Evidence map›Paper›PMID 30583528›Full record

ArticleCancers2018

Mifepristone Overcomes Tumor Resistance to Temozolomide Associated with DNA Damage Repair and Apoptosis in an Orthotopic Model of Glioblastoma.

Monserrat Llaguno-Munive, Mario Romero-Piña, Janeth Serrano-Bello, Luis A Medina, Norma Uribe-Uribe, Ana Maria Salazar, Mauricio Rodríguez-Dorantes, Patricia Garcia-Lopez

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2018. 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, 24 citations in OpenAlex.

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  12. Antiproliferative effect of mifepristone (RU486) on human neuroblastoma cells (SK-N-SH): in vitro and in vivo studies.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020
    Article
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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

8 authors at 4 institutions in 1 country.

Monserrat Llaguno-MuniveLaboratorio de Farmacología, Subdirección de Investigación Básica, Instituto Nacional de Cancerología, Ciudad de México 14080, Mexico. muniv1250@hotmail.com.
Mario Romero-PiñaLaboratorio de Farmacología, Subdirección de Investigación Básica, Instituto Nacional de Cancerología, Ciudad de México 14080, Mexico. esau1708@gmail.com.
Janeth Serrano-BelloFacultad de Odontología, Universidad Nacional Autónoma de México (UNAM), Ciudad de México 04510, Mexico. janserbe@hotmail.com.
Luis A MedinaInstituto de Física, Universidad Nacional Autónoma de México (UNAM), Unidad de Investigación Biomédica en Cáncer INCan-UNAM, Ciudad de México, 14080, Mexico. medina@fisica.unam.mx.ORCID 0000-0001-9301-5823
Norma Uribe-UribeInstituto Nacional de Ciencias Médicas y de la Nutrición Salvador Zubirán, Ciudad de México 14080, Mexico. nofeliauribe@yahoo.com.mx.
Ana Maria SalazarInstituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México (UNAM), Ciudad de México 04510, Mexico. anamsm@biomedicas.unam.mx.
Mauricio Rodríguez-DorantesInstituto de Medicina Genómica, Ciudad de México 14080, Mexico. mrodriguez@inmegen.gob.mx.
Patricia Garcia-LopezLaboratorio de Farmacología, Subdirección de Investigación Básica, Instituto Nacional de Cancerología, Ciudad de México 14080, Mexico. pgarcia_lopez@yahoo.com.mx.
Instituto Nacional de Cancerología · MXUniversidad Nacional Autónoma de México · MXInstituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán · MXNational Institute of Genomic Medicine · MX

Funding

Consejo Nacional de Ciencia y Tecnología CB-258823
6 · The paper itself

Abstract

The standard treatment for glioblastoma multiforme (GBM) is surgery followed by chemo/radiotherapy. A major limitation on patient improvement is the high resistance of tumors to drug treatment, likely responsible for their subsequent recurrence and rapid progression. Therefore, alternatives to the standard therapy are necessary. The aim of the present study was to evaluate whether mifepristone, an antihormonal agent, has a synergistic effect with temozolomide (used in standard therapy for gliomas). Whereas the mechanism of temozolomide involves damage to tumor DNA leading to apoptosis, tumor resistance is associated with DNA damage repair through the O⁶-methylguanine-DNA-methyltransferase (MGMT) enzyme. Temozolomide/mifepristone treatment, herein examined in Wistar rats after orthotopically implanting C6 glioma cells, markedly reduced proliferation. This was evidenced by a decreased level of the following parameters: a proliferation marker (Ki-67), a tumor growth marker (

Indexed as

apoptosisdrug resistanceglioblastomaMGMTmifepristonetemozolomide

Identifiers

PMID30583528
PMCPMC6356343
OpenAlexW2906379041

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.