Background: Endometrial hyperplasia and carcinoma are among the most common gynecological disorders, with abnormal regulation of cell cycle proteins playing a central role in their pathogenesis. Cyclin D1, a key regulator of the G1/S phase transition, has been implicated in uncontrolled proliferation and malignant progression of endometrial tissue. This comprehensive analysis aimed to evaluate the role of Cyclin D1 dysregulation in the development and progression of endometrial hyperplasia and carcinoma.
Methods: A systematic review of relevant studies published up to [insert date] was conducted using PubMed, Scopus, Web of Science, and Google Scholar databases. Eligible articles assessing Cyclin D1 expression through immunohistochemistry, molecular profiling, or gene amplification in endometrial hyperplasia and carcinoma were included. Data were synthesized to examine expression patterns, clinicopathological correlations, and prognostic significance.
Results: Evidence consistently demonstrated overexpression of Cyclin D1 in endometrial hyperplasia with atypia and in endometrial carcinoma compared with normal endometrium, suggesting its role in early tumorigenesis. High Cyclin D1 expression was associated with increased proliferative activity, higher tumor grade, and poor prognostic markers in some studies. However, findings on its correlation with patient survival and disease recurrence remain heterogeneous. Mechanistic insights indicate that Cyclin D1 interacts with estrogen receptor signaling and other oncogenic pathways, contributing to endometrial carcinogenesis.
Conclusion: Cyclin D1 dysregulation plays a significant role in the initiation and progression of endometrial hyperplasia and carcinoma, with potential diagnostic and prognostic implications. Standardized methods for assessing Cyclin D1 expression and large-scale clinical studies are needed to clarify its utility as a biomarker and therapeutic target in endometrial pathology.
