Evidence map›Paper›PMID 18340357›Full record

ArticleCancer gene therapy2008

In vivo restoration of RhoB expression leads to ovarian tumor regression.

B Couderc, A Pradines, A Rafii, M Golzio, A Deviers, C Allal, D Berg, M Penary, J Teissie, G Favre

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 62 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

10 authors at 4 institutions in 1 country.

B CoudercINSERM U563, CPTP, Toulouse, France. couderc.bettina@claudiusregaud.fr
A Pradines
A Rafii
M Golzio
A Deviers
C Allal
D Berg
M Penary
J Teissie
G Favre
Institut Claudius Regaud · FRInserm · FRCentre National de la Recherche Scientifique · FRInstitut de Pharmacologie et de Biologie Structurale · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancers are very aggressive cancers most often diagnosed when metastasis has already occurred in the entire peritoneal cavity. Ovarian adenocarcinoma cells present an undetectable level of RhoB GTPase. Using preclinical ovarian cancer models, we aimed to evaluate the potential use of RhoB cDNA as a tumor suppressor gene in gene therapy. RhoB restoration in vitro, through recombinant adenovirus transduction, resulted in the apoptosis of endogenous RhoB protein low-expressing cell lines (OVCAR-3 and IGROV-1) through the activation of the intrinsic apoptotic caspase cascade. We showed that a single injection of 10(8) p.f.u. of adenoviral vector encoding a reporter gene into the peritoneal cavity of ovarian tumor bearing mice can induce the gene modification of a large quantity of cells throughout the cavity. We thereby tested the effect of AdRhoB injections to treat ovarian cancer-bearing mice. The ectopic expression of RhoB, following its introduction via viral transduction into nude mice in vivo, was highly effective in suppressing tumor growth of ovarian cancer xenografts. Therapeutic agents designed to correct defects of RhoB at the molecular level may thereby provide innovative treatment options for patients not responding to standard therapies.

Indexed as

AdenocarcinomaAdenoviridaeAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticGenetic TherapyGenetic VectorsHumansImmunoblottingMiceMicroscopy, FluorescenceOvarian NeoplasmsrhoB GTP-Binding ProteinrhoB GTP-Binding Protein

Identifiers

PMID18340357
OpenAlexW1978465526

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.