Evidence map›Paper›PMID 32225105›Full record

ArticleInternational journal of molecular sciences2020

Regulative Loop between β-catenin and Protein Tyrosine Receptor Type γ in Chronic Myeloid Leukemia.

Luisa Tomasello, Marzia Vezzalini, Christian Boni, Massimiliano Bonifacio, Luigi Scaffidi, Mohamed Yassin, Nader Al-Dewik, Paul Takam Kamga, Mauro Krampera, Claudio Sorio

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 21 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

10 authors at 3 institutions in 3 countries.

Luisa TomaselloDepartment of Medicine, General Pathology Division, University of Verona, 37134 Verona, Italy.
Marzia VezzaliniDepartment of Medicine, General Pathology Division, University of Verona, 37134 Verona, Italy.ORCID 0000-0002-5476-0844
Christian BoniDepartment of Medicine, General Pathology Division, University of Verona, 37134 Verona, Italy.ORCID 0000-0002-9982-4100
Massimiliano BonifacioDepartment of Medicine, Section of Hematology, University of Verona, 37134 Verona, Italy.
Luigi ScaffidiDepartment of Medicine, Section of Hematology, University of Verona, 37134 Verona, Italy.
Mohamed YassinNational Center for Cancer Care and Research, Department of Hematology and BMT, Hamad Medical Corporation, Doha, Qatar and College of Medicine Qatar University, Doha, Qatar.ORCID 0000-0002-1144-8076
Nader Al-DewikPediatrics department, Women's Wellness and Research Center (WWRC), Interim Translational Research Institute (iTRI), Hamad Medical Corporation (HMC) and College of Health and Life Science (CHLS), Hamad Bin Khalifa University (HBKU), Doha, Qatar.ORCID 0000-0001-5739-1135
Paul Takam KamgaStem Cell Research Laboratory, Section of Hematology, Department of Medicine, University of Verona, 37134 Verona, Italy.ORCID 0000-0002-8586-1381
Mauro KramperaStem Cell Research Laboratory, Section of Hematology, Department of Medicine, University of Verona, 37134 Verona, Italy.ORCID 0000-0002-7280-2040
Claudio SorioDepartment of Medicine, General Pathology Division, University of Verona, 37134 Verona, Italy.
University of Verona · ITHamad Medical Corporation · QANational Center for Cancer Care and Research · QA

Funding

Associazione Italiana per la Ricerca sul Cancro IG 4667Qatar National Research Fund 4-157-3-052
6 · The paper itself

Abstract

Protein tyrosine phosphatase receptor type γ (PTPRG) is a tumor suppressor gene, down-regulated in Chronic Myeloid Leukemia (CML) cells by the hypermethylation of its promoter region. β-catenin (CTNNB1) is a critical regulator of Leukemic Stem Cells (LSC) maintenance and CML proliferation. This study aims to demonstrate the antagonistic regulation between β-catenin and PTPRG in CML cells. The specific inhibition of PTPRG increases the activation state of BCR-ABL1 and modulates the expression of the BCR-ABL1- downstream gene β-Catenin. PTPRG was found to be capable of dephosphorylating β-catenin, eventually causing its cytosolic destabilization and degradation in cells expressing PTPRG. Furthermore, we demonstrated that the increased expression of β-catenin in PTPRG-negative CML cell lines correlates with DNA (cytosine-5)-methyl transferase 1 (DNMT1) over-expression, which is responsible for

Indexed as

Gene Expression Regulation, Neoplasticbeta CateninDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationDown-RegulationFusion Proteins, bcr-ablHumansK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositivePromoter Regions, GeneticReceptor-Like Protein Tyrosine Phosphatases, Class 5Tumor Cells, CulturedBCR-ABL1 fusion protein, humanbeta CateninCTNNB1 protein, humanDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanFusion Proteins, bcr-ablPTPRG protein, humanReceptor-Like Protein Tyrosine Phosphatases, Class 55-azacytidinechronic myeloid leukemiaDNMTmethylationPTPRGtumor suppressortyrosine phosphataseβ-catenin

Identifiers

PMID32225105
PMCPMC7177637
OpenAlexW3013247720

What OpenQuestion holds

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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.