Evidence map›Paper›PMID 30910960›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Inflammatory regulatory network mediated by the joint action of NF-kB, STAT3, and AP-1 factors is involved in many human cancers.

Zhe Ji, Lizhi He, Aviv Regev, Kevin Struhl

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed
11.5field-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

133 citing papers in PubMed, 223 citations in OpenAlex.

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  14. EBV Triggers a Distinct Antiviral Response in HMC3 Cells.bioRxiv : the preprint server for biology · 2026
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  16. TET1 deficiency amplifies macrophage inflammatory signaling associated with Crohn's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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73 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

4 authors at 2 institutions in 1 country.

Zhe JiDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115.
Lizhi HeDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115.
Aviv RegevBroad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, MA 02142.
Kevin StruhlDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115; kevin@hms.harvard.edu.
Broad Institute · USHarvard University · US

Funding

Genomic targets of oncoproteins and tumor suppressorsR01CA107486 · NCI · HARVARD MEDICAL SCHOOL · PI STRUHL, KEVIN · 2006 to 2020
$9.4M
Dissect regulation of RNA translation in human cancersR00CA207865 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI JI, ZHE · 2018 to 2020
$705k
Dissect regulation of RNA translation in human cancersK99CA207865 · NCI · HARVARD MEDICAL SCHOOL · PI JI, ZHE · 2016 to 2017
$200k
Howard Hughes Medical InstituteNCI NIH HHS K99 CA207865NCI NIH HHS R00 CA207865NCI NIH HHS R01 CA107486
6 · The paper itself

Abstract

Using an inducible, inflammatory model of breast cellular transformation, we describe the transcriptional regulatory network mediated by STAT3, NF-κB, and AP-1 factors on a genomic scale. These proinflammatory regulators form transcriptional complexes that directly regulate the expression of hundreds of genes in oncogenic pathways via a positive feedback loop. This transcriptional feedback loop and associated network functions to various extents in many types of cancer cells and patient tumors, and it is the basis for a cancer inflammation index that defines cancer types by functional criteria. We identify a network of noninflammatory genes whose expression is well correlated with the cancer inflammatory index. Conversely, the cancer inflammation index is negatively correlated with the expression of genes involved in DNA metabolism, and transformation is associated with genome instability. We identify drugs whose efficacy in cell lines is correlated with the cancer inflammation index, suggesting the possibility of using this index for personalized cancer therapy. Inflammatory tumors are preferentially associated with infiltrating immune cells that might be recruited to the site of the tumor via inflammatory molecules produced by the cancer cells.

Indexed as

Gene Expression Regulation, NeoplasticCell Line, TumorDNA, NeoplasmHumansInflammationNeoplasm ProteinsNeoplasmsNF-kappa BSTAT3 Transcription FactorTranscription Factor AP-1DNA, NeoplasmNeoplasm ProteinsNF-kappa BSTAT3 protein, humanSTAT3 Transcription FactorTranscription Factor AP-1cancerepignetic switchgene regulatory networkinflammation

Identifiers

PMID30910960
PMCPMC6511065
OpenAlexW2924391634

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.