Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-1-27
pubmed:abstractText
The study of the genetics of complex human disease has met with limited success. Many findings with candidate genes fail to replicate despite seemingly overwhelming physiological data implicating the genes. In contrast, animal model studies of the same genes and disease models usually have more consistent results. We propose that one important reason for this is the ability to control genetic background in animal studies. The fact that controlling genetic background can produce more consistent results suggests that the failure to replicate human findings in the same diseases is due to variation in interacting genes. Hence, the contrasting nature of the findings from the different study designs indicates the importance of non-additive genetic effects on human disease. We discuss these issues and some methodological approaches that can detect multilocus effects, using hypertension as a model disease. This article contains supplementary material, which may be viewed at the BioEssays website at http://www.interscience.wiley.com/jpages/0265-9247/suppmat/index.html.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0265-9247
pubmed:author
pubmed:copyrightInfo
Copyright 2004 Wiley Periodicals, Inc.
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
170-9
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
The use of animal models in the study of complex disease: all else is never equal or why do so many human studies fail to replicate animal findings?
pubmed:affiliation
Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN 37232, USA. smwilliams@chgr.mc.vanderbilt.edu
pubmed:publicationType
Journal Article