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|Title:||PPARδ status and mismatch repair mediated neoplasia in the mouse intestine|
Gescher, Andreas J.
|Publisher:||BioMed Central Ltd|
|Citation:||BMC Cancer 2006, 6:113|
|Abstract:||Background:Therapeutic regulation of PPARδ activity using selective agonists has been proposed for various disorders. However, the consequences of altered peroxisome proliferator-activated receptor delta (PPARδ) activity in the context of intestinal tumourigenesis remain somewhat unclear. Contradictory evidence suggesting PPARδ either attenuates or potentiates intestinal neoplasia. To further investigate the PPARδ dependency of intestinal tumourigenesis, we have analysed the consequences of PPARδ deficiency upon intestinal neoplasia occurring in mice with impaired mismatch DNA repair. Methods:Mice deficient for both PPARδ and the mismatch repair gene Mlh1 were produced and the incidence and severity of intestinal neoplasia recorded. Results:No significant differences between the control genotypes and the double mutant genotypes were recorded indicating that deficiency of PPARδ does not modify impaired mismatch repair induced neoplasia. Conclusion:In contrast with the previously observed acceleration of intestinal neoplasia in the context of the Apc[superscript Min/+]mouse, PPARδ deficiency does not alter the phenotype of mismatch repair deficiency. This data supports the notion that PPARδ is not required for adenoma formation and indicate that any pro-tumourigenic effect of PPARδ inactivation may be highly context dependent.|
|Rights:||Copyright © 2006 Reed et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.|
|Appears in Collections:||Published Articles, Dept. of Cancer Studies and Molecular Medicine|
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|10.1186_1471-2407-6-113.pdf||Post-review (final submitted)||248.26 kB||Adobe PDF||View/Open|
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