Immediate ureterovaginal fistula following oocyte retrieval: A case and systematic review of the literature.

The aim of this study is to report a case of acute ureterovaginal fistula (UVF) formation with immediate symptomatic presentation after transvaginal ultrasound-guided oocyte retrieval (TVOR) for in vitro fertilization (IVF) and to perform a systematic literature review of ureteral injuries during TVOR. A 33-year-old woman with a history of anovulatory infertility presented with severe abdominal pain and vaginal leakage immediately following TVOR for IVF. We systematically reviewed the current literature regarding ureteral injury resulting from TVOR and present a case of timely identification and management of a UVF followed by a successful pregnancy. Computed tomography cystogram with intravenous contrast and left retrograde pyelogram confirmed the diagnosis of UVF which was managed by placement of the left ureteral stent. The IVF cycle was converted to a freeze-all cycle. The ureteral stent was removed 4 weeks later, and a subsequent frozen embryo transfer cycle resulted in pregnancy. We present the 13th case of ureteral injury and the fourth case of UVF following TVOR. UVF formation is a rare complication after TVOR and may result in serious long-term morbidity if it is not identified and treated promptly. Clinicians must exercise a high degree of suspicion and prompt evaluation for potential ureteral injuries in women presenting with abdominal pain, urinary symptoms, or vaginal leakage following TVOR.

Exploring the 3 A's of cystectomy access to care for muscle-invasive bladder cancer.

Despite a known survival benefit, gross underutilization of radical cystectomy in the treatment of muscle-invasive bladder cancer (MIBC) continues. The leading hypothesis for these low utilization rates is access to care, with barriers that can be classified into 3 categories: acceptability, availability, and affordability. Acceptability is highlighted by patient miseducation, fears, and cultural beliefs, which can lead to poor treatment decisions and emphasizes the need for decision-making research for MIBC. Availability is defined by structural barriers such as facility type and physician access. Understanding and improving differences in treatment among community vs. academic centers may improve access to cystectomy among patients who are treated locally. Affordability is marked by both direct (e.g., hospital) and indirect (e.g., travel) costs, with insurance type and travel distance notably affecting cystectomy receipt. Understanding the interplay of the "3 A's" that comprise cystectomy access to care is needed before we can successfully increase utilization of cystectomy in the vulnerable MIBC population.

PPP2R2C loss promotes castration-resistance and is associated with increased prostate cancer-specific mortality.

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 using signaling programs and growth factors that bypass canonical AR ligand-mediated mechanisms. We used an in vitro high-throughput RNA interference (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 downregulated 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 show 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.