Evidence map›Paper›PMID 20527044›Full record

ArticleThe journal of gene medicine2010

Docetaxel increases antitumor efficacy of oncolytic prostate-restricted replicative adenovirus by enhancing cell killing and virus distribution.

Xiong Li, Youhong Liu, Yong Tang, Phipps Roger, Meei-Huey Jeng, Chinghai Kao

Open access · greenAbstract read
In one paragraph

Article in The journal of gene medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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

6 authors at 3 institutions in 2 countries.

Xiong LiMaine Institute for Human Genetics and Health, Bangor, ME, USA.
Youhong Liu
Yong Tang
Phipps Roger
Meei-Huey Jeng
Chinghai Kao
Indiana University – Purdue University Indianapolis · USIndiana University School of MedicineJinan University · CN

Funding

BASIC SCIENCE STUDIES ON GENE THERAPY OF BLOOD DISEASEST32HL007910 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI Roland W. Herzog, Reuben Kapur · 1999 to 2026
$7.6M
Tissue Specific Gene Therapy for Human Prostate CancerR01CA074042 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KAO, CHINGHAI · 2004 to 2008
$1.4M
TISSUE SPECIFIC GENE THERAPY FOR HUMAN PROSTATE CANCERR29CA074042 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI KAO, CHINGHAI · 1997 to 2001
$216k
NCI NIH HHS R01 CA074042NCI NIH HHS R29 CA074042NHLBI NIH HHS 1 T32 HL007910NHLBI NIH HHS T32 HL007910
6 · The paper itself

Abstract

backgroundWe explored multiple molecular mechanisms of the combination of docetaxel and an oncolytic prostate-restricted replication competent adenovirus (Ad) (PRRA) in advanced prostate cancer (PCa) models. The combinational therapy has potential to overcome the therapeutic limitations of poor virus distribution inside solid tumors.

methodsWe evaluated the effect of docetaxel on the antitumor efficacy and efficiency of virus transduction, transgene expression and virus distribution of PRRA in a prostate-specific antigen/prostate-specific membrane antigen-positive tumor xenograft model. We also evaluated the effect of docetaxel on apoptosis induction, cell killing and the efficiency of transgene expression and virus replication in vitro.

resultsTumor growth inhibition was significantly enhanced when docetaxel was administrated before intratumor injection of PRRA. In vivo dual-photon microscopy and ex vivo fluorescence microscopy and immunohistochemistry showed that docetaxel increased transgene expression and expanded virus distribution. The combination of docetaxel and PRRA also increased cell apoptosis. In vitro, docetaxel significantly increased cell killing in PRRA-treated PCa cells. Docetaxel significantly increased Ad-mediated trangene expression independent of Ad binding receptors and replication capability. Docetaxel increased the activity of cytomegalovirus (CMV) promoter but not of a chimeric prostate-specific enhancer, resulting in higher transgene expression. The enhanced CMV promoter activity resulted from activation of p38 mitogen-activated protein kinase (MAPK) because inhibition of p38 MAPK blocked the docetaxel-induced increase in CMV promoter activity.

conclusionsCombining docetaxel with an oncolytic PRRA improved therapeutic potential by expanding virus distribution and enhancing cell apoptosis and killing. These studies suggested a novel mechanism for enhancing the effect of therapeutic genes delivered by a PRRA.

Indexed as

AdenoviridaeGenetic VectorsAnimalsCell DeathCell Line, TumorDocetaxelEnzyme ActivationGene Expression Regulation, NeoplasticGenes, ReporterGenetic TherapyHumansIntegrin beta1Integrin beta3MaleNeoplasm Transplantationp38 Mitogen-Activated Protein KinasesDocetaxelIntegrin beta1Integrin beta3p38 Mitogen-Activated Protein KinasesTaxoids

Identifiers

PMID20527044
PMCPMC9126185
OpenAlexW1978452952

What OpenQuestion holds

Textmetadata
LicenceTDM
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.