Evidence map›Paper›PMID 34564680›Full record

ArticleMedicina oral, patologia oral y cirugia bucal2021

Expression profile of components of the β-catenin destruction complex in oral dysplasia and oral cancer.

F-J Goñi, D Peña-Oyarzún, V-A Torres, M Reyes

Open access · diamondAbstract read
In one paragraph

Article in Medicina oral, patologia oral y cirugia bucal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.2field-weighted citation impact, top 46% 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

5 citing papers in PubMed, 6 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

4 authors at 2 institutions in 2 countries.

F-J GoñiDepartment of Pathology and Oral Medicine Faculty of Dentistry, Universidad de Chile Calle Sergio Livingstone 943, Independencia, Santiago, Chile mreyes@odontologia.uchile.cl.
D Peña-Oyarzún
V-A Torres
M Reyes
University of Chile · CLUniversity of Valparaíso · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOral cancer represents the sixth most common cancer in the world and is associated with 40-50% survival at 5 years. Within oral malignancies, oral squamous cell carcinoma (OSCC) is commonly preceded by potentially malignant lesions, which, according to histopathological criteria, are referred to as oral dysplasia and their diagnosis are associated with higher rates of malignant transformation towards cancer. We recently reported that aberrant activation of the Wnt/β‑catenin pathway is due to overexpression of Wnt ligands in oral dysplasia. However, the expression of other regulators of this pathway, namely components of the β-catenin destruction complex has not been explored in oral dysplasia. MATERIAL AND

methodsUsing immunohistochemical analyses, we evaluated nuclear expression of β‑catenin and its association with Wnt3a and Wnt5a. Likewise, components of the β-catenin destruction complex, including Adenomatous Polyposis Coli (APC), Axin and Glycogen Synthase Kinase 3 beta (GSK-3β) were also evaluated in oral dysplasia and OSCC biopsies.

resultsWe found that moderate and severe dysplasia samples, which harbored increased expression of nuclear β‑catenin, depicted augmented cytoplasmic expression of GSK‑3β, Axin and APC, in comparison with OSCC samples. Also, GSK-3β was found nuclear in mild dysplasia and OSCC samples, when compared with other study samples.

conclusionsCytoplasmic levels of components of the β-catenin destruction complex are increased in oral dysplasia and might be responsible of augmented nuclear β‑catenin.

Indexed as

Carcinoma, Squamous CellMouth NeoplasmsAxin Signaling Complexbeta CateninGlycogen Synthase Kinase 3 betaHumansSquamous Cell Carcinoma of Head and NeckWnt Signaling PathwayAxin Signaling Complexbeta CateninCTNNB1 protein, humanGlycogen Synthase Kinase 3 beta

Identifiers

PMID34564680
PMCPMC8601647
OpenAlexW3204821663

What OpenQuestion holds

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LicenceCC BY
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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.