Evidence map›Paper›PMID 31531023›Full record

ArticleJournal of oncology2019

Live Cell Imaging Supports a Key Role for Histone Deacetylase as a Molecular Target during Glioblastoma Malignancy Downgrade through Tumor Competence Modulation.

Aline Menezes, Gustavo Henrique Dos Reis, Maria Cecília Oliveira-Nunes, Fernanda Mariath, Mariana Cabanel, Bruno Pontes, Newton Gonçalves Castro, José Marques de Brito, Katia Carneiro

Open access · hybridAbstract read
In one paragraph

Article in Journal of oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

7 citing papers in PubMed, 11 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

9 authors at 1 institution in 1 country.

Aline Menezes *Laboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373, Bloco F Sala F2-01, Rio de Janeiro 21941-902, Brazil.
Gustavo Henrique Dos Reis *Laboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373, Bloco F Sala F2-01, Rio de Janeiro 21941-902, Brazil.
Maria Cecília Oliveira-NunesLaboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373, Bloco F Sala F2-01, Rio de Janeiro 21941-902, Brazil.
Fernanda MariathLaboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373, Bloco F Sala F2-01, Rio de Janeiro 21941-902, Brazil.
Mariana CabanelLaboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373, Bloco F Sala F2-01, Rio de Janeiro 21941-902, Brazil.
Bruno PontesLaboratório de Pinças Ópticas, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373, Bloco F Sala F1-26, Rio de Janeiro 21941-902, Brazil.
Newton Gonçalves CastroLaboratório de Farmacologia Molecular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373, Bloco J Sala J1-10, Rio de Janeiro 21941-902, Brazil.
José Marques de BritoLaboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373, Bloco F Sala F2-01, Rio de Janeiro 21941-902, Brazil.ORCID https://orcid.org/0000-0002-5772-5999
Katia CarneiroLaboratório de Proliferação e Diferenciação Celular, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Av. Carlos Chagas Filho 373, Bloco F Sala F2-01, Rio de Janeiro 21941-902, Brazil.ORCID https://orcid.org/0000-0001-5915-5486
Universidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is the most aggressive tumor of the central nervous system, and the identification of the mechanisms underlying the biological basis of GBM aggressiveness is essential to develop new therapies. Due to the low prognosis of GBM treatment, different clinical studies are in course to test the use of histone deacetylase inhibitors (iHDACs) in anticancer cocktails. Here, we seek to investigate the impact of HDAC activity on GBM cell behavior and plasticity by live cell imaging. We pharmacologically knock down HDAC activity using two different inhibitors (TSA and SAHA) in two different tumor cell types: a commercial GBM cell line (U87-MG) and primary tumor (GBM011). Upon 72 hours of

Identifiers

PMID31531023
PMCPMC6720048
OpenAlexW2967438247

What Socratic 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 Socratic graph.