Evidence map›Paper›PMID 31254352›Full record

ArticleFEBS letters2019

HDAC2-dependent miRNA signature in acute myeloid leukemia.

Mariarosaria Conte, Carmela Dell'Aversana, Giulia Sgueglia, Annamaria Carissimo, Lucia Altucci

Open access · hybridAbstract read
In one paragraph

Article in FEBS letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 14 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

5 authors at 2 institutions in 1 country.

Mariarosaria ConteIRCCS, SDN, Naples, Italy.
Carmela Dell'AversanaDepartment of Precision Medicine, University of Campania "L. Vanvitelli", Naples, Italy.
Giulia SguegliaDepartment of Precision Medicine, University of Campania "L. Vanvitelli", Naples, Italy.
Annamaria CarissimoDepartment of Precision Medicine, University of Campania "L. Vanvitelli", Naples, Italy.
Lucia AltucciDepartment of Precision Medicine, University of Campania "L. Vanvitelli", Naples, Italy.
University of Campania "Luigi Vanvitelli" · ITSDN Istituto di Ricerca Diagnostica e Nucleare · IT

Funding

AIRC 17217Campania Regional Government FASE2: IDEAL CUP B53D18000080007Campania Regional Government Lotta Alle Patologie Oncologiche, iCURE CUP B21C17000030007MIUR Proof of Concept EpiCUREVALERE: Vanvitelli per la Ricerca
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) arises from a complex sequence of biological and finely orchestrated events that are still poorly understood. Increasingly, epigenetic studies are providing exciting findings that may be exploited in promising and personalized cutting-edge therapies. A more appropriate and broader screening of possible players in cancer could identify a master molecular mechanism in AML. Here, we build on our previously published study by evaluating a histone deacetylase (HDAC)2-mediated miRNA regulatory network in U937 leukemic cells. Following a comparative miRNA profiling analysis in genetically and enzymatically HDAC2-downregulated AML cells, we identified miR-96-5p and miR-92a-3p as potential regulators in AML etiopathology by targeting defined genes. Our findings support the potentially beneficial role of alternative physiopathological interventions.

Indexed as

Cell Line, TumorGene Regulatory NetworksGenes, MHC Class IIHistone Deacetylase 2HumansLeukemia, Myeloid, AcuteMicroRNAsHDAC2 protein, humanHistone Deacetylase 2MicroRNAsepigeneticsHDAC2immunoregulationleukemiamiRNASAHA

Identifiers

PMID31254352
PMCPMC6790563
OpenAlexW2956002315

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.