It should be noted that for our cohort there are patients in the moderate/low nuclear BETA-catenin group

A wide range of ��-catenin staining phenotypes was observed for PIN, cancer, and perineural invasion lesions. Based on staining in normal basal cells we set a cutoff for high nuclear ��-catenin score as anything over the 75th percentile of normal. The nuclear ��-catenin score was high in 73.7% of PIN locations and this was statistically significant compared to normal basal cells. Comparison with normal luminal cells showed the nuclear ��catenin score was also significantly increased in PIN. As shown previously, we observed a decrease in the percent ciliated cells in a subset of PIN. This decrease in percent cilia in a subset of PIN correlates with an increase in nuclear ��-catenin for a subset of patients. In cancer locations, high nuclear ��-catenin scores were not significantly different from normal basal or luminal cells. To determine if primary cilia in the cancers that had higher nuclear ��-catenin were dysfunctional, we added cilia lengths to this analysis. Although not statistically significant, likely due to insufficient sample size, the average cilia length was shorter for cancers with higher nuclear ��-catenin compared to cancers with lower nuclear ��-catenin. This data suggests that cancers with shorter and therefore dysfunctional cilia have increased nuclear ��-catenin. Analysis of nuclear ��-catenin in perineural invasion lesions showed high staining in 78.3% of perineural invasion locations compared to normal basal cells. Comparison with normal luminal cells showed that nuclear ��-catenin was again increased in perineural invasion lesions. As shown previously, perineural invasion lesions showed a significant loss of cilia. The increase in nuclear ��-catenin correlates with loss of cilia. This is novel data, and may suggest canonical Wnt signaling as a mechanism which is activated to drive prostate cancer perineural invasion. To determine if differences in nuclear ��-catenin reflects differences in clinical data, we correlated clinical data with nuclear ��-catenin scores by breaking up scores into low/ moderate or high. The clinical data analyzed were: age at surgery, pathological tumor stage, pre-operative free PSA levels, biochemical recurrence, time to biochemical recurrence, capsular penetration, and largest tumor volume. Significant differences in incidence of capsular penetration and biochemical recurrence were found. A greater number of patients with high nuclear ��-catenin had capsular penetration compared to patients with moderate/low nuclear ��-catenin. In contrast, a greater number of patients with lower nuclear ��-catenin had biochemical recurrence compared to patients with higher nuclear ��-catenin. Both presence of capsular penetration and biochemical recurrence are thought to be poor prognostic markers in prostate cancer. Our results demonstrate that high nuclear ��-catenin correlates with capsular penetration but not with biochemical recurrence.