Evidence map›Paper›PMID 29295936›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

Gene regulation and suppression of type I interferon signaling by STAT3 in diffuse large B cell lymphoma.

Li Lu, Fen Zhu, Meili Zhang, Yangguang Li, Amanda C Drennan, Shuichi Kimpara, Ian Rumball, Christopher Selzer, Hunter Cameron, Ashley Kellicut and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
10.8field-weighted citation impact, top 1% 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

60 citing papers in PubMed, 112 citations in OpenAlex.

  1. Interferon regulatory factors orchestrate CD8International journal of molecular medicine · 2026
    Review
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  14. TRAF3 loss-of-function reveals the noncanonical NF-κB pathway as a therapeutic target in diffuse large B cell lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

14 authors at 3 institutions in 1 country.

Li LuDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792.
Fen ZhuDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792.
Meili ZhangLymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Yangguang LiDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792.
Amanda C DrennanDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792.
Shuichi KimparaDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792.
Ian RumballDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792.
Christopher SelzerDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792.
Hunter CameronDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792.
Ashley KellicutDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792.
Amanda KelmDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792.
Fangyu WangDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792.
Thomas A WaldmannLymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; tawald@mail.nih.gov lrui@medicine.wisc.edu.
Lixin RuiDepartment of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792; tawald@mail.nih.gov lrui@medicine.wisc.edu.
University of Wisconsin–Madison · USUniversity of Wisconsin Carbone Cancer Center · USNational Institutes of Health · US

Funding

Institutional Clinical and Translational Science AwardUL1TR000427 · NCATS · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2012 to 2016
$32.2M
IL-2:IL-15 : implications for cancer therapy (Investigator -Initiated Project)ZIASC004002 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI WALDMANN, THOMAS · 2009 to 2022
$22.9M
RESEARCH TRAINING IN HEMATOLOGYT32HL007899 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI Jane Ellen Churpek · 1998 to 2026
$8.2M
Institutional Clinical and Translational Science AwardKL2TR000428 · NCATS · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2012 to 2016
$6.2M
Epigenetic Gene Regulation by JAK1 Kinase in Diffuse Large B-Cell LymphomaR01CA187299 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI RUI, LIXIN · 2015 to 2019
$1.7M
NCATS NIH HHS KL2 TR000428NCATS NIH HHS UL1 TR000427NCI NIH HHS R01 CA187299NHLBI NIH HHS T32 HL007899
6 · The paper itself

Abstract

STAT3 is constitutively activated in many cancers and regulates gene expression to promote cancer cell survival, proliferation, invasion, and migration. In diffuse large B cell lymphoma (DLBCL), activation of STAT3 and its kinase JAK1 is caused by autocrine production of IL-6 and IL-10 in the activated B cell-like subtype (ABC). However, the gene regulatory mechanisms underlying the pathogenesis of this aggressive lymphoma by STAT3 are not well characterized. Here we performed genome-wide analysis and identified 2,251 STAT3 direct target genes, which involve B cell activation, survival, proliferation, differentiation, and migration. Whole-transcriptome profiling revealed that STAT3 acts as both a transcriptional activator and a suppressor, with a comparable number of up- and down-regulated genes. STAT3 regulates multiple oncogenic signaling pathways, including NF-κB, a cell-cycle checkpoint, PI3K/AKT/mTORC1, and STAT3 itself. In addition, STAT3 negatively regulates the lethal type I IFN signaling pathway by inhibiting expression of

Indexed as

Cell DifferentiationCell Line, TumorCell MovementCell ProliferationCell SurvivalCytokinesGene Expression Regulation, NeoplasticGenome-Wide Association StudyHumansImmunologic FactorsInterferon Type ILenalidomideLymphoma, Large B-Cell, DiffuseNitrilesPyrazolesPyrimidinesCytokinesImmunologic FactorsInterferon Type ILenalidomideNitrilesPyrazolesPyrimidinesruxolitinibSTAT3 protein, humanSTAT3 Transcription FactorThalidomidediffuse large B cell lymphomainterferonSTAT3

Identifiers

PMID29295936
PMCPMC5776985
OpenAlexW2782201456

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.