Evidence map›Paper›PMID 31353847›Full record

ArticleCancer medicine2019

Aberrant accumulation of Dickkopf 4 promotes tumor progression via forming the immune suppressive microenvironment in gastrointestinal stromal tumor.

Ming Wang, Bo Ni, Chun Zhuang, Wen-Yi Zhao, Lin Tu, Xin-Li Ma, Lin-Xi Yang, Zhi-Gang Zhang, Hui Cao

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

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  10. Low Distribution of TIM-3Journal of immunology research · 2021
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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

9 authors at 2 institutions in 1 country.

Ming WangDepartment of Gastrointestinal Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Bo NiDepartment of Gastrointestinal Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0001-9154-1213
Chun ZhuangDepartment of Gastrointestinal Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Wen-Yi ZhaoDepartment of Gastrointestinal Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Lin TuDepartment of Gastrointestinal Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Xin-Li MaDepartment of Gastrointestinal Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Lin-Xi YangDepartment of Gastrointestinal Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Zhi-Gang ZhangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hui CaoDepartment of Gastrointestinal Surgery, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Renji Hospital · CNShanghai Jiao Tong University · CN

Funding

Clinical Research Plan of SHDC 16CR3001AShanghai Municipal Commission of Health and Family Planning 201540071Shanghai Outstanding Academic Leaders Plan
6 · The paper itself

Abstract

backgroundDrug resistance and tumor recurrence are the major concerns in clinical practices of gastrointestinal stromal tumor (GIST), with the urgent requirement for exploring undiscovered pathways driving malignancy. To deal with these, recent studies have made many efforts to explore prognosis indicators and establish potential therapeutic targets.

methodsExpression profiles of different risks of GISTs were described and abundant clinical evidences supported our findings in this study. Following exploration in vitro by cell experiments and verification in vivo using tumor microarray were taken to elucidate the underlying mechanism, which drove the malignancy in GIST.

resultsDickkopf 4 (DKK4), as the canonical Wnt pathway antagonist, was unexpectedly and universally upregulated in high-risk GISTs, and aberrant accumulation of DKK4 was closely correlated with poor prognosis. In addition, tumor-derived DKK4 could decrease immune cells infiltration and activation in the tumor microenvironment, which decreased the antitumor effects in return. And this phenomenon was recurrent in human tumor specimens.

conclusionsOur findings identified DKK4 as a proper tumor biomarker for prognosis predicting and recurrence monitoring, and suggested a novel immune-escape mechanism driving malignancy in GIST, which might be a potential therapeutic target to improve the effects of canonical RTK therapy and combined immunotherapy.

Indexed as

AgedBiomarkersCell Line, TumorCytotoxicity, ImmunologicDisease ProgressionFemaleFluorescent Antibody TechniqueGastrointestinal Stromal TumorsGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansIntercellular Signaling Peptides and ProteinsMaleMiddle AgedPrognosisBiomarkersDKK4 protein, humanIntercellular Signaling Peptides and ProteinsDKK4GISTimmune suppressionprognosis indicatorprogression

Identifiers

PMID31353847
PMCPMC6718536
OpenAlexW2965317114

What OpenQuestion holds

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LicenceCC BY
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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.