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Carcinogenesis Advance Access first published online on March 26, 2007
This version published online on May 14, 2007
Carcinogenesis, doi:10.1093/carcin/bgm071
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Swedish moist snuff accelerates gastric cancer development in Helicobacter pylori-infected wild-type and gastrin transgenic mice

Björn Stenström1, Chun-Mei Zhao1, Arlin B. Rogers2, Hans-Olof Nilsson3, Erik Sturegård3,4, Steinar Lundgren1,5, James G. Fox2, Timothy C. Wang6, Torkel Wadström3 and Duan Chen1,*

1 Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway
2 Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, Massachusetts
3 Department of Medical Microbiology, Lund University, Lund, Sweden
4 Department of Clinical Microbiology, Malmö University Hospital, Malmö, Sweden
5 Department of Oncology, St. Olav's Hospital, Trondheim, Norway
6 Division of Digestive and Liver Diseases, Columbia University Medical Center and Irving Cancer Research Center, New York

* Corresponding author. Tel: +47 725 73320; Fax: +47 725 76412; Email: duan.chen{at}ntnu.no

The Swedish variant of moist oral smokeless tobacco (snus) is popular in Sweden and Norway, banned from sale within the EU, and is currently being introduced in the U.S. The aim of the present study was to determine if snus is carcinogenic to the stomach, particularly in Helicobacter pylori infected hosts at increased risk for gastric cancer development. Snus (GeneralTM; Swedish Match, Sweden) was mixed with powdered standard mouse chow at a concentration of 5-9% (w/w) and given to wild-type (WT, FVB) and gastrin transgenic (INS-GAS, FVB) mice for 6 months with or without Helicobacter pylori (strain 67:21, CagA+, VacA+) infection. At necropsy, pathological evaluation of stomachs from uninfected snus-treated WT mice showed mild morphological changes, while 50% snus-treated INS-GAS mice developed carcinoma in situ (CIS), compared to 25% not exposed to snus. When snus was given to Helicobacter pylori-infected mice, 9 of 17 WT mice developed CIS with intramucosal invasion, and the remaining 8 of 17 WT mice developed high grade dysplasia (score >1.5) that was associated with increased gastritis, epithelial defects, oxyntic atrophy, hyperplasia, and intestinal metaplasia. Twelve of 12 Helicobacter pylori-infected INS-GAS mice developed CIS with intramucosal invasion and submucosal herniation. We suggest that snus is a potential gastric carcinogen in mice. The development of CIS was associated with increased rates of the epithelial cell proliferation and apoptosis, common features of gastric carcinogenesis.

Key Words: gastric cancer • Helicobacter pylori • Swedish snus • oral moist snuff • mice

Received January 24, 2007; revised March 16, 2007; accepted March 20, 2007.


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