In order to resolve these contradictory results, further analysis with a larger cohort of patients is needed. This is the first study that has carefully characterized the frequency of primary cilia in human tissue types of different stages of AbMole Folinic acid calcium salt pentahydrate prostate cancer. We have demonstrated that primary cilia are decreased early on epithelial cells in a subset of PIN lesions, and primary cilia are further reduced in cancers including perineural invasion lesions. We also show that primary cilia length is decreased in preinvasive and invasive prostate cancer, suggesting a potential dysfunctionality of the remaining cilia on preinvasive and malignant cells. The loss of primary cilia in preinvasive and invasive prostate cancer was correlated to the canonical Wnt signaling pathway, and we showed an association between primary cilia loss and increased nuclear ��-catenin in normal tissue, and nuclear ��catenin is shown to be increased in PIN, a subset of cancers, and perineural invasion lesions. We also investigated associations between primary cilia frequency and clinical parameters, and most notably found that decreased cilia frequency correlated with increased tumor size. Consistent with our findings in human prostate cancer tissue, Zhang et al. demonstrate that prostate cancer cell lines fail to express primary cilia in vitro. Primary cilia in normal tissue adjacent to cancer, BPH, and prostate cancer were examined by electron microscopy in a study published in 1979. This study did not characterize cilia frequency in prostate cancer. However, it did demonstrate that the primary cilia expressed in prostate cancers often are of abnormal microtubule patterns, instead of the typical ��9+0�� pattern. Structural abnormalities of microtubule patterning in primary cilia likely affects signaling function. Taken together, these findings, along with data presented in this report, support the hypothesis that primary cilia are dysfunctional in prostate cancer either by being absent, shortened, or having abnormal microtubule structures. We report low nuclear ��-catenin, and therefore low canonical Wnt pathway activation, in the majority of invasive prostate cancers in our cohort. There are numerous contradictory studies in the literature reporting on Wnt signaling activity measured by ��-catenin staining in prostate cancer. Consistent with our report, some studies demonstrate absent or relatively low nuclear staining, and therefore low activation of the Wnt signaling pathway. Other studies report an activated canonical Wnt signaling phenotype as a common event in prostate cancer. Tissue fixation variations and differing primary antibody concentrations likely contribute to the differences observed. Our results, which do not suggest Wnt signaling is activated in the majority of invasive prostate cancers, are surprising because we show the majority of prostate cancers have a loss of primary cilia.