Hari K. Koul, MSc, PhD, presents the take home messages on basic science research at the AUA annual meeting in San Diego.
Presented by Hari K. Koul, MSc, PhD
University of Colorado, Anschutz Medical Campus, Aurora
• The combination of bombesin/gastrin-releasing peptide antagonist plus growth hormone-releasing hormone antagonist prevented and decreased tissue growth in a mouse model of BPH.
• The combination of candidate genes KISS1R, CSAD, and SEPT9 could serve as a prognostic marker panel for determining the metastatic risk of primary bladder tumors.
• Expression of histone deacetylase 2 in urothelial bladder cancer tissue was associated with more aggressive tumors compared to histone deacetylase 1 and 3.
• Findings from in vitro cell culture studies and a mouse model suggest dual inhibition of mTORC1 and mTORC2 may be a useful treatment for renal cell carcinoma harboring TFE3 gene fusions.
• 4-MU, an investigational hyaluronic acid synthesis inhibitor, prevented growth and progression of prostate cancer in a mouse model and is considered to have promise as a nontoxic, oral chemopreventive agent.
• Small numbers of RANK ligand-positive prostate cancer cells may be sufficient to drive bone metastasis, suggesting a possible therapeutic target.
• Androgen receptor knockdown via molecular techniques suppresses enzalutamide (Xtandi)-resistant prostate cancer cell growth.
• Tetrandrine, a bisbenzylisoquinoline, inhibits both androgen-stimulated and androgen-independent androgen receptor signaling, and may be useful for treating castration-resistant prostate cancer.
• Findings from a rat study suggest a link between oral exposure to bisphenol A and erectile dysfunction.
• In a mouse model, anti-inflammatory M2 macrophages reduced renal crystal formation via a colony-stimulating factor-1 dependent pathway, providing prophylactic activity against kidney stone formation.
• Inhibition of p38 MAP kinase may be a strategy for decreasing oxalate nephrotoxicity, crystal retention, and nephrolithiasis.
• The inflammatory cascade initiated by NF-kappaB may be responsible for tissue necrosis factor-alpha-induced bladder smooth muscle contraction.
• Nerve growth factor and prostaglandin E receptors may be targets for treatment or prevention of diabetes mellitus-associated hyposensitive bladder.UT