The rates of trichomonas infection in US males are lower than in women. Infections are strongly associated with black males, HSV-2 infection and other factors known to increase STI rates. This information may be helpful for counseling, screening and management of patients.

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BackgroundPrevention of bladder cancer recurrence is a central challenge in the management of this highly prevalent disease. The histone deacetylase inhibitor valproic acid (sodium valproate) has anti-angiogenic properties and has been shown to decrease bladder cancer growth in model systems. We have previously shown reduced expression of thrombospondin-1 in a mouse model and in human bladder cancer relative to normal urothelium. We speculated that inhibition of angiogenesis by valproate might be mediated by this anti-angiogenic protein.MethodsBladder cancer cell lines UMUC3 and T24 were treated with valproate or another histone deacetylase inhibitor, vorinostat, in culture for a period of three days. Proliferation was assessed by alamar blue reduction. Gene expression was evaluated by reverse transcription of RNA and quantitative PCR.ResultsProliferation assays showed treatment with valproate or vorinostat decreased proliferation in both cell lines. Histone deacetylase inhibition also increased relative expression of thrombospondin-1 up to 8 fold at 5 mM valproate.ConclusionsHistone deacetylase inhibitors warrant further study for the prevention or treatment of bladder cancer.

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Abstract. Background In 2015, there were an estimated 220,800 incident cases of prostate cancer (PCa) with 27,540 patient deaths (1). Despite these sobering statistics, a majority of disease continues to be low-grade in nature with an excellent prognosis. Often, the complications of therapy can outweigh the risk of lowgrade cancers that have reduced oncologic potential. There remains a need for therapy in these low-risk cancers that can halt progression to higher-risk disease while minimizing the morbidity of treatment.Chemoprevention via anti-angiogenic therapy (AAT) is a targeted strategy that could limit further tumor growth. As a tumor continues to grow, there is development of an impaired blood supply and a resultant hypoxic tumor microenvironment. It is hypothesized that this stress may allow cancerous lesions to evade immune surveillance and, ultimately, may apply selective pressure favoring cells that possess invasive and metastatic capability (2). With this in mind, AAT early in PCa development could restore a normal tumor microenvironment by alleviating hypoxia and, thus, halting progression. These effects stem from the "normalizing" effects on the vasculature by prudent AAT use. Consistent with this, in vitro and murine models have demonstrated that AAT is more effective when the PCa burden is minimal (3).While some AAT directly target vascular endothelial growth factor (VEGF) or its effectors, one mechanism that has received less investigation is epigenetic modification, in particular the acetylation of histones. Cancerous cells are able to alter their histone acetylation status and, thus, gene expression (4). Therapies that act as histone deacetylase inhibitors (HDACi) can modulate this phenomenon (5). HDACi have been tested in multiple in vitro and in vivo cancer models (6), as well as progressing to clinical trials (7).One of the well-known and commonly used HDAC inhibitors is valproic acid (VPA) (8), which has been safely used for over 50 years as an anti-seizure medication. We have previously shown that VPA decreases urothelial cancer cell proliferation and induces the expression of thrombospondin-1 (TSP1), an extracellular matrix protein that functions as a potent inhibitor of angiogenesis (9). We sought to investigate the intracellular signaling alterations caused by VPA administration to PCa cells. Our hypothesis was that VPA would inhibit PCa growth through modifications in both angiogenic signaling and pathways known to be associated with PCa growth and progression. Furthermore, we postulated that TSP1 would be a central regulator in these signaling cascades. 5079