Evidence map›Paper›PMID 26776202›Full record

ArticlePacific Symposium on Biocomputing. Pacific Symposium on Biocomputing2016

SEPARATING THE CAUSES AND CONSEQUENCES IN DISEASE TRANSCRIPTOME.

Yong Fuga Li, Fuxiao Xin, Russ B Altman

Open access · goldAbstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 42% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Yong Fuga LiDepartment of Bioengineering, Stanford University, USA2Stanford Genome Technology Center, Stanford University, USA.
Fuxiao Xin
Russ B Altman
Stanford University · USGE Global Research (United States) · US

Funding

Pilot Study: POPULATION PHARMACOLOGYU54HL117798 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 2012 to 2016
$18.5M
Modeling the temporal succession of phenotypes & environnnental cuesP50MH094267 · NIMH · UNIVERSITY OF CHICAGO · PI RZHETSKY, ANDREY · 2011 to 2015
$10.2M
Text Mining for High-fidelity Curation and Discovery of Gene-drug-phenotype RelationshipsR01LM005652 · NLM · STANFORD UNIVERSITY · PI ALTMAN, RUSS BIAGIO · 2000 to 2018
$6.2M
Undergraduate Summer Research Experiences Support for Combining systems biology and structural biology to find new therapeuticsR01GM102365 · NIGMS · STANFORD UNIVERSITY · PI ALTMAN, RUSS BIAGIO · 2012 to 2021
$3.0M
MODELING AND COMPUTING WITH UNCERTAIN STRUCTURESR29LM005652 · NLM · STANFORD UNIVERSITY · PI ALTMAN, RUSS BIAGIO · 1994 to 1998
–
NHLBI NIH HHS HL117798NHLBI NIH HHS U54 HL117798NIGMS NIH HHS GM102365NIGMS NIH HHS R01 GM102365NIMH NIH HHS MH094267NIMH NIH HHS P50 MH094267NLM NIH HHS LM005652NLM NIH HHS R01 LM005652
6 · The paper itself

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

Genetic Predisposition to DiseaseTranscriptomeAlgorithmsComputational BiologyDiabetes MellitusGene Expression ProfilingGene Regulatory NetworksGenome-Wide Association StudyHumansMental DisordersModels, GeneticMultifactorial InheritanceUnsupervised Machine Learning

Identifiers

PMID26776202
PMCPMC4722949
OpenAlexW2327165221

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.