#33 - Cigarette Smoke Exposure Upregulation of Phospholipase A₂ Metabolic Pathway Expression in the Bladder as a Promoter of Tumorigenesis

Author #1

Abstract

Cigarette smoking remains the leading cause of preventable death and disease in the United States. Despite known risks, 42.1 million Americans continue to smoke, making research into tobacco-related pathologies relevant and necessary. We previously discovered that cigarette smoke exposure leads to tumor progression in the breast via platelet activating factor (PAF) and other phospholipase A₂ (PLA₂) metabolic pathways. In addition, pilot studies in the bladder have shown urothelial cell destruction, promoting a tumorigenic environment. Cigarette smoking has been identified as a primary risk factor for developing bladder cancer, yet the pathways involved remains to be elucidated. Our results in the breast and the lack of research in the bladder have led us to examine the PLA2metabolite, prostaglandin E₂ (PGE₂), cyclooxygenase-2 (COX-2), 15-prostaglandin hydrogenase (15-PGDH), and prostaglandin E-synthase (PGES). We will observe the expression of these proteins in mouse bladder from nonsmokers and long-term smokers via immunohistochemistry. We hypothesize that we will see a significant increase in the expression of the PLA₂ pathway proteins when compared to the nonsmokers via immunohistochemical analysis. Our studies would show for the first-time evidence to support cigarette smoke exposure dysregulation of PLA₂ metabolite pathway. These studies could provide potential therapeutic targets for cigarette smoked-induced tumorigenesis and progression.

 
Nov 2nd, 10:20 AM Nov 2nd, 11:30 AM

#33 - Cigarette Smoke Exposure Upregulation of Phospholipase A₂ Metabolic Pathway Expression in the Bladder as a Promoter of Tumorigenesis

Cleveland Ballroom

Cigarette smoking remains the leading cause of preventable death and disease in the United States. Despite known risks, 42.1 million Americans continue to smoke, making research into tobacco-related pathologies relevant and necessary. We previously discovered that cigarette smoke exposure leads to tumor progression in the breast via platelet activating factor (PAF) and other phospholipase A₂ (PLA₂) metabolic pathways. In addition, pilot studies in the bladder have shown urothelial cell destruction, promoting a tumorigenic environment. Cigarette smoking has been identified as a primary risk factor for developing bladder cancer, yet the pathways involved remains to be elucidated. Our results in the breast and the lack of research in the bladder have led us to examine the PLA2metabolite, prostaglandin E₂ (PGE₂), cyclooxygenase-2 (COX-2), 15-prostaglandin hydrogenase (15-PGDH), and prostaglandin E-synthase (PGES). We will observe the expression of these proteins in mouse bladder from nonsmokers and long-term smokers via immunohistochemistry. We hypothesize that we will see a significant increase in the expression of the PLA₂ pathway proteins when compared to the nonsmokers via immunohistochemical analysis. Our studies would show for the first-time evidence to support cigarette smoke exposure dysregulation of PLA₂ metabolite pathway. These studies could provide potential therapeutic targets for cigarette smoked-induced tumorigenesis and progression.