Evidence map›Paper›PMID 21738649›Full record

ArticlePloS one2011

Epigenetic activation of SOX11 in lymphoid neoplasms by histone modifications.

Maria Carmela Vegliante, Cristina Royo, Jara Palomero, Itziar Salaverria, Balazs Balint, Idoia Martín-Guerrero, Xabier Agirre, Amaia Lujambio, Julia Richter, Silvia Xargay-Torrent and 14 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

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  8. Sox11 promotes head and neck cancer progression via the regulation of SDCCAG8.Journal of experimental & clinical cancer research : CR · 2019
    Article
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  10. SOX11: friend or foe in tumor prevention and carcinogenesis?Therapeutic advances in medical oncology · 2019
    Review
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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

24 authors at 11 institutions in 2 countries.

Maria Carmela VeglianteHematopathology Section, Laboratory of Pathology, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, Barcelona, Spain.
Cristina Royo
Jara Palomero
Itziar Salaverria
Balazs Balint
Idoia Martín-Guerrero
Xabier Agirre
Amaia Lujambio
Julia Richter
Silvia Xargay-Torrent
Silvia Bea
Luis Hernandez
Anna Enjuanes
María José Calasanz
Andreas Rosenwald
German Ott
José Roman-Gomez
Felipe Prosper
Manel Esteller
Pedro Jares
Reiner Siebert
Elias Campo
José I Martín-Subero
Virginia Amador
Consorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESUniversitat de Barcelona · ESInstitut d'Investigació Biomédica de Bellvitge · ESUniversidad de Navarra · ESUniversity Hospital Schleswig-Holstein · DEClinica Universidad de Navarra · ESHospital Universitario Reina Sofía · ESKiel University · DERobert Bosch Hospital · DEUniversity of Lübeck · DEUniversity of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have shown aberrant expression of SOX11 in various types of aggressive B-cell neoplasms. To elucidate the molecular mechanisms leading to such deregulation, we performed a comprehensive SOX11 gene expression and epigenetic study in stem cells, normal hematopoietic cells and different lymphoid neoplasms. We observed that SOX11 expression is associated with unmethylated DNA and presence of activating histone marks (H3K9/14Ac and H3K4me3) in embryonic stem cells and some aggressive B-cell neoplasms. In contrast, adult stem cells, normal hematopoietic cells and other lymphoid neoplasms do not express SOX11. Such repression was associated with silencing histone marks H3K9me2 and H3K27me3. The SOX11 promoter of non-malignant cells was consistently unmethylated whereas lymphoid neoplasms with silenced SOX11 tended to acquire DNA hypermethylation. SOX11 silencing in cell lines was reversed by the histone deacetylase inhibitor SAHA but not by the DNA methyltransferase inhibitor AZA. These data indicate that, although DNA hypermethylation of SOX11 is frequent in lymphoid neoplasms, it seems to be functionally inert, as SOX11 is already silenced in the hematopoietic system. In contrast, the pathogenic role of SOX11 is associated with its de novo expression in some aggressive lymphoid malignancies, which is mediated by a shift from inactivating to activating histone modifications.

Indexed as

Blotting, WesternCell Line, TumorChromatin ImmunoprecipitationDNA MethylationEpigenesis, GeneticHistone Deacetylase InhibitorsHistonesHumansIn Vitro TechniquesLymphomaOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionSOXC Transcription FactorsHistone Deacetylase InhibitorsHistonesSOX11 protein, humanSOXC Transcription Factors

Identifiers

PMID21738649
PMCPMC3124503
OpenAlexW1989700029

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.