Evidence map›Paper›PMID 28481875›Full record

ArticleOncogene2017

Identification of a TLR2-regulated gene signature associated with tumor cell growth in gastric cancer.

A C West, K Tang, H Tye, L Yu, N Deng, M Najdovska, S J Lin, J J Balic, E Okochi-Takada, P McGuirk and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 63 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

18 authors at 6 institutions in 4 countries.

A C WestCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
K TangCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
H TyeCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
L YuCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
N DengGenome Institute of Singapore, Singapore, Singapore.
M NajdovskaCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
S J LinGenome Institute of Singapore, Singapore, Singapore.
J J BalicCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
E Okochi-TakadaDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
P McGuirkOpsona Therapeutics Ltd, Dublin, Ireland.
B KeoghOpsona Therapeutics Ltd, Dublin, Ireland.
W McCormackOpsona Therapeutics Ltd, Dublin, Ireland.
P S BhathalDepartment of Molecular Translational Science, Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Victoria, Australia.
M ReillyOpsona Therapeutics Ltd, Dublin, Ireland.
M OshimaDivision of Genetics, Cancer Research Institute, Kanazawa University, Kanazawa, Japan.
T UshijimaDivision of Epigenomics, National Cancer Center Research Institute, Tokyo, Japan.
P TanGenome Institute of Singapore, Singapore, Singapore.
B J JenkinsCentre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Victoria, Australia.
Hudson Institute of Medical Research · AUOpsona Therapeutics (Ireland) · IEMonash University · AUGenome Institute of Singapore · SGDuke-NUS Medical School · SGKanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptors (TLRs) are key regulators of innate immune responses, and their dysregulation is observed in numerous inflammation-associated malignancies, including gastric cancer (GC). However, the identity of specific TLRs and their molecular targets which promote the pathogenesis of human GC is ill-defined. Here, we sought to determine the clinical utility of TLR2 in human GC. TLR2 mRNA and protein expression levels were elevated in >50% of GC patient tumors across multiple ethnicities. TLR2 was also widely expressed among human GC cell lines, and DNA microarray-based expression profiling demonstrated that the TLR2-induced growth responsiveness of human GC cells corresponded with the up-regulation of six anti-apoptotic (BCL2A1, BCL2, BIRC3, CFLAR, IER3, TNFAIP3) and down-regulation of two tumor suppressor (PDCD4, TP53INP1) genes. The TLR2-mediated regulation of these anti-apoptotic and tumor suppressor genes was also supported by their increased and reduced expression, respectively, in two independent genetic GC mouse models (gp130

Indexed as

Cell ProliferationGene Expression ProfilingAnimalsApoptosisBiomarkers, TumorFemaleHumansMiceMice, Inbred NODNeoplasm InvasivenessNeoplasm StagingPrognosisStomach NeoplasmsSurvival RateToll-Like Receptor 2Tumor Cells, CulturedBiomarkers, TumorTLR2 protein, humanToll-Like Receptor 2

Identifiers

PMID28481875
OpenAlexW2612260650

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.