Evidence map›Paper›PMID 26709919›Full record

ArticlePloS one2015

The Macrophage Inhibitor CNI-1493 Blocks Metastasis in a Mouse Model of Ewing Sarcoma through Inhibition of Extravasation.

Anthony J Hesketh, Caroline Maloney, Christopher A Behr, Morris C Edelman, Richard D Glick, Yousef Al-Abed, Marc Symons, Samuel Z Soffer, Bettie M Steinberg

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  7. The Chemokine Receptor CCR1 Mediates Microglia Stimulated Glioma Invasion.International journal of molecular sciences · 2023
    Article
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  14. The immune system in cancer metastasis: friend or foe?Journal for immunotherapy of cancer · 2017
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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

9 authors at 3 institutions in 1 country.

Anthony J HeskethThe Elmezzi Graduate School of Molecular Medicine, North Shore-LIJ Health System, Manhasset, New York, United States of America.
Caroline MaloneyThe Elmezzi Graduate School of Molecular Medicine, North Shore-LIJ Health System, Manhasset, New York, United States of America.
Christopher A BehrCenter for Oncology and Cell Biology, The Feinstein Institute for Medical Research, North Shore-LIJ Health System, Manhasset, New York, United States of America.
Morris C EdelmanDepartment of Pathology and Laboratory Medicine, Hofstra North Shore-LIJ School of Medicine, New Hyde Park, New York, United States of America.
Richard D GlickDepartment of Surgery, Hofstra North Shore-LIJ School of Medicine, New Hyde Park, New York, United States of America.
Yousef Al-AbedThe Elmezzi Graduate School of Molecular Medicine, North Shore-LIJ Health System, Manhasset, New York, United States of America.
Marc SymonsThe Elmezzi Graduate School of Molecular Medicine, North Shore-LIJ Health System, Manhasset, New York, United States of America.
Samuel Z SofferCenter for Oncology and Cell Biology, The Feinstein Institute for Medical Research, North Shore-LIJ Health System, Manhasset, New York, United States of America.
Bettie M SteinbergThe Elmezzi Graduate School of Molecular Medicine, North Shore-LIJ Health System, Manhasset, New York, United States of America.
Feinstein Institute for Medical Research · USHofstra University · USNorthwell Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastatic Ewing Sarcoma carries a poor prognosis, and novel therapeutics to prevent and treat metastatic disease are greatly needed. Recent evidence demonstrates that tumor-associated macrophages in Ewing Sarcoma are associated with more advanced disease. While some macrophage phenotypes (M1) exhibit anti-tumor activity, distinct phenotypes (M2) may contribute to malignant progression and metastasis. In this study, we show that M2 macrophages promote Ewing Sarcoma invasion and extravasation, pointing to a potential target of anti-metastatic therapy. CNI-1493 is a selective inhibitor of macrophage function and has shown to be safe in clinical trials as an anti-inflammatory agent. In a xenograft mouse model of metastatic Ewing Sarcoma, CNI-1493 treatment dramatically reduces metastatic tumor burden. Furthermore, metastases in treated animals have a less invasive morphology. We show in vitro that CNI-1493 decreases M2-stimulated Ewing Sarcoma tumor cell invasion and extravasation, offering a functional mechanism through which CNI-1493 attenuates metastasis. These data indicate that CNI-1493 may be a safe and effective adjuvant agent for the prevention and treatment of metastatic Ewing Sarcoma.

Indexed as

AnilidesAnimalsCell Line, TumorCell ProliferationDisease Models, AnimalEndotheliumFemaleGuanidinesHumansHydrazonesMacrophagesMiceMice, NudeNeoplasm InvasivenessNeoplasm MetastasisSarcoma, EwingAnilidesGuanidinesHydrazonessemapimod

Identifiers

PMID26709919
PMCPMC4692435
OpenAlexW2201194739

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.