Evidence map›Paper›PMID 23028051›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Anaphylatoxin C5a creates a favorable microenvironment for lung cancer progression.

Leticia Corrales, Daniel Ajona, Stavros Rafail, Juan J Lasarte, Jose I Riezu-Boj, John D Lambris, Ana Rouzaut, Maria J Pajares, Luis M Montuenga, Ruben Pio

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers.

0numbers the graph read from it
0cells of the map it votes in
176citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

176 citing papers in PubMed, 274 citations in OpenAlex.

  1. Complement-Regulatory Proteins CFHR1 and CFHR3 and Patient Response to Anti-CD20 Monoclonal Antibody Therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
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116 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

10 authors at 2 institutions in 2 countries.

Leticia CorralesDivision of Oncology, Center for Applied Medical Research, University of Navarra, Pamplona 31008, Spain.
Daniel Ajona
Stavros Rafail
Juan J Lasarte
Jose I Riezu-Boj
John D Lambris
Ana Rouzaut
Maria J Pajares
Luis M Montuenga
Ruben Pio
Universidad de Navarra · ESUniversity of Pennsylvania · US

Funding

Role of complement in kidney disorders: from hemodialysis to transportationP01AI068730 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI LAMBRIS, JOHN D · 2007 to 2018
$16.0M
NIAID NIH HHS AI068730NIAID NIH HHS P01 AI068730
6 · The paper itself

Abstract

The complement system contributes to various immune and inflammatory diseases, including cancer. In this study, we investigated the capacity of lung cancer cells to activate complement and characterized the consequences of complement activation on tumor progression. We focused our study on the production and role of the anaphylatoxin C5a, a potent immune mediator generated after complement activation. We first measured the capacity of lung cancer cell lines to deposit C5 and release C5a. C5 deposition, after incubation with normal human serum, was higher in lung cancer cell lines than in nonmalignant bronchial epithelial cells. Notably, lung malignant cells produced complement C5a even in the absence of serum. We also found a significant increase of C5a in plasma from patients with non-small cell lung cancer, suggesting that the local production of C5a is followed by its systemic diffusion. The contribution of C5a to lung cancer growth in vivo was evaluated in the Lewis lung cancer model. Syngeneic tumors of 3LL cells grew slower in mice treated with an antagonist of the C5a receptor. C5a did not modify 3LL cell proliferation in vitro but induced endothelial cell chemotaxis and blood-vessels formation. C5a also contributed to the immunosuppressive microenvironment required for tumor growth. In particular, blockade of C5a receptor significantly reduced myeloid-derived suppressor cells and immunomodulators ARG1, CTLA-4, IL-6, IL-10, LAG3, and PDL1 (B7H1). In conclusion, lung cancer cells have the capacity to generate C5a, a molecule that creates a favorable tumor microenvironment for lung cancer progression.

Indexed as

AdenocarcinomaAnimalsCarcinoma, Lewis LungCarcinoma, Non-Small-Cell LungCarcinoma, Squamous CellCell Line, TransformedCell Line, TumorComplement ActivationComplement C5aDisease Models, AnimalDisease ProgressionFemaleHumansHuman Umbilical Vein Endothelial CellsImmune ToleranceLung NeoplasmsComplement C5aReceptor, Anaphylatoxin C5a

Identifiers

PMID23028051
PMCPMC3478398
OpenAlexW1900099842

What OpenQuestion holds

Textmetadata
LicenceTDM
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.