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Widespread hyperplasia induced by transgenic TGFalpha in ApcMin mice is associated with only regional effects on tumorigenesis. Carcinogenesis 2008 Sep;29(9):1825-30

Date

03/04/2008

Pubmed ID

18310091

Pubmed Central ID

PMC2547353

DOI

10.1093/carcin/bgn038

Scopus ID

2-s2.0-51849136546 (requires institutional sign-in at Scopus site)   7 Citations

Abstract

Using a mouse predisposed to neoplasia by a germ line mutation in Apc (Apc(Min)), 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.

Author List

Bilger A, Sullivan R, Prunuske AJ, Clipson L, Drinkwater NR, Dove WF

Author

Amy Jeanette Prunuske PhD Associate Professor in the Medical School Regional Campuses department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Apoptosis
Colonic Neoplasms
Duodenal Neoplasms
Ethylnitrosourea
Female
Genes, APC
Hyperplasia
Ileal Neoplasms
Jejunal Neoplasms
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Mitosis
Mutation
Transforming Growth Factor alpha
Transgenes
Zinc