Evidence map›Paper›PMID 36293473›Full record

ArticleInternational journal of molecular sciences2022

GPER Agonist G1 Prevents Wnt-Induced

Maria Abancens, Brian J Harvey, Jean McBryan

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.4field-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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. 17β-estradiol in colorectal cancer: friend or foe?Cell communication and signaling : CCS · 2024
    Review
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  6. Review
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  8. 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

3 authors at 1 institution in 2 countries.

Maria AbancensDepartment of Surgery, RCSI University of Medicine and Health Sciences, ERC Beaumont Hospital, D09 YD60 Dublin, Ireland.
Brian J HarveyDepartment of Molecular Medicine, RCSI University of Medicine and Health Sciences, ERC Beaumont Hospital, D09 YD60 Dublin, Ireland.ORCID 0000-0002-7388-8034
Jean McBryanDepartment of Surgery, RCSI University of Medicine and Health Sciences, ERC Beaumont Hospital, D09 YD60 Dublin, Ireland.ORCID 0000-0002-7568-2208
Beaumont Hospital · IE

Funding

DOCTRID n/aHigher Education Authority n/aPhysiological Society n/a
6 · The paper itself

Abstract

Women consistently show lower incidence and mortality rates for colorectal cancer (CRC) compared to men. Epidemiological evidence supports a pivotal role for estrogen in protecting women against CRC. Estrogen protective effects in CRC have been mainly attributed to the estrogen receptor beta (ERβ) however its expression is lost during CRC progression. The role of the G-protein coupled membrane estrogen receptor (GPER/GPER1/GPR30), which remains expressed after ERβ loss in CRC, is currently under debate. We hypothesise that estrogen can protect against CRC progression via GPER by modulating the Wnt/β-catenin proliferative pathway which is commonly hyperactivated in CRC. We sought evidence of sexual dimorphism within the Wnt/β-catenin pathway by conducting Kaplan-Meier analyses based on gene expression of the Wnt receptor

Indexed as

beta CateninColorectal NeoplasmsCell Line, TumorCell ProliferationEstrogen Receptor betaEstrogensFemaleGene Expression Regulation, NeoplasticHT29 CellsHumansMaleNeoplasm Recurrence, LocalReceptors, EstrogenUp-RegulationWnt Signaling Pathwaybeta CateninEstrogen Receptor betaEstrogensReceptors, Estrogenbeta-catenincolorectal cancerGPERWnt

Identifiers

PMID36293473
PMCPMC9603962
OpenAlexW4306925953

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.