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Cell Growth & Differentiation, Vol 7, Issue 10 1361-1368, Copyright © 1996 by American Association of Cancer Research


ARTICLES

Action of Min and Mom1 on neoplasia in ectopic intestinal grafts

KA Gould and WF Dove
McArdle Laboratory for Cancer Research and Laboratory of Genetics, University of Wisconsin, Madison, 53706, USA.

Mice heterozygous for Min, a mutant allele of Apc, develop adenomas throughout the intestinal tract. Tumor multiplicity in Min mice is influenced by genetic modifier loci. Previously, we mapped one of these modifier loci, Mom1, to distal mouse chromosome 4. Mom1 is a semidominant modifier of both tumor size and multiplicity in Min mice. Recent evidence suggests that Mom1 may encode a secretory phospholipase, Pla2g2a. Pla2g2a is expressed in a variety of cell types and seems to be involved in inflammatory responses and bacterial defense mechanisms. Here, we determine whether Min and Mom1 act in a tissue-autonomous fashion using ectopic intestinal isografts. Within the small intestinal grafts, both Min and Mom1 act in a tissue-autonomous manner. There is no evidence that either Min or Mom1 has a systemic effect on tumor development. However, within the colonic grafts, the Min phenotype does not appear to be autonomous; the development of colonic tumors in Min mice seems dependent on factors beyond the Min genotype of the colonic epithelium. Micro-environmental factors, such as digestive secretions, dietary components, or intestinal flora, may be critical factors contributing to the development of Min-induced colonic tumors. However, these factors are not required for the action of Min or Mom1 within the small intestine.


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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1996 by the American Association of Cancer Research.