Abstract
Endometrial cancer (EC) is the sixth most common cancer in women worldwide, with rising incidence, particularly in economically developed countries where obesity and type 2 diabetes are prevalent risk factors. EC comprises various histological subtypes with distinct behaviors: Type I tumors are generally estrogen-driven with favorable prognosis, while Type II tumors are hormone-independent, aggressive, and associated with poorer outcomes. Dysregulation of the cell cycle, particularly through cyclin-dependent kinases (CDKs) and their regulators like Cyclin D1 (CCND1), plays a crucial role in EC progression and recurrence. Cyclin D1 overexpression is often observed in the early stages of endometrioid carcinoma and complex hyperplasia, marking potential early carcinogenic events, while lower expression levels are common in high-grade subtypes like serous carcinoma. Although CDK inhibitors targeting Cyclin D1/CDK4/6 complexes have shown therapeutic potential in cancers such as breast and lung, their role in EC remains underexplored. This study integrates immunohistochemical evaluations of Cyclin D1 expression in EC patient samples with data from The Cancer Genome Atlas (TCGA) to assess its prognostic significance across EC subtypes. By correlating molecular, histopathological, and clinical outcomes, we aim to clarify the impact of Cyclin D1 dysregulation on EC progression and recurrence. Our findings may inform more personalized therapeutic approaches, particularly for high-grade and treatment-resistant forms of EC.