Evidence map›Paper›PMID 29438108›Full record

ArticleThe Journal of clinical investigation2018

STAT3-enhancing germline mutations contribute to tumor-extrinsic immune evasion.

Daniel Kogan, Alexander Grabner, Christopher Yanucil, Christian Faul, Vijay Kumar Ulaganathan

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

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  12. FGFR4 Gene Polymorphism Reduces the Risk of Distant Metastasis in Lung Adenocarcinoma in Taiwan.International journal of environmental research and public health · 2020
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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

5 authors at 4 institutions in 2 countries.

Daniel KoganTechnische Universität München, Munich, Germany.
Alexander GrabnerDivision of Nephrology, Department of Medicine, Duke University Medical Center, Duke University, Durham, North Carolina, USA.
Christopher YanucilDivision of Nephrology, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama, USA.
Christian FaulDivision of Nephrology, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama, USA.
Vijay Kumar UlaganathanMax Planck Institute of Biochemistry, Department of Molecular Biology, Martinsried, Germany.
University of Alabama at Birmingham · USDuke Medical Center · USMax Planck Institute of Biochemistry · DETechnical University of Munich · DE

Funding

ACTIVATION OF CARDIAC FGFR4 CAUSES LEFT VENTRICULAR HYPERTROPHYR01HL128714 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI FAUL, CHRISTIAN · 2015 to 2019
$1.9M
Vitamin D and soluble Klotho inhibit FGF23-mediated cardiac hypertrophy in Chronic Kidney DiseaseF31DK115074 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YANUCIL, CHRISTOPHER · 2017 to 2019
$106k
NHLBI NIH HHS R01 HL128714NIDDK NIH HHS F31 DK115074
6 · The paper itself

Abstract

Immune evasion and the suppression of antitumor responses during cancer progression are considered hallmarks of cancer and are typically attributed to tumor-derived factors. Although the molecular basis for the crosstalk between tumor and immune cells is an area of active investigation, whether host-specific germline variants can dictate immunosuppressive mechanisms has remained a challenge to address. A commonly occurring germline mutation (c.1162G>A/rs351855 G/A) in the FGFR4 (CD334) gene enhances signal transducer and activator of transcription 3 (STAT3) signaling and is associated with poor prognosis and accelerated progression of multiple cancer types. Here, using rs351855 SNP-knockin transgenic mice and Fgfr4-knockout mice, we reveal the genotype-specific gain of immunological function of suppressing the CD8/CD4+FOXP3+CD25+ regulatory T cell ratio in vivo. Furthermore, using knockin transgenic mouse models for lung and breast cancers, we establish the host-specific, tumor-extrinsic functions of STAT3-enhancing germline variants in impeding the tumor infiltration of CD8 T cells. Thus, STAT3-enhancing germline receptor variants contribute to immune evasion through their pleiotropic functions in immune cells.

Indexed as

Tumor EscapeAnimalsCD8-Positive T-LymphocytesGerm-Line MutationMiceMice, KnockoutNeoplasm ProteinsNeoplasms, ExperimentalReceptor, Fibroblast Growth Factor, Type 4STAT3 Transcription FactorT-Lymphocytes, RegulatoryFgfr4 protein, mouseNeoplasm ProteinsReceptor, Fibroblast Growth Factor, Type 4Stat3 protein, mouseSTAT3 Transcription FactorComplex traitsGeneticsGenetic variationHomeostasisOncology

Identifiers

PMID29438108
PMCPMC5919827
OpenAlexW2787209010

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.