Widespread hyperplasia induced by transgenic TGFα in ApcMin mice is associated with only regional effects on tumorigenesis

Andrea Bilger, Ruth Sullivan, Amy J. Prunuske, Linda Clipson, Norman R. Drinkwater, William F. Dove

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Using a mouse predisposed to neoplasia by a germ line 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 multiple intestinal neoplasia (Min) mutation partially suppressed both mitosis and transforming growth factor alpha-induced hyperplasia throughout the intestine; and zinc treatment alone increased tumor multiplicity in the duodenum of Min mice.

Original languageEnglish (US)
Pages (from-to)1825-1830
Number of pages6
Issue number9
StatePublished - 2008

Bibliographical note

Funding Information:
National Research Service Award and a National Cancer Institute Postdoctoral Fellowship to A.B.; National Cancer Institute (P30-CA014520) to UW Comprehensive Cancer Center and (R37-CA63677) to W.F.D.


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