results: The results showed that 73% of the tissues were infected by HPV.

Conclusion: This finding confirm the previous results based of correlation between HPV,and cervical cancer.

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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.