Evidence map›Paper›PMID 28506205›Full record

ArticleBMC genomics2017

In silico pathway analysis and tissue specific cis-eQTL for colorectal cancer GWAS risk variants.

Lenora W M Loo, Mathieu Lemire, Loïc Le Marchand

Abstract read
In one paragraph

Article in BMC genomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  9. Identifying Transcriptomic Signatures and Rules for SARS-CoV-2 Infection.Frontiers in cell and developmental biology · 2020
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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.

Lenora W M LooCancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI, USA. lloo@cc.hawaii.edu.
Mathieu LemireOntario Institute for Cancer Research, MaRS Centre, 661 University Avenue, Suite 510, Toronto, ON, M5G 0A3, Canada.
Loïc Le MarchandCancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenome-wide association studies have identified 55 genetic variants associated with colorectal cancer risk to date. However, potential causal genes and pathways regulated by these risk variants remain to be characterized. Therefore, we performed gene ontology enrichment and pathway analyses to determine if there was an enrichment of genes in proximity to the colorectal cancer risk variants that could further elucidate the probable causal genes and pathways involved in colorectal cancer biology.

resultsFor the 65 unique genes that either contained, or were immediately neighboring up- and downstream, of these variants there was a significant enrichment for the KEGG pathway, Pathways in Cancer (p-value = 2.67 × 10

conclusionsOur data reaffirm the potential to identify an enrichment for biological processes and candidate causal genes based on expression profiles correlated with genetic risk alleles of colorectal cancer, however, the identification of these significant cis-eQTLs is context and tissue specific.

Indexed as

Computer SimulationGenetic VariationGenome-Wide Association StudyAllelesColorectal NeoplasmsComputational BiologyGene OntologyGenetic Predisposition to DiseaseHumansOrgan SpecificityQuantitative Trait LociColorectal cancereQTLGene expressionRisk variant

Identifiers

PMID28506205
PMCPMC5432975

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.