ArticlePacific Symposium on Biocomputing. Pacific Symposium on Biocomputing2016
SEPARATING THE CAUSES AND CONSEQUENCES IN DISEASE TRANSCRIPTOME.
Article in Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- The E2F4 transcriptional repressor is a key mechanistic regulator of colon cancer resistance tobioRxiv : the preprint server for biology · 2025Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The causes of complex diseases are multifactorial and the phenotypes of complex diseases are typically heterogeneous, posting significant challenges for both the experiment design and statistical inference in the study of such diseases. Transcriptome profiling can potentially provide key insights on the pathogenesis of diseases, but the signals from the disease causes and consequences are intertwined, leaving it to speculations what are likely causal. Genome-wide association study on the other hand provides direct evidences on the potential genetic causes of diseases, but it does not provide a comprehensive view of disease pathogenesis, and it has difficulties in detecting the weak signals from individual genes. Here we propose an approach diseaseExPatho that combines transcriptome data, regulome knowledge, and GWAS results if available, for separating the causes and consequences in the disease transcriptome. DiseaseExPatho computationally deconvolutes the expression data into gene expression modules, hierarchically ranks the modules based on regulome using a novel algorithm, and given GWAS data, it directly labels the potential causal gene modules based on their correlations with genome-wide gene-disease associations. Strikingly, we observed that the putative causal modules are not necessarily differentially expressed in disease, while the other modules can show strong differential expression without enrichment of top GWAS variations. On the other hand, we showed that the regulatory network based module ranking prioritized the putative causal modules consistently in 6 diseases. We suggest that the approach is applicable to other common and rare complex diseases to prioritize causal pathways with or without genome-wide association studies.
Indexed as
Identifiers
26776202PMC4722949W2327165221What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.