Evidence map›Paper›PMID 34680231›Full record

ArticleCancers2021

Tumor-Derived Factors Differentially Affect the Recruitment and Plasticity of Neutrophils.

Ludovica Arpinati, Naomi Kaisar-Iluz, Merav E Shaul, Christopher Groth, Viktor Umansky, Zvi G Fridlender

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026
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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.

Ludovica ArpinatiHadassah Medical Center, Institute of Pulmonary Medicine, Faculty of Medicine, Hebrew University of Jerusalem, P.O. Box 12000, Jerusalem 9112001, Israel.
Naomi Kaisar-IluzHadassah Medical Center, Institute of Pulmonary Medicine, Faculty of Medicine, Hebrew University of Jerusalem, P.O. Box 12000, Jerusalem 9112001, Israel.
Merav E ShaulHadassah Medical Center, Institute of Pulmonary Medicine, Faculty of Medicine, Hebrew University of Jerusalem, P.O. Box 12000, Jerusalem 9112001, Israel.
Christopher GrothGerman Cancer Research Center (DKFZ), Skin Cancer Unit, 69120 Heidelberg, Germany.
Viktor UmanskyGerman Cancer Research Center (DKFZ), Skin Cancer Unit, 69120 Heidelberg, Germany.ORCID 0000-0003-0259-1839
Zvi G FridlenderHadassah Medical Center, Institute of Pulmonary Medicine, Faculty of Medicine, Hebrew University of Jerusalem, P.O. Box 12000, Jerusalem 9112001, Israel.
Hebrew University of Jerusalem · ILGerman Cancer Research Center · DE

Funding

Cooperation Program in Cancer Research of the Deutsches Krebsforschungszentrum (DKFZ) and Israel's Ministry of Science and Technology (MOST) CA2656Deutsche Forschungsgemeinschaft 259332240/RTG 2099Israel Lung Association N/ASasson and Luisa Naor Fund N/A
6 · The paper itself

Abstract

Neutrophils play a key role in cancer biology. In contrast to circulating normal-density neutrophils (NDN), the amount of low-density neutrophils (LDN) significantly increases with tumor progression. The correlation between these neutrophil subpopulations and intratumoral neutrophils (TANs) is still under debate. Using 4T1 (breast) and AB12 (mesothelioma) tumor models, we aimed to elucidate the source of TANs and to assess the mechanisms driving neutrophils' plasticity in cancer. Both NDN and LDN were found to migrate in response to CXCL1 and CXCL2 exposure, and co-infiltrate the tumor site ex vivo and in vivo, although LDN migration into the tumor was higher than NDN. Tumor-derived factors and chemokines, particularly CXCL1, were found to drive neutrophil phenotypical plasticity, inducing NDN to transition towards a low-density state (LD-NDN). LD-NDN appeared to differ from NDN by displaying a phenotypical profile similar to LDN in terms of nuclear morphology, surface receptor markers, decreased phagocytic abilities, and increased ROS production. Interestingly, all three subpopulations displayed comparable cytotoxic abilities towards tumor cells. Our data suggest that TANs originate from both LDN and NDN, and that a portion of LDN derives from NDN undergoing phenotypical changes. NDN plasticity resulted in a change in surface marker expression and functional activity, gaining characteristics of LDN.

Indexed as

cancer immunologycell plasticityCXCL1CXCR2 and CXCR4neutrophils

Identifiers

PMID34680231
PMCPMC8534125
OpenAlexW3206800014

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.