2017
DOI: 10.1186/s12920-017-0293-y
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Differential gene expression in disease: a comparison between high-throughput studies and the literature

Abstract: BackgroundDifferential gene expression is important to understand the biological differences between healthy and diseased states. Two common sources of differential gene expression data are microarray studies and the biomedical literature.MethodsWith the aid of text mining and gene expression analysis we have examined the comparative properties of these two sources of differential gene expression data.ResultsThe literature shows a preference for reporting genes associated to higher fold changes in microarray d… Show more

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Cited by 74 publications
(51 citation statements)
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“…Perhaps even more interesting are the 6 genes (ABCB1, GRN, LHFPL2, NAP1L3, TCN2, and VSIG1) that are not linked to the immune system, plausible pathogenic mechanisms, or autoimmune diseases. Scientists often fall prey to the "streetlight effect" -looking for answers where the light is better rather than where the truth is more likely to lie (118)(119)(120)(121). Although many of the underappreciated SLE MetaSignature genes make mechanistic sense, we should not lose sight of the 6 genes that had previously been in the shadows but are now illuminated.…”
Section: Tcn2mentioning
confidence: 99%
“…Perhaps even more interesting are the 6 genes (ABCB1, GRN, LHFPL2, NAP1L3, TCN2, and VSIG1) that are not linked to the immune system, plausible pathogenic mechanisms, or autoimmune diseases. Scientists often fall prey to the "streetlight effect" -looking for answers where the light is better rather than where the truth is more likely to lie (118)(119)(120)(121). Although many of the underappreciated SLE MetaSignature genes make mechanistic sense, we should not lose sight of the 6 genes that had previously been in the shadows but are now illuminated.…”
Section: Tcn2mentioning
confidence: 99%
“…Recent studies have demonstrated the highly imbalanced research effort directed towards individual human protein-coding genes [ 1 8 ], which manifests itself in several ways, including the number of publications per gene, the number of human-curated and computationally predicted functional annotations, the number of gene names and gene symbols, and the number of patents containing their nucleotide sequences ( S1 Fig ). Plausibly, this observed disparity could reflect a lack of importance of many genes, but more likely it could also reflect existing social structures of research [ 9 , 10 ], scientific and economic reward systems [ 11 , 12 ], medical and societal relevance [ 13 15 ], preceding discoveries [ 2 , 16 ], serendipity [ 17 , 18 ], the availability of technologies [ 19 , 20 ] and reagents [ 6 , 21 ], and other intrinsic characteristics of genes [ 22 24 ]. It remains unclear, however, if any of these factors can significantly explain the observed number of publications on individual human genes.…”
Section: Introductionmentioning
confidence: 99%
“…We hypothesized that this experimental paradigm has led to a gene-centric disease research bias where hypotheses are confounded by the streetlight effect of looking for “answers where the light is better rather than where the truth is more likely to lie” 13 – 16 . To test this hypothesis, we examined the annotation inequality for the human genome across a number of biomedical databases using the Gini coefficient, which is a measure of inequality such that high coefficient value indicates higher inequality 17 .…”
Section: Introductionmentioning
confidence: 99%