Article ID Journal Published Year Pages File Type
3946925 Gynecologic Oncology 2012 6 Pages PDF
Abstract

ObjectiveOvarian cancer is the most lethal of all gynecologic malignancies. It is characterized by the spread of intraperitoneal tumors, accumulation of ascites, and formation of tumor blood vessels. Cyclin I has been linked with angiogenesis-related proteins, like vascular endothelial growth factor (VEGF) and VEGF receptor 2 (VEGFR-2), in human breast cancer. We examined whether an association exists between expression of cyclin I, VEGFR-2, clinicopathologic parameters and survival of patients with epithelial ovarian cancer (EOC).MethodsCyclin I and VEGFR-2 expressions were analyzed by immunohistochemistry in 55 human primary EOC tissue specimens.ResultsCyclin I immunoreactivity was significantly correlated with VEGFR-2 (R = 0.4587, P = 0.0004), and immunolabeling of cyclin I and VEGFR-2 significantly correlated with cancer cells' proliferative activity evaluated using cyclin A labeling index as a marker (R = 0.3107, P = 0.0209 and R = 0.4183, P = 0.0015, respectively). VEGFR-2 immunostaining was significantly higher in advanced, poorly differentiated, and suboptimally resected EOCs compared to their counterparts (P < 0.05). Finally, higher VEGFR-2 expression was significantly associated with shorter disease-free survival (P = 0.0437).ConclusionsOur results indicate that elevated expression of cyclin I and VEGFR-2 is likely to provide a proliferative advantage to the EOC cells, and that cyclin I may be linked with angiogenesis in EOC. Higher expression of VEGFR-2 is associated with more advanced disease. Further investigation of cyclin I in ovarian cancer is needed to evaluate if cyclin I may become a novel target for an anticancer therapy.

► Cyclin I correlates with VEGFR-2 and proliferation of EOC cells. ► Cyclin I may be linked with angiogenesis in EOC. ► VEGFR-2 expression is higher in advanced EOCs.

Related Topics
Health Sciences Medicine and Dentistry Obstetrics, Gynecology and Women's Health
Authors
, , , , , ,