Best of AUA 2013: Basic Science Research


Hari K. Koul, MSc, PhD, presents the take home messages on basic science research at the AUA annual meeting in San Diego.

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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

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