Skip Navigation



Carcinogenesis Advance Access published online on February 28, 2008
Carcinogenesis, doi:10.1093/carcin/bgn038
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
29/9/1825    most recent
bgn038v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Bilger, A.
Right arrow Articles by Dove, W. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bilger, A.
Right arrow Articles by Dove, W. F.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Widespread hyperplasia induced by transgenic TGF{alpha} in ApcMin mice is associated with only regional effects on tumorigenesis

Andrea Bilger1, Ruth Sullivan2, Amy J. Prunuske1,4, Linda Clipson1, Norman Drinkwater1 and William F. Dove1,3

1 McArdle Laboratory for Cancer Research
2 Comprehensive Cancer Center
3 Laboratory of Genetics, University of Wisconsin School of Medicine and Public Health
4 Present Address: Department of Biochemistry, University of Wisconsin, Madison, Wisconsin 53706

Corresponding Author: William F. Dove, McArdle Laboratory for Cancer Research, 1400 University Avenue, Madison, WI 53706, Phone: (608) 262-4977, Email: dove{at}oncology.wisc.edu

Using a mouse predisposed to neoplasia by a germline mutation in Apc (ApcMin), we tested whether induced hyperplasia is sufficient to increase intestinal tumor multiplicity or size in the intestine. We found that hyperplasia in the jejunum correlated with a significant increase in tumor multiplicity. However, tumor multiplicity was unchanged in the hyperplastic colon. This result indicates that even an intestine predisposed to neoplasia can, in certain regions including the colon, accommodate net increased cell growth without developing more neoplasms. Where hyperplasia correlated with increased tumor multiplicity, it did not increase the size or net growth of established tumors. This result suggests that the event linking hyperplasia and neoplasia in the jejunum is tumor establishment. Two novel observations arose in our study: the Min mutation partially suppressed both mitosis and TGF{alpha}-induced hyperplasia throughout the intestine; and zinc treatment alone increased tumor multiplicity in the duodenum of Min mice.

Key Words: Hyperplasia • regionality • zinc • intestine • tumor • Apc

Received August 30, 2007; revised January 11, 2008; accepted January 29, 2008.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.