Evidence map›Paper›PMID 35948568›Full record

ArticleScientific reports2022

Transcriptional dynamics of colorectal cancer risk associated variation at 11q23.1 correlate with tuft cell abundance and marker expression in silico.

Bradley T Harris, Vidya Rajasekaran, James P Blackmur, Alan O'Callaghan, Kevin Donnelly, Maria Timofeeva, Peter G Vaughan-Shaw, Farhat V N Din, Malcolm G Dunlop, Susan M Farrington

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
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  5. Review
  6. Genetic mapping revealsScience immunology · 2023
    Article
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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

10 authors at 3 institutions in 2 countries.

Bradley T HarrisEdinburgh Cancer Research, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.
Vidya RajasekaranEdinburgh Cancer Research, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.
James P BlackmurEdinburgh Cancer Research, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.
Alan O'CallaghanMRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.
Kevin DonnellyEdinburgh Cancer Research, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.
Maria TimofeevaEdinburgh Cancer Research, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.
Peter G Vaughan-ShawEdinburgh Cancer Research, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.
Farhat V N DinEdinburgh Cancer Research, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.
Malcolm G DunlopEdinburgh Cancer Research, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK.
Susan M FarringtonEdinburgh Cancer Research, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK. susan.farrington@ed.ac.uk.
Edinburgh Cancer Research · GBUniversity of Edinburgh · GBMRC Institute of Genetics and Molecular Medicine · GB

Funding

Cancer Research UK 18927Cancer Research UK C157/A23218Cancer Research UK DRCPGM\100012Medical Research Council MR/K018647/1Medical Research Council MR/M004007/1
6 · The paper itself

Abstract

Colorectal cancer (CRC) is characterised by heritable risk that is not well understood. Heritable, genetic variation at 11q23.1 is associated with increased colorectal cancer (CRC) risk, demonstrating eQTL effects on 3 cis- and 23 trans-eQTL targets. We sought to determine the relationship between 11q23.1 cis- and trans-eQTL target expression and test for potential cell-specificity. scRNAseq from 32,361 healthy colonic epithelial cells was aggregated and subject to weighted gene co-expression network analysis (WGCNA). One module (blue) included 19 trans-eQTL targets and was correlated with POU2AF2 expression only. Following unsupervised clustering of single cells, the expression of 19 trans-eQTL targets was greatest and most variable in cluster number 11, which transcriptionally resembled tuft cells. 14 trans-eQTL targets were found to demarcate this cluster, 11 of which were corroborated in a second dataset. Intra-cluster WGCNA and module preservation analysis then identified twelve 11q23.1 trans-eQTL targets to comprise a network that was specific to cluster 11. Finally, linear modelling and differential abundance testing showed 11q23.1 trans-eQTL target expression was predictive of cluster 11 abundance. Our findings suggest 11q23.1 trans-eQTL targets comprise a POU2AF2-related network that is likely tuft cell-specific and reduced expression of these genes correlates with reduced tuft cell abundance in silico.

Indexed as

Colorectal NeoplasmsQuantitative Trait LociCluster AnalysisHumans

Identifiers

PMID35948568
PMCPMC9365857
OpenAlexW4291019300

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.