Evidence map›Paper›PMID 26668367›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

Lung inflammation promotes metastasis through neutrophil protease-mediated degradation of Tsp-1.

Tina El Rayes, Raúl Catena, Sharrell Lee, Marcin Stawowczyk, Natasha Joshi, Claudia Fischbach, Charles A Powell, Andrew J Dannenberg, Nasser K Altorki, Dingcheng Gao and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

136 citing papers in PubMed, 201 citations in OpenAlex.

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  9. Targeting neutrophils for cancer therapy.Nature reviews. Drug discovery · 2025
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76 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

11 authors at 2 institutions in 1 country.

Tina El RayesDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, New York, NY 10065; Department of Cell and Developmental Biology, Weill Cornell Medical College of Cornell University, New York, NY 10065; Neuberger Berman Lung Cancer Center, Weill Cornell Medical College of Cornell University, New York, NY 10065;
Raúl CatenaDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, New York, NY 10065; Department of Cell and Developmental Biology, Weill Cornell Medical College of Cornell University, New York, NY 10065; Neuberger Berman Lung Cancer Center, Weill Cornell Medical College of Cornell University, New York, NY 10065;
Sharrell LeeDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, New York, NY 10065; Neuberger Berman Lung Cancer Center, Weill Cornell Medical College of Cornell University, New York, NY 10065;
Marcin StawowczykDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, New York, NY 10065; Department of Cell and Developmental Biology, Weill Cornell Medical College of Cornell University, New York, NY 10065; Neuberger Berman Lung Cancer Center, Weill Cornell Medical College of Cornell University, New York, NY 10065;
Natasha JoshiDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, New York, NY 10065; Department of Cell and Developmental Biology, Weill Cornell Medical College of Cornell University, New York, NY 10065; Neuberger Berman Lung Cancer Center, Weill Cornell Medical College of Cornell University, New York, NY 10065;
Claudia FischbachNancy E. and Peter C. Meinig School of Biomedical Engineering, Cornell University, Ithaca, NY 14853;
Charles A PowellDivision of Pulmonary, Critical Care, and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029;
Andrew J DannenbergDepartment of Medicine, Weill Cornell Medical College of Cornell University, New York, NY 10065.
Nasser K AltorkiDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, New York, NY 10065; Neuberger Berman Lung Cancer Center, Weill Cornell Medical College of Cornell University, New York, NY 10065;
Dingcheng GaoDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, New York, NY 10065; Department of Cell and Developmental Biology, Weill Cornell Medical College of Cornell University, New York, NY 10065; Neuberger Berman Lung Cancer Center, Weill Cornell Medical College of Cornell University, New York, NY 10065;
Vivek MittalDepartment of Cardiothoracic Surgery, Weill Cornell Medical College of Cornell University, New York, NY 10065; Department of Cell and Developmental Biology, Weill Cornell Medical College of Cornell University, New York, NY 10065; Neuberger Berman Lung Cancer Center, Weill Cornell Medical College of Cornell University, New York, NY 10065; vim2010@med.cornell.edu.
Cornell University · USIcahn School of Medicine at Mount Sinai · US

Funding

Lung Adenocarcinoma Invasion GenomicsR01CA163772 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MASSION, PIERRE P., POWELL, CHARLES A. · 2013 to 2017
$2.9M
NCI NIH HHS R01 CA163772NCI NIH HHS U54CA14387
6 · The paper itself

Abstract

Inflammation is inextricably associated with primary tumor progression. However, the contribution of inflammation to tumor outgrowth in metastatic organs has remained underexplored. Here, we show that extrinsic inflammation in the lungs leads to the recruitment of bone marrow-derived neutrophils, which degranulate azurophilic granules to release the Ser proteases, elastase and cathepsin G, resulting in the proteolytic destruction of the antitumorigenic factor thrombospondin-1 (Tsp-1). Genetic ablation of these neutrophil proteases protected Tsp-1 from degradation and suppressed lung metastasis. These results provide mechanistic insights into the contribution of inflammatory neutrophils to metastasis and highlight the unique neutrophil protease-Tsp-1 axis as a potential antimetastatic therapeutic target.

Indexed as

AnimalsBlotting, WesternBone Marrow TransplantationCathepsin GCell Line, TumorFemaleFlow CytometryGene ExpressionLeukocyte ElastaseLipopolysaccharidesLung NeoplasmsMice, Inbred C57BLMice, KnockoutNeoplasms, ExperimentalNeutrophilsPeptide HydrolasesCathepsin GLeukocyte ElastaseLipopolysaccharidesPeptide HydrolasesSerine ProteasesThrombospondin 1inflammationmetastasisneutrophilsproteasesthrombospondin-1

Identifiers

PMID26668367
PMCPMC4703007
OpenAlexW2203076610

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.