Spatially Uniform ReliefF (SURF) for computationally-efficient filtering of gene-gene interactions 英文参考文献.docVIP
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Spatially Uniform ReliefF (SURF) for computationally-efficient filtering of gene-gene interactions 英文参考文献
BioData Mining
BioMedCentral
Methodology
Open Access
Spatially Uniform ReliefF (SURF) for computationally-efficient
filtering of gene-gene interactions
Casey S Greene1, Nadia M Penrod1, Jeff Kiralis1 and Jason H Moore*1,2,3,4,5
Address: 1Department of Genetics, Norris Cotton Cancer Center, Dartmouth Medical School, Lebanon, NH, USA, 2Department of Community
and Family Medicine, Dartmouth Medical School, Lebanon, NH, USA, 3Department of Computer Science, University of New Hampshire,
Lebanon, NH, USA, 4Department of Computer Science, University of Vermont, Burlington, VT, USA and 5Translational Genomics Research
Institute, Phoenix, AZ, USA
Email: Casey S Greene - casey.s.greene@; Nadia M Penrod - nadia.m.penrod@;
Jeff Kiralis - jeff.kiralis@; Jason H Moore* - jason.h.moore@
* Corresponding author
Published: 22 September 2009
Received: 9 April 2009
Accepted: 22 September 2009
BioData Mining 2009, 2:5
doi:10.1186/1756-0381-2-5
This article is available from: /content/2/1/5
? 2009 Greene et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background: Genome-wide association studies are becoming the de facto standard in the genetic
analysis of common human diseases. Given the complexity and robustness of biological networks
such diseases are unlikely to be the result of single points of failure but instead likely arise from the
joint failure of two or more interacting components. The hope in genome-wide screens is that
these points of failure can be linked to single nucleotide polymorphisms (SNPs) which confer
disease susceptibility. Detecting interacting variants that lead to disease in the absence of single-
gene effects is difficult however, and methods to exhaustively analyze sets of
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