E2F-1 is a transcriptional factor that mediates cell cycle progression from G1 to S phase, thereby influencing tumor progression. However, only a few clinicopathologic studies have been carried out using surgically removed specimens for defining its role in tumor biology. Therefore, we studied the expression of this cell cycle regulator on surgical specimens at the immunohistochemical level, and examined its possible relationship with proliferative index, assessed by analysis of MIB-1 expression, and clinicopathologic factors in pancreatic ductal carcinomas. E2F-1 and MIB-1 were immunostained on 54 surgically removed specimens, and nuclear reactivity was evaluated. The percentage of E2F-1 positive cells (E2F-1 PI) ranged from 3.8% to 71.4%. We found a statistically significant correlation between E2F-1 PI and the histologic grade of tumor differentiation (p = 0.0133), i.e. E2F-1 PI was higher in less-differentiated carcinomas. Furthermore, there was a positive correlation between E2F-1 PI and the percentage of MIB-1 PI (r = 0.763; p < 0.0001). The patients with higher E2F-1 PI (E2F-1 PI > or = 38.0 = median) showed a significantly shorter disease-associated survival time in R0 resection cases (n = 49, p = 0.015). The present analysis seems to support the theory that E2F-1 is upregulated in cell cycle, and its expression reflects the effector function of G1/S progression as far as pancreatic ductal carcinoma is concerned.