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Background: Living kidney donor pools are expanding with the use of "medically complex" donors. Whether or not to include cigarette smokers as living kidney donors remains unclear. The aim of this study was to determine the relationship between donor smoking and recipient outcomes. We hypothesized that donor smoking would increase donor complications and decrease allograft and recipient survival over time., Methods: The charts of 602 living kidney donors and their recipients were retrospectively reviewed. Kaplan-Meier survival analysis and Cox modeling were used to assess the relationships between smoking and recipient and allograft survival., Results: No difference in postoperative complications was seen in smoking versus non-smoking donors. Donor smoking at time of evaluation did not significantly decrease allograft survival (HR = 1.19, p = 0.52), but recipient smoking at evaluation did reduce allograft survival (HR = 1.74, p = 0.05). Both donor and recipient smoking decreased recipient survival (HR = 1.93, p < 0.01 vs HR = 1.74, p = 0.048)., Discussion: When controlled for donor and recipient factors, cigarette smoking by living kidney donors significantly reduced recipient survival. This datum suggests that careful attention to smoking history is an important clinical measure in which to counsel potential donors and recipients. Policy efforts to limit donors with a recent smoking history should be balanced with the overall shortage of appropriate kidney donors., (© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Smoking is highly associated with pancreatic cancer. Nicotine, the addictive component of tobacco, is involved in pancreatic cancer tumorigenesis, metastasis, and chemoresistance. This work aimed to describe the role of nicotine within the pancreatic cancer tumor microenvironment. Nicotine treatment was used in vitro to assess its effect on tumor-associated stromal cells and pancreatic cancer cells. Nicotine treatment was then used in a pancreatic cancer patient-derived xenograft model to study the effects in vivo. Nicotine induced secretion of interleukin 8 (IL-8) by tumor-associated stroma cells in an extracellular signal-regulated kinase (ERK)-dependent fashion. The secreted IL-8 and nicotine acted on the pancreatic cancer cell, resulting in upregulation of IL-8 receptor. Nicotine treatment of mice bearing pancreatic cancer patient-derived xenografts had significantly increased tumor mass, increased tumor-free weight loss, and decreased muscle mass. These represent important pathways through which nicotine acts within the tumor microenvironment and worsens pancreatic cancer-induced cachexia, potentially representing future therapeutic targets. [ABSTRACT FROM AUTHOR]