Evidence map›Paper›PMID 24652767›Full record

ArticleDisease models & mechanisms2014

Histopathology reveals correlative and unique phenotypes in a high-throughput mouse phenotyping screen.

Hibret A Adissu, Jeanne Estabel, David Sunter, Elizabeth Tuck, Yvette Hooks, Damian M Carragher, Kay Clarke, Natasha A Karp, Sanger Mouse Genetics Project, Susan Newbigging and 4 more

Abstract read
In one paragraph

Article in Disease models & mechanisms, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
–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

32 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Eye manifestations in theInternational journal of molecular epidemiology and genetics · 2021
    Article
  8. Histopathologic Evaluation and Scoring of Viral Lung Infection.Methods in molecular biology (Clifton, N.J.) · 2020
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Principles and approaches for reproducible scoring of tissue stains in research.Laboratory investigation; a journal of technical methods and pathology · 2018
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

14 authors.

Hibret A AdissuCentre for Modeling Human Disease, Toronto Centre for Phenogenomics, 25 Orde Street, Toronto, ON M5T 3H7, Canada.
Jeanne Estabel
David Sunter
Elizabeth Tuck
Yvette Hooks
Damian M Carragher
Kay Clarke
Natasha A Karp
Sanger Mouse Genetics Project
Susan Newbigging
Nora Jones
Lily Morikawa
Jacqueline K White
Colin McKerlie

Funding

KOMP Phase II Mouse Production and CryopreservationU42OD011175 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LLOYD, KC KENT · 2012 to 2015
$18.9M
KOMP Phase II Mouse PhenotypingU54HG006364 · NHGRI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LLOYD, KC KENT · 2011 to 2015
$16.3M
NHGRI NIH HHS U54 HG006364NIH HHS U42 OD011175Wellcome TrustWellcome Trust 098051
6 · The paper itself

Abstract

The Mouse Genetics Project (MGP) at the Wellcome Trust Sanger Institute aims to generate and phenotype over 800 genetically modified mouse lines over the next 5 years to gain a better understanding of mammalian gene function and provide an invaluable resource to the scientific community for follow-up studies. Phenotyping includes the generation of a standardized biobank of paraffin-embedded tissues for each mouse line, but histopathology is not routinely performed. In collaboration with the Pathology Core of the Centre for Modeling Human Disease (CMHD) we report the utility of histopathology in a high-throughput primary phenotyping screen. Histopathology was assessed in an unbiased selection of 50 mouse lines with (n=30) or without (n=20) clinical phenotypes detected by the standard MGP primary phenotyping screen. Our findings revealed that histopathology added correlating morphological data in 19 of 30 lines (63.3%) in which the primary screen detected a phenotype. In addition, seven of the 50 lines (14%) presented significant histopathology findings that were not associated with or predicted by the standard primary screen. Three of these seven lines had no clinical phenotype detected by the standard primary screen. Incidental and strain-associated background lesions were present in all mutant lines with good concordance to wild-type controls. These findings demonstrate the complementary and unique contribution of histopathology to high-throughput primary phenotyping of mutant mice.

Indexed as

PathologyPhenotypeAllelesAnimalsFemaleHigh-Throughput Screening AssaysMaleMiceMice, KnockoutOrgan SpecificityHigh-throughput phenotypingHistopathologyMousePathology

Identifiers

PMID24652767
PMCPMC4007403

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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.