Evidence map›Paper›PMID 24349422›Full record

ArticlePloS one2013

HDAC inhibitors repress BARD1 isoform expression in acute myeloid leukemia cells via activation of miR-19a and/or b.

Ilaria Lepore, Carmela Dell'Aversana, Maxim Pilyugin, Mariarosaria Conte, Angela Nebbioso, Floriana De Bellis, Francesco P Tambaro, Tiziana Izzo, Guillermo Garcia-Manero, Felicetto Ferrara and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 43 citations in OpenAlex.

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  3. BARD1: A Friend or Foe in Pancreatic Ductal Adenocarcinoma?International journal of molecular sciences · 2025
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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

12 authors at 4 institutions in 2 countries.

Ilaria LeporeDepartment of Biochemistry, Biophysics and General Pathology, Seconda Università degli Studi di Napoli, Naples, Italy.
Carmela Dell'AversanaDepartment of Biochemistry, Biophysics and General Pathology, Seconda Università degli Studi di Napoli, Naples, Italy ; Institute of Genetics and Biophysics (IGB), Naples, Italy.
Maxim PilyuginMolecular Gynecology and Obstetrics Laboratory, Department of Gynecology and Obstetrics and Department of Genetic and Laboratory Medicine, University Hospitals of Geneva, HUG, Genève, Switzerland.
Mariarosaria ConteDepartment of Biochemistry, Biophysics and General Pathology, Seconda Università degli Studi di Napoli, Naples, Italy.
Angela NebbiosoDepartment of Biochemistry, Biophysics and General Pathology, Seconda Università degli Studi di Napoli, Naples, Italy.
Floriana De BellisDepartment of Biochemistry, Biophysics and General Pathology, Seconda Università degli Studi di Napoli, Naples, Italy.
Francesco P TambaroDepartment of Biochemistry, Biophysics and General Pathology, Seconda Università degli Studi di Napoli, Naples, Italy ; Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America.
Tiziana IzzoDivision of Hematology and Stem Cell Transplantation Unit, Cardarelli Hospital, Naples, Italy.
Guillermo Garcia-ManeroDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America.
Felicetto FerraraDivision of Hematology and Stem Cell Transplantation Unit, Cardarelli Hospital, Naples, Italy.
Irmgard Irminger-FingerMolecular Gynecology and Obstetrics Laboratory, Department of Gynecology and Obstetrics and Department of Genetic and Laboratory Medicine, University Hospitals of Geneva, HUG, Genève, Switzerland.
Lucia AltucciDepartment of Biochemistry, Biophysics and General Pathology, Seconda Università degli Studi di Napoli, Naples, Italy ; Institute of Genetics and Biophysics (IGB), Naples, Italy.
University of Naples Federico II · ITFatebenefratelli Hospital · ITInstitute of Genetics and Biophysics · ITThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the past years BARD1 (BRCA1-associated RING domain 1) has been considered as both a BRCA1 (BReast Cancer susceptibility gene 1, early onset) interactor and tumor suppressor gene mutated in breast and ovarian cancers. Despite its role as a stable heterodimer with BRCA1, increasing evidence indicates that BARD1 also has BRCA1-independent oncogenic functions. Here, we investigate BARD1 expression and function in human acute myeloid leukemias and its modulation by epigenetic mechanism(s) and microRNAs. We show that the HDACi (histone deacetylase inhibitor) Vorinostat reduces BARD1 mRNA levels by increasing miR-19a and miR-19b expression levels. Moreover, we identify a specific BARD1 isoform, which might act as tumor diagnostic and prognostic markers.

Indexed as

Epigenesis, GeneticGene Expression Regulation, LeukemicHistone Deacetylase InhibitorsHL-60 CellsHumansHydroxamic AcidsK562 CellsLeukemia, Myeloid, AcuteMicroRNAsProtein IsoformsRNA, NeoplasmTumor Suppressor ProteinsU937 CellsUbiquitin-Protein LigasesVorinostatBARD1 protein, humanHistone Deacetylase InhibitorsHydroxamic AcidsMicroRNAsMIRN19A microRNA, humanProtein IsoformsRNA, NeoplasmTumor Suppressor ProteinsUbiquitin-Protein LigasesVorinostat

Identifiers

PMID24349422
PMCPMC3859623
OpenAlexW2144368903

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.