Evidence map›Paper›PMID 27471643›Full record

ArticleOncoimmunology2016

Epithelial NF-κB signaling promotes EGFR-driven lung carcinogenesis via macrophage recruitment.

Jamie A Saxon, Taylor P Sherrill, Vasiliy V Polosukhin, Jiqing Sai, Rinat Zaynagetdinov, Allyson G McLoed, Peter M Gulleman, Whitney Barham, Dong-Sheng Cheng, Raphael P Hunt and 5 more

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 18 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

15 authors at 2 institutions in 1 country.

Jamie A SaxonDepartment of Cancer Biology, Vanderbilt University , Nashville, TN, USA.
Taylor P SherrillDepartment of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center , Nashville, TN, USA.
Vasiliy V PolosukhinDepartment of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center , Nashville, TN, USA.
Jiqing SaiDepartment of Cancer Biology, Vanderbilt University , Nashville, TN, USA.
Rinat ZaynagetdinovDepartment of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center , Nashville, TN, USA.
Allyson G McLoedDepartment of Cancer Biology, Vanderbilt University , Nashville, TN, USA.
Peter M GullemanDepartment of Pediatrics, Division of Pulmonary Medicine, Vanderbilt University Medical Center , Nashville, TN, USA.
Whitney BarhamDepartment of Cancer Biology, Vanderbilt University , Nashville, TN, USA.
Dong-Sheng ChengDepartment of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center , Nashville, TN, USA.
Raphael P HuntDepartment of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center , Nashville, TN, USA.
Linda A GleavesDepartment of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center , Nashville, TN, USA.
Ann RichmondDepartment of Cancer Biology, Vanderbilt University, Nashville, TN, USA; Department of Veterans Affairs Medical Center, Nashville, TN, USA.
Lisa R YoungDepartment of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Pediatrics, Division of Pulmonary Medicine, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN, USA.
Fiona E YullDepartment of Cancer Biology, Vanderbilt University , Nashville, TN, USA.
Timothy S BlackwellDepartment of Cancer Biology, Vanderbilt University, Nashville, TN, USA; Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Veterans Affairs Medical Center, Nashville, TN, USA; Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN, USA.
Vanderbilt University Medical Center · USVanderbilt University · US

Funding

MELANOMA GROWTH STIMULATORY ACTIVITYR01CA034590 · NCI · VANDERBILT UNIVERSITY · PI RICHMOND, ANN · 1986 to 2017
$5.2M
Mechanisms of Pulmonary Fibrosis in Hermansky-Pudlak SyndromeR01HL119503 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI YOUNG, LISA R. · 2013 to 2021
$3.6M
BLRD VA IK6 BX005225NCI NIH HHS R01 CA034590NHLBI NIH HHS R01 HL119503
6 · The paper itself

Abstract

Several studies have demonstrated that NF-κB activation is common in lung cancer; however, the mechanistic links between NF-κB signaling and tumorigenesis remain to be fully elucidated. We investigated the function of NF-κB signaling in epidermal growth factor receptor (EGFR)-mutant lung tumors using a transgenic mouse model with doxycycline (dox)-inducible expression of oncogenic EGFR in the lung epithelium with or without a dominant inhibitor of NF-κB signaling. NF-κB inhibition resulted in a significant reduction in tumor burden in both EGFR tyrosine kinase inhibitor (TKI)-sensitive and resistant tumors. However, NF-κB inhibition did not alter epithelial cell survival in vitro or in vivo, and no changes were detected in activation of EGFR downstream signaling pathways. Instead, we observed an influx of inflammatory cells (macrophages and neutrophils) in the lungs of mice with oncogenic EGFR expression that was blocked in the setting of NF-κB inhibition. To investigate whether inflammatory cells play a role in promoting EGFR-mutant lung tumors, we depleted macrophages and neutrophils during tumorigenesis and found that neutrophil depletion had no effect on tumor formation, but macrophage depletion caused a significant reduction in tumor burden. Together, these data suggest that epithelial NF-κB signaling supports carcinogenesis in a non-cell autonomous manner in EGFR-mutant tumors through recruitment of pro-tumorigenic macrophages.

Indexed as

EGFRlung cancermacrophageneutrophilNF-κB

Identifiers

PMID27471643
PMCPMC4938365
OpenAlexW2316823859

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.