Evidence map›Paper›PMID 27694902›Full record

ArticleOncogene2017

Functional redundancy between Apc and Apc2 regulates tissue homeostasis and prevents tumorigenesis in murine mammary epithelium.

C S Daly, P Shaw, L D Ordonez, G T Williams, J Quist, A Grigoriadis, J H Van Es, H Clevers, A R Clarke, K R Reed

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed, 28 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

C S DalyEuropean Cancer Stem Cell Research Institute, Cardiff University School of Biosciences, Cardiff, Wales, UK.
P ShawEuropean Cancer Stem Cell Research Institute, Cardiff University School of Biosciences, Cardiff, Wales, UK.
L D OrdonezEuropean Cancer Stem Cell Research Institute, Cardiff University School of Biosciences, Cardiff, Wales, UK.
G T WilliamsDivision of Cancer and Genetics, School of Medicine, Cardiff University, Cardiff, UK.
J QuistBreast Cancer Now Unit, King's College London, Guy's Hospital London, London, UK.
A GrigoriadisBreast Cancer Now Unit, King's College London, Guy's Hospital London, London, UK.
J H Van EsHubrecht Laboratory, Netherlands Institute for Developmental Biology, Utrecht, The Netherlands.
H CleversHubrecht Laboratory, Netherlands Institute for Developmental Biology, Utrecht, The Netherlands.
A R ClarkeEuropean Cancer Stem Cell Research Institute, Cardiff University School of Biosciences, Cardiff, Wales, UK.
K R ReedEuropean Cancer Stem Cell Research Institute, Cardiff University School of Biosciences, Cardiff, Wales, UK.
Cardiff University · GBHubrecht Institute for Developmental Biology and Stem Cell Research · NLBreast Cancer Now · GBGuy's Hospital · GB

Funding

Cancer Research UK 15937Cancer Research UK A15937
6 · The paper itself

Abstract

Aberrant Wnt signaling within breast cancer is associated with poor prognosis, but regulation of this pathway in breast tissue remains poorly understood and the consequences of immediate or long-term dysregulation remain elusive. The exact contribution of the Wnt-regulating proteins adenomatous polyposis coli (APC) and APC2 in the pathogenesis of human breast cancer are ill-defined, but our analysis of publically available array data sets indicates that tumors with concomitant low expression of both proteins occurs more frequently in the 'triple negative' phenotype, which is a subtype of breast cancer with particularly poor prognosis. We have used mouse transgenics to delete Apc and/or Apc2 from mouse mammary epithelium to elucidate the significance of these proteins in mammary homeostasis and delineate their influences on Wnt signaling and tumorigenesis. Loss of either protein alone failed to affect Wnt signaling levels or tissue homeostasis. Strikingly, concomitant loss led to local disruption of β-catenin status, disruption in epithelial integrity, cohesion and polarity, increased cell division and a distinctive form of ductal hyperplasia with 'squamoid' ghost cell nodules in young animals. Upon aging, the development of Wnt activated mammary carcinomas with squamous differentiation was accompanied by a significantly reduced survival. This novel Wnt-driven mammary tumor model highlights the importance of functional redundancies existing between the Apc proteins both in normal homeostasis and in tumorigenesis.

Indexed as

Adenomatous Polyposis Coli ProteinAnimalsbeta CateninBreast NeoplasmsCarcinogenesisCell Transformation, NeoplasticCytoskeletal ProteinsDNA Copy Number VariationsEpitheliumFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHomeostasisHumansHyperplasiaAdenomatous Polyposis Coli ProteinAPC2 protein, humanbeta CateninCytoskeletal Proteins

Identifiers

PMID27694902
PMCPMC5219933
OpenAlexW2527877839

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.