This low nuclear ��-catenin could be due to lack of canonical Wnt ligands in the tissue, or loss of pathway components needed to translocate ��-catenin into the nucleus, such as Jouberin. Interestingly, cancers surrounding nerves were shown to have increased nuclear ��catenin compared to other cancers. Perhaps the microenvironment of perineural invasion preferentially allows for pathway activation. We did see a group of prostate cancers that had high nuclear ��-catenin, and these cancers had both low percentage of ciliated cells and a decrease in cilia length. We hypothesize that shorter cilia may be dysfunctional and would fail to suppress the Wnt pathway. The low sample sizes of our cohort should be acknowledged. Our data suggests that other factors besides primary cilia may be controlling canonical Wnt signaling in the majority of prostate cancers. Upon investigation of a correlation between clinical parameters and nuclear ��-catenin, we found that high nuclear ��-catenin correlates with increased incidence of capsular penetration and that moderate/low ��-catenin correlates with increased incidence of biochemical recurrence. These results appear to be contradictory given biochemical recurrence and capsular penetration have been associated with disease-recurrence. However, several published reports on ��-catenin agree with both of our results. Chen et al. demonstrated that higher total expression of ��-catenin was found in higher tumor stage cancers versus 
lower tumor stage cancers. Also in agreement with our findings, Horvath et al. investigated biochemical survival and correlated lower nuclear ��-catenin with biochemical relapse. These seemingly contradictory data, where high nuclear ��-catenin correlated with capsular penetration and moderate/low nuclear ��-catenin correlated with biochemical recurrence, may be explained by the biology of biochemical recurrence. Biochemical recurrence can occur as a result of PSA production by disseminated tumors cells that expand months following surgical removal of the primary tumor and this does not necessarily correlate with capsular penetration which is a pathologic diagnosis made at the time of surgery. This lack of correlation between biochemical recurrence and capsular penetration is also evident in our cohort. While this lack of correlation may explain our contradictory clinical correlations, further studies with a larger cohort are needed. Our findings have shown that prostate cancer cells have a very low frequency of primary cilia. An important question for therapeutics is whether this loss of primary cilia is a driver of prostate cancer. A future direction is to determine if primary cilia loss is causal in tumor formation in the prostate. If cilia are causal in cancer formation, use of drugs that result in reexpression of primary cilia in cancers may be a promising therapy. This would require the determination of the cause of primary cilia loss in prostate cancers.