Evidence map›Paper›PMID 18723878›Full record

ArticleGenetics2008

The pleiotropic phenotype of Apc mutations in the mouse: allele specificity and effects of the genetic background.

Richard B Halberg, Xiaodi Chen, James M Amos-Landgraf, Alanna White, Kristin Rasmussen, Linda Clipson, Cheri Pasch, Ruth Sullivan, Henry C Pitot, William F Dove

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Genetic reconstitution of tumorigenesis in primary intestinal cells.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  5. Vavien: an algorithm for prioritizing candidate disease genes based on topological similarity of proteins in interaction networks.Journal of computational biology : a journal of computational molecular cell biology · 2011
    Article
  6. Article
  7. Review
  8. Article
  9. 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

10 authors at 2 institutions in 2 countries.

Richard B HalbergMcArdle Laboratory for Cancer Research, University of Wisconsin, Madison, Wisconsin 53706, USA.
Xiaodi Chen
James M Amos-Landgraf
Alanna White
Kristin Rasmussen
Linda Clipson
Cheri Pasch
Ruth Sullivan
Henry C Pitot
William F Dove
Center for Cancer Research · USGenetic Resources Center · JP

Funding

GENES CONTROLLING NEOPLASIA OF THE INTESTINAL EPITHELIUMR37CA063677 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI DOVE, WILLIAM FRANKLIN · 1998 to 2008
$6.3M
NCI NIH HHS R37 CA063677NCI NIH HHS R37 CA63677NCI NIH HHS U01 CA-58085
6 · The paper itself

Abstract

Familial adenomatous polyposis (FAP) is a human cancer syndrome characterized by the development of hundreds to thousands of colonic polyps and extracolonic lesions including desmoid fibromas, osteomas, epidermoid cysts, and congenital hypertrophy of the pigmented retinal epithelium. Afflicted individuals are heterozygous for mutations in the APC gene. Detailed investigations of mice heterozygous for mutations in the ortholog Apc have shown that other genetic factors strongly influence the phenotype. Here we report qualitative and quantitative modifications of the phenotype of Apc mutants as a function of three genetic variables: Apc allele, p53 allele, and genetic background. We have found major differences between the Apc alleles Min and 1638N in multiplicity and regionality of intestinal tumors, as well as in incidence of extracolonic lesions. By contrast, Min mice homozygous for either of two different knockout alleles of p53 show similar phenotypic effects. These studies illustrate the classic principle that functional genetics is enriched by assessing penetrance and expressivity with allelic series. The mouse permits study of an allelic gene series on multiple genetic backgrounds, thereby leading to a better understanding of gene action in a range of biological processes.

Indexed as

Genes, APCMutationAdenomatous Polyposis ColiAdenomatous Polyposis Coli ProteinAllelesAnimalsCrosses, GeneticGene Expression Regulation, NeoplasticHomozygoteHumansIntestinal NeoplasmsMiceMice, KnockoutPancreatic NeoplasmsPhenotypeAdenomatous Polyposis Coli Protein

Identifiers

PMID18723878
PMCPMC2535708
OpenAlexW2001674444

What OpenQuestion holds

Textmetadata
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.