Evidence map›Paper›PMID 18309355›Full record

ArticleCancer gene therapy2008

Cisplatin enhances the antitumor effect of tumor necrosis factor-related apoptosis-inducing ligand gene therapy via recruitment of the mitochondria-dependent death signaling pathway.

S Shamimi-Noori, W-S Yeow, M F Ziauddin, H Xin, T L N Tran, J Xie, A Loehfelm, P Patel, J Yang, D S Schrump and 2 more

Abstract read
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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 40 citations in OpenAlex.

  1. Identification and experimental verification of a novel cisplatin resistance-related lncRNA signature for predicting prognosis and immune response in lung adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  8. Mesenchymal stem cells as vectors for lung cancer therapy.Respiration; international review of thoracic diseases · 2013
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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

12 authors at 6 institutions in 1 country.

S Shamimi-NooriSection of Thoracic Oncology, Surgery Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
W-S Yeow
M F Ziauddin
H Xin
T L N Tran
J Xie
A Loehfelm
P Patel
J Yang
D S Schrump
B L Fang
D M Nguyen
Center for Cancer Research · USNational Cancer Institute · USNational Institutes of Health Clinical Center · USJackson Memorial Hospital · USNational Institutes of Health · USThe University of Texas MD Anderson Cancer Center · US

Funding

Core Research Services for Molecular Imaging and Imaging SciencesZ01CL040013 · CLC · CLINICAL CENTER · PI WOOD, BRADFORD · 2008 to 2008
$51k
Core Research Services for Molecular Imaging and Imaging SciencesZICCL040013 · CLC · CLINICAL CENTER · PI FRANK, JOSEPH · 2009 to 2025
$0k
Intramural NIH HHS
6 · The paper itself

Abstract

Despite adequately expressing tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptors DR4/DR5, malignant cells are frequently refractory to the cytotoxic effect of this apoptosis-inducing ligand. The susceptibility of cancer cells to TRAIL can be potentiated by cisplatin (CDDP). This study was designed to evaluate the ability of cisplatin to enhance the cytotoxic effect of TRAIL gene therapy using the recombinant adenovirus-mediated tumor-selective expression of membrane-bound green fluorescence protein (GFP)-TRAIL fusion protein (AdVgTRAIL) on thoracic cancer cells and to elucidate the putative mechanisms responsible for this synergistic combination effect. While causing little death of cultured thoracic cancer cells by itself, AdVgTRAIL in combination with CDDP, on the other hand, mediated profound supra-additive cytotoxicity and apoptosis via a strong bystander effect. CDDP/AdVgTRAIL-induced cytotoxicity was completely abrogated either by the pancaspase inhibitor zVAD-fmk or by the selective caspase 9 inhibitor or by transient knockdown of caspase 9 by siRNA, indicating that this process was caspase-mediated and mitochondria-dependent. This was confirmed by the observation that Bcl2 overexpression protected the cells from combination-induced cytotoxicity. Robust activation of caspase 8 activity in combination-treated cells was blocked by overexpression of Bcl2, indicating that caspase 8 activation was secondary to the mitochondria-mediated amplification feedback loop. Combining CDDP with AdVgTRAIL greatly enhances its tumoricidal efficacy in cultured thoracic cancer cells in vitro. The two agents interact to mediate profound activation of caspase cascade via recruitment of the mitochondria and positive feedback loop. The CDDP/AdVgTRAIL combination also exhibits a strong antitumor effect in in vivo animal model of human cancer xenografts.

Indexed as

AdenoviridaeAnimalsAntineoplastic AgentsCaspase 9Cell Line, TumorCell SurvivalCisplatinEsophageal NeoplasmsFemaleGenetic TherapyHumansLung NeoplasmsMiceMice, NudeMitochondriaNeoplasmsAntineoplastic AgentsCaspase 9CisplatinRNA, Small InterferingTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, human

Identifiers

PMID18309355
OpenAlexW1965549497

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.