Evidence map›Paper›PMID 34294033›Full record

ArticleBMC genomics2021

Genetic mapping of novel modifiers for Apc

Alexandra Dorman, Ilona Binenbaum, Hanifa J Abu-Toamih Atamni, Aristotelis Chatziioannou, Ian Tomlinson, Richard Mott, Fuad A Iraqi

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

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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

7 authors at 5 institutions in 3 countries.

Alexandra DormanDepartment of Clinical Microbiology & Immunology, Sackler Faculty of Medicine, Ramat Aviv, 69978, Tel-Aviv, Israel.
Ilona BinenbaumDepartment of Biology, University of Patras, Patras, Greece.
Hanifa J Abu-Toamih AtamniDepartment of Clinical Microbiology & Immunology, Sackler Faculty of Medicine, Ramat Aviv, 69978, Tel-Aviv, Israel.
Aristotelis ChatziioannouCenter of Systems Biology, Biomedical Research Foundation of the Academy of Athens, Athens, Greece.
Ian TomlinsonCancer Research UK Edinburgh Centre, Charles and Ethel Barr Chair of Cancer Research, University of Edinburgh, Edinburgh, UK.
Richard MottDepartment of Genetics, University Collage of London, London, UK.
Fuad A IraqiDepartment of Clinical Microbiology & Immunology, Sackler Faculty of Medicine, Ramat Aviv, 69978, Tel-Aviv, Israel. fuadi@tauex.tau.ac.il.ORCID http://orcid.org/0000-0001-5525-206X
Tel Aviv University · ILBiomedical Research Foundation of the Academy of Athens · GREdinburgh Cancer Research · GBUniversity College London · GBUniversity of Patras · GR

Funding

Cancer Research UK 27327Wellcome TrustWellcome Trust Wellcome Trust grants 090532/Z/09/Z, 085906/Z/08/Z, 083573/Z/07/Z, and 075491/Z/04
6 · The paper itself

Abstract

backgroundFamilial adenomatous polyposis is an inherited genetic disease, characterized by colorectal polyps. It is caused by inactivating mutations in the Adenomatous polyposis coli (Apc) gene. Mice carrying a nonsense mutation in the Apc gene at R850, which is designated Apc

resultsThe number of polyps in all these sub-regions and colon varied significantly between the different CC lines. At 95% genome-wide significance, we mapped nine novel QTL for variation in polyp number, with distinct QTL associated with each intestinal sub-region. QTL confidence intervals varied in width between 2.63-17.79 Mb. We extracted all genes in the mapped QTL at 90 and 95% CI levels using the BioInfoMiner online platform to extract, significantly enriched pathways and key linker genes, that act as regulatory and orchestrators of the phenotypic landscape associated with the Apc

conclusionsGenomic structure of the CC lines has allowed us to identify novel modifiers and confirmed some of the previously mapped modifiers. Key genes involved mainly in metabolic and immunological processes were identified. Future steps in this analysis will be to identify regulatory elements - and possible epistatic effects - located in the mapped QTL.

Indexed as

Adenomatous Polyposis ColiCollaborative Cross MiceAnimalsFemaleIntestinal PolypsMaleMiceMice, Inbred C57BLQuantitative Trait LociApc MinCandidate genesCollaborative crossColorectal cancerFamilial adenomatous polyposisGenetic modifierMomsPhenotypingQTL mappingRecombinant inbred lines

Identifiers

PMID34294033
PMCPMC8299641
OpenAlexW3186877660

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.