Purpose The proportion of women in urology has increased from <0.5% in 1981 to 10% today. Furthermore, 33% of students matching in urology are now female. This analysis sought to characterize the female workforce in urology in comparison to men with regard to income, workload, and job satisfaction. Materials and Methods We collaborated with the American Urologic Association to survey its domestic membership of practicing urologists regarding socioeconomic, workforce, and quality of life issues. 6,511 survey invitations were sent via e-mail. The survey consisted of 26 questions and took approximately 13 minutes to complete. Linear regression models were used to evaluate bivariable and multivariable associations with job satisfaction and compensation. Results A total of 848 responses (n=660 (90%) male, n=73 (10%) female) were collected for a total response rate of 13%. On bivariable analysis, female urologists were younger (p<0.0001), more likely to be fellowship trained (p=0.002), worked in academics (p=0.008), were less likely to be self-employed, and worked fewer hours (p=0.03) compared to males. On multivariable analysis, female gender was a significant predictor of lower compensation (p = 0.001) when controlling for work hours, call frequency, age, practice setting and type, fellowship training, and Advance Practice Provider employment. Adjusted salaries among female urologists were $76,321 less than men. Gender was not a predictor for job satisfaction. Conclusions Female urologists are significantly less compensated compared to males, after adjusting for several factors likely contributing to compensation. There is no difference in job satisfaction between male and female urologists.

Metastatic prostate cancers generally rely on androgen receptor (AR) signaling for growth and survival, even following systemic androgen deprivation therapy (ADT). However, recent evidence suggests that some advanced prostate cancers escape ADT by utilizing signaling programs and growth factors that bypass canonical AR ligand-mediated mechanisms. We utilized an in vitro high-throughput RNAi screen to identify pathways in androgen-dependent prostate cancer cell lines whose loss of function promotes androgen ligand-independent growth. We identified 40 genes where knockdown promoted proliferation of both LNCaP and VCaP prostate cancer cells in the absence of androgen. Of these, 14 were down-regulated in primary and metastatic prostate cancer, including two subunits of the protein phosphatase 2 (PP2A) holoenzyme complex: PPP2R1A, a structural subunit with known tumor-suppressor properties in several tumor types; and PPP2R2C, a PP2A substrate-binding regulatory subunit that has not been previously identified as a tumor suppressor. We demonstrate that loss of PPP2R2C promotes androgen ligand depletion-resistant prostate cancer growth without altering AR expression or canonical AR-regulated gene expression. Furthermore, cell proliferation induced by PPP2R2C loss was not inhibited by the AR antagonist MDV3100, indicating that PPP2R2C loss may promote growth independently of known AR-mediated transcriptional programs. Immunohistochemical analysis of PPP2R2C protein levels in primary prostate tumors determined that low PPP2R2C expression significantly associated with an increased likelihood of cancer recurrence and cancer-specific mortality. These findings provide insights into mechanisms by which prostate cancers resist AR-pathway suppression, and support inhibiting PPP2R2C complexes or the growth pathway(s) activated by PPP2R2C as a therapeutic strategy.