alexa Epistatic Control of Mammary Cancer Susceptibility in M
ISSN: 2161-1041

Hereditary Genetics: Current Research
Open Access

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Research Article

Epistatic Control of Mammary Cancer Susceptibility in Mice may Depend on the Dietary Environment

Larry J. Leamy*1, Ryan R. Gordon2 and Daniel Pomp3

1Department of Biology, University of North Carolina at Charlotte, Charlotte, North Carolina, 28223

2Department of Nutrition, University of North Carolina, Chapel Hill, North Carolina 27599

3Department of Biology, Nutrition, and Cell and Molecular Physiology, University of North Carolina, Chapel Hill North Carolina, 27599

*Corresponding Author:
Larry Leamy
Department of Biology
University of North Carolina at Charlotte
9201 University City Blvd, Charlotte, NC 28223, USA
E-mail: [email protected]

Received date: December 21, 2011; Accepted date: May 05, 2012; Published date: May 10, 2012

Citation: Leamy LJ, Gordon RR , Pomp D (2012) Epistatic Control of Mammary Cancer Susceptibility in Mice may Depend on the Dietary Environment. Hereditary Genetics 1:108 doi: 10.4172/2161-1041.1000108

Copyright: © 2012 Leamy LJ, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Abstract Recent studies have linked a high fat diet to the development of breast cancer, but any genetic basis for this association is poorly understood. We investigated this association with an epistatic analysis of seven cancer traits in a segregating population of mice with metastatic mammary cancer that were fed either a control or a high-fat diet. We used an interval mapping approach with single nucleotide polymorphisms to scan all 19 autosomes, and discovered a number of diet-independent epistatic interactions of quantitative trait loci (QTLs) affecting these traits. More importantly, we also discovered significant epistatic by diet interactions affecting some of the traits that suggested these epistatic effects varied depending on the dietary environment. An analysis of these interactions showed some were due to epistasis that occurred in mice fed only the control diet or only the high-fat diet whereas other interactions were generated by differential effects of epistasis in the two dietary environments. Some of the epistatic QTLs appeared to colocalize with cancer QTLs mapped in other mouse populations and with candidate genes identified from eQTLs previously mapped in this population, but others represented novel modifying loci affecting these cancer traits. It was concluded that these diet dependent epistatic QTLs contribute to a genetic susceptibility of dietary effects on breast cancer, and their identification may eventually lead to a better understanding that will be needed for the design of more effective treatments for this disease.


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