Evidence map›Paper›PMID 33186461›Full record

ArticleBlood advances2020

Che-1/AATF-induced transcriptionally active chromatin promotes cell proliferation in multiple myeloma.

Tiziana Bruno, Francesca De Nicola, Giacomo Corleone, Valeria Catena, Frauke Goeman, Matteo Pallocca, Cristina Sorino, Gianluca Bossi, Bruno Amadio, Giovanni Cigliana and 21 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 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
1.3field-weighted citation impact, top 19% 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, 19 citations in OpenAlex.

  1. Article
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  7. The new world of RNA diagnostics and therapeutics.Journal of experimental & clinical cancer research : CR · 2023
    Article
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  11. CK2-mediated phosphorylation of Che-1/AATF is required for its pro-proliferative activity.Journal of experimental & clinical cancer research : CR · 2021
    Article
  12. 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

31 authors at 9 institutions in 2 countries.

Tiziana BrunoSAFU Laboratory.
Francesca De NicolaSAFU Laboratory.
Giacomo CorleoneSAFU Laboratory.
Valeria CatenaSAFU Laboratory.
Frauke GoemanSAFU Laboratory.
Matteo PalloccaSAFU Laboratory.
Cristina SorinoSAFU Laboratory.
Gianluca BossiOncogenomic and Epigenetic Unit, and.
Bruno AmadioSAFU Laboratory.
Giovanni CiglianaClinical Pathology Unit, Department of Research, Advanced Diagnostics, and Technological Innovation, Translational Research Area, IRCCS Regina Elena National Cancer Institute, Rome, Italy.
Maria Rosaria RicciardiHematology, Department of Clinical and Molecular Medicine, "Sant'Andrea" Hospital-Sapienza, University of Rome, Rome, Italy.
Maria Teresa PetrucciDepartment of Cellular Biotechnologies and Haematology, Sapienza University of Rome, Rome, Italy.
Enrico Pierluigi SpugniniSAFU Laboratory.
Alfonso BaldiDepartment of Environmental, Biological and Pharmaceutical Sciences and Technologies, Campania University "Luigi Vanvitelli," Caserta, Italy.
Mario CioceOncogenomic and Epigenetic Unit, and.
Giancarlo CorteseSAFU Laboratory.
Elisabetta MatteiCNR-Institute of Cell Biology and Neurobiology, IRCCS Fondazione Santa Lucia, Rome, Italy.
Roberta MerolaClinical Pathology Unit, Department of Research, Advanced Diagnostics, and Technological Innovation, Translational Research Area, IRCCS Regina Elena National Cancer Institute, Rome, Italy.
Umberto GianelliPathology Unit, Department of Pathophysiology and Transplantation, University of Milan, IRCCS Ca' Granda-Maggiore Policlinico, Hospital Foundation, Milan, Italy.
Luca BaldiniPathology Unit, Department of Pathophysiology and Transplantation, University of Milan, IRCCS Ca' Granda-Maggiore Policlinico, Hospital Foundation, Milan, Italy.
Francesco PisaniHematology Unit, IRCCS Regina Elena National Cancer Institute, Rome, Italy.
Svitlana GumenyukHematology Unit, IRCCS Regina Elena National Cancer Institute, Rome, Italy.
Andrea MengarelliHematology Unit, IRCCS Regina Elena National Cancer Institute, Rome, Italy.
Katja HöpkerDepartment II of Internal Medicine, University Hospital of Cologne, Cologne, Germany.
Thomas BenzingDepartment II of Internal Medicine, University Hospital of Cologne, Cologne, Germany.
Bruno VincenziCampus Biomedico University, Rome, Italy; and.
Aristide FloridiSAFU Laboratory.
Claudio PassanantiCNR-Institute of Molecular Biology and Pathology, Department of Molecular Medicine, Sapienza University, Rome, Italy.
Giovanni BlandinoOncogenomic and Epigenetic Unit, and.
Simona IezziSAFU Laboratory.
Maurizio FanciulliSAFU Laboratory.
Istituti di Ricovero e Cura a Carattere Scientifico · ITSapienza University of Rome · ITUniversity of Milan · ITFondazione Santa Lucia · ITInstitute of Molecular Biology and Pathology · ITUniversità Campus Bio-Medico · ITUniversity Hospital Cologne · DEUniversity of Campania "Luigi Vanvitelli" · ITUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is a hematologic malignancy produced by a clonal expansion of plasma cells and characterized by abnormal production and secretion of monoclonal antibodies. This pathology exhibits an enormous heterogeneity resulting not only from genetic alterations but also from several epigenetic dysregulations. Here we provide evidence that Che-1/AATF (Che-1), an interactor of RNA polymerase II, promotes MM proliferation by affecting chromatin structure and sustaining global gene expression. We found that Che-1 depletion leads to a reduction of "active chromatin" by inducing a global decrease of histone acetylation. In this context, Che-1 directly interacts with histones and displaces histone deacetylase class I members from them. Strikingly, transgenic mice expressing human Che-1 in plasma cells develop MM with clinical features resembling those observed in the human disease. Finally, Che-1 downregulation decreases BRD4 chromatin accumulation to further sensitize MM cells to bromodomain and external domain inhibitors. These findings identify Che-1 as a promising target for MM therapy, alone or in combination with bromodomain and external domain inhibitors.

Indexed as

Multiple MyelomaNuclear ProteinsCell ProliferationChromatinHumansTranscription FactorsChromatinNuclear ProteinsTranscription Factors

Identifiers

PMID33186461
PMCPMC7686885
OpenAlexW3101190001

What OpenQuestion holds

Textmetadata
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.