Evidence map›Paper›PMID 21931799›Full record

ArticlePloS one2011

Gene expression signature analysis identifies vorinostat as a candidate therapy for gastric cancer.

Sofie Claerhout, Jae Yun Lim, Woonyoung Choi, Yun-Yong Park, Kyounghyun Kim, Sang-Bae Kim, Ju-Seog Lee, Gordon B Mills, Jae Yong Cho

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

68 citing papers in PubMed, 122 citations in OpenAlex.

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  15. Programmed cell death, redox imbalance, and cancer therapeutics.Apoptosis : an international journal on programmed cell death · 2021
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  20. Article

8 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

Sofie ClaerhoutDivision of Cancer Medicine, Department of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America.
Jae Yun Lim
Woonyoung Choi
Yun-Yong Park
Kyounghyun Kim
Sang-Bae Kim
Ju-Seog Lee
Gordon B Mills
Jae Yong Cho
The University of Texas MD Anderson Cancer Center · USGangnam Severance Hospital · KRMitchell Institute · USYonsei University · KR

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Targeting the PI3K Signaling Pathway in Endometrial CarcinomaP50CA098258 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BODURKA, DIANE · 2003 to 2020
$32.0M
NCI NIH HHS P50 CA098258
6 · The paper itself

Abstract

backgroundGastric cancer continues to be one of the deadliest cancers in the world and therefore identification of new drugs targeting this type of cancer is thus of significant importance. The purpose of this study was to identify and validate a therapeutic agent which might improve the outcomes for gastric cancer patients in the future. METHODOLOGY/PRINCIPAL

findingsUsing microarray technology, we generated a gene expression profile of human gastric cancer-specific genes from human gastric cancer tissue samples. We used this profile in the Broad Institute's Connectivity Map analysis to identify candidate therapeutic compounds for gastric cancer. We found the histone deacetylase inhibitor vorinostat as the lead compound and thus a potential therapeutic drug for gastric cancer. Vorinostat induced both apoptosis and autophagy in gastric cancer cell lines. Pharmacological and genetic inhibition of autophagy however, increased the therapeutic efficacy of vorinostat, indicating that a combination of vorinostat with autophagy inhibitors may therapeutically be more beneficial. Moreover, gene expression analysis of gastric cancer identified a collection of genes (ITGB5, TYMS, MYB, APOC1, CBX5, PLA2G2A, and KIF20A) whose expression was elevated in gastric tumor tissue and downregulated more than 2-fold by vorinostat treatment in gastric cancer cell lines. In contrast, SCGB2A1, TCN1, CFD, APLP1, and NQO1 manifested a reversed pattern. CONCLUSIONS/SIGNIFICANCE: We showed that analysis of gene expression signature may represent an emerging approach to discover therapeutic agents for gastric cancer, such as vorinostat. The observation of altered gene expression after vorinostat treatment may provide the clue to identify the molecular mechanism of vorinostat and those patients likely to benefit from vorinostat treatment.

Indexed as

Antineoplastic AgentsApolipoprotein C-IBlotting, WesternCell Line, TumorChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneGene Expression ProfilingGene Expression Regulation, NeoplasticGroup II Phospholipases A2Histone Deacetylase InhibitorsHumansHydroxamic AcidsIn Vitro TechniquesKinesinsOligonucleotide Array Sequence AnalysisStomach NeoplasmsAntineoplastic AgentsAPOC1 protein, humanApolipoprotein C-ICBX5 protein, humanChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneGroup II Phospholipases A2Histone Deacetylase InhibitorsHydroxamic AcidsKIF20A protein, humanKinesinsPLA2G2A protein, humanVorinostat

Identifiers

PMID21931799
PMCPMC3170379
OpenAlexW1985481481

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.