Evidence map›Paper›PMID 31428521›Full record

ArticleOncoimmunology

Neutrophil Cathepsin G and Tumor Cell RAGE Facilitate Neutrophil Anti-Tumor Cytotoxicity.

Ronit Vogt Sionov, Tanya Fainsod-Levi, Tamir Zelter, Lola Polyansky, Christine T Pham, Zvi Granot

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

43 citing papers in PubMed, 61 citations in OpenAlex.

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  9. Harnessing myeloid cells in cancer.Molecular cancer · 2025
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  10. Cannabidiol (CBD) Acts as an Antioxidant onAntibiotics (Basel, Switzerland) · 2025
    Article
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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

6 authors at 2 institutions in 2 countries.

Ronit Vogt SionovDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel Canada, Hebrew University Medical School, Jerusalem, Israel.
Tanya Fainsod-LeviDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel Canada, Hebrew University Medical School, Jerusalem, Israel.
Tamir ZelterDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel Canada, Hebrew University Medical School, Jerusalem, Israel.
Lola PolyanskyDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel Canada, Hebrew University Medical School, Jerusalem, Israel.
Christine T PhamDivision of Rheumatology, Washington University in St. Louis, St. Louis, MO, USA.
Zvi GranotDepartment of Developmental Biology and Cancer Research, Institute for Medical Research Israel Canada, Hebrew University Medical School, Jerusalem, Israel.
Hebrew University of Jerusalem · ILWashington University in St. Louis · US

Funding

Washington University Rheumatic DiseasesResearch Resource-based CenterP30AR073752 · NIAMS · WASHINGTON UNIVERSITY · PI Alfred Hyoungju Kim · 2018 to 2026
$7.6M
NIAMS NIH HHS P30 AR073752
6 · The paper itself

Abstract

Neutrophils are a heterogeneous population of myeloid cells which may either promote or hinder tumor growth and progression. Anti-tumor neutrophils have the capacity to kill tumor cells in a contact-dependent manner. However, the molecular mechanisms underlying tumor cell recognition by neutrophils remained unexplored. Tumor cells were shown to express aberrant glycosylation patterns and neutrophils are equipped with receptors capable of recognizing such glycosylations. Accordingly, we hypothesized that the receptor for advanced glycation end products (RAGE) may facilitate neutrophil recognition of tumor cells. Indeed, RAGE decoy receptors and RAGE-specific blocking antibodies dramatically reduce tumor cell susceptibility to neutrophil cytotoxicity. Unexpectedly, we found that tumor cell RAGE rather than neutrophil RAGE is important for the killing process. We further identified neutrophil Cathepsin G as the neutrophil component interacting with tumor cell RAGE. Cathepsin G-deficient neutrophils show impaired ability to kill tumor cells, suggesting that RAGE-Cathepsin G interaction is required for neutrophil cytotoxicity. These data unravel new aspects of neutrophil anti-tumor activity and identify a novel role for RAGE and Cathepsin G in neutrophil-mediated cytotoxicity.

Indexed as

Cathepsin Gneutrophil cytotoxicityRAGEtumor cell killing

Identifiers

PMID31428521
PMCPMC6685517
OpenAlexW2951876433

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.