Introduction: Endometrial carcinoma is a common gynaecological malignancy all over the world. It typically occurs in elderly women, approximately 80% are post menopausal at the time of diagnosis1. Endometrial carcinoma can be broadly divided in to two groups, based on differences in their clinical presentation, behaviour and pathogenesis. Endometrial carcinoma is often preceded by characteristic histopathologic lesions designated as endometrial hyperplasia.2 Currently it is accepted that there is continuum of changes that evolve to endometrioid carcinoma.3
Hyperplasia is usually associated with exogenous estrogen stimulation, and thus estrogen is considered as an endometrial carcinogen4,5,6.Other mechanisms of endometrial carcinogenesis include mutations in p53 and PTEN tumor suppressor genes and over expression of cyclin D1 .Over expression of cyclin D1 has been observed in endometrial carcinoma7.
The cyclin D1 proto-oncogene is an important regulator of G1 to S-phase transition and an important cofactor for several transcription factors in numerous cell types8.
This study was done to investigate the pattern of cyclin D1 expression in normal,, metaplastic, and neoplastic endometrium, and thereby evaluate the possibility of a role in the genesis of endometrial neoplastic and preneoplastic lesions.
Aims and Objectives
To investigate the role of cyclin D1 in simple hyperplasia, complex hyperplsia and endometrial carcinoma.
To recognize the subset of endometrial lesions that may be precancerous.
To exclude the lesions that may be responsive to harmonal manipulation.
To know the prognosis and treatment by drug induced cyclin D1 chemo- ablation.
Materials and Methods: This study was conducted in the department of pathology of hostipals attached to the osmania medical college and Gandhi Medical College . This is a restrospective study done for a period of 2 years .
A total of 60 uterine resection and endometrial biopsy specimens from 60 patients were studied. Cases for the study were selected on the basis of adequacy of tissue material on paraffin embedded blocks ensuring minimal amount of necrosis and haemorrhage. They were examined and categorized under the different groups on haematoxylin and Eosin section. Immunohistochemical stains were performed on freshly cut 4microns thick paraffin embedded tissue section. Cyclin D1 staining was evaluated in the glandular epithelium component and in the superficial epithelium component (except carcinoma cases) in each group of, simple hyperplasia, complex hyperplasia and adenocarcinoma. No attempt was made to separate complex hyperplasias as those with and without nuclear atypia.
Results: The present study was conducted to evaluate the expression of cyclin D1 in simple hyperplasia, complex hyperplasia and endometrial carcinoma. None of the cases of simple hyperplasia showed cyclin D1 immunopositivity. 6 out of 15 (40%) cases of complex hyperplasia.
Conclusion: Endometrial carcinoma is often preceded by characterstic histopathological lesions known as endometrial hyperplasia. Over expression of cyclin D1 in endometrial glands increases progressively in intensity and extent from simple hyperplasia to complex hypjerplasia and carcinoma, suggests that it may play a role in endometrial carcinogenesis. The present study support the significance of complex hyperplasia as a precancerous lesion, but apparently do not support the notion that simple hyperplasia is precancerous.