BACKGROUND: Cell-proliferating activity is one of the prominent parameters for evaluating the biological aggressiveness of carcinomas. Pancreatic adenocarcinoma has been studied to identify modulators of the G1-S boundary. In the present study we investigated the modulators of another important checkpoint, the G2-M checkpoint. METHODS: We immunohistochemically studied three representative G2-M modulators, cdc2, cyclin A and cyclin B1 in 62 pancreatic adenocarcinomas and 7 cystadenomas. RESULTS: Overexpression of cdc2, cyclin A and cyclin B1, was observed in 54.8, 54.9 and 56.4%, respectively, of the pancreatic adenocarcinomas. cdc2 overexpression was directly related to lymph node metastasis, Ki-67 labeling index (LI), and cyclin A overexpression which was significantly linked to the stage, carcinoma differentiation, tumor size, and lymphatic invasion. On the other hand, cyclin B1 was not linked to clinicopathological parameters including Ki-67 LI and cdc2 overexpression, except for tumor size. CONCLUSION: The findings suggest that cdc2 and cyclin A play a role in the progression of pancreatic adenocarcinoma, while the clinical significance of cyclin B1 remains to be clarified because of its more random expression.
BACKGROUND: Cell-proliferating activity is one of the prominent parameters for evaluating the biological aggressiveness of carcinomas. Pancreatic adenocarcinoma has been studied to identify modulators of the G1-S boundary. In the present study we investigated the modulators of another important checkpoint, the G2-M checkpoint. METHODS: We immunohistochemically studied three representative G2-M modulators, cdc2, cyclin A and cyclin B1 in 62 pancreatic adenocarcinomas and 7 cystadenomas. RESULTS: Overexpression of cdc2, cyclin A and cyclin B1, was observed in 54.8, 54.9 and 56.4%, respectively, of the pancreatic adenocarcinomas. cdc2 overexpression was directly related to lymph node metastasis, Ki-67 labeling index (LI), and cyclin A overexpression which was significantly linked to the stage, carcinoma differentiation, tumor size, and lymphatic invasion. On the other hand, cyclin B1 was not linked to clinicopathological parameters including Ki-67 LI and cdc2 overexpression, except for tumor size. CONCLUSION: The findings suggest that cdc2 and cyclin A play a role in the progression of pancreatic adenocarcinoma, while the clinical significance of cyclin B1 remains to be clarified because of its more random expression.