Evidence map›Paper›PMID 37149684›Full record

ArticleNature communications2023

Type I interferon response in astrocytes promotes brain metastasis by enhancing monocytic myeloid cell recruitment.

Weili Ma, Maria Cecília Oliveira-Nunes, Ke Xu, Andrew Kossenkov, Benjamin C Reiner, Richard C Crist, James Hayden, Qing Chen

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
13.7field-weighted citation impact, top 1% 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

51 citing papers in PubMed, 53 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Weili Ma *Immunology, Microenvironment and Metastasis Program, The Wistar Institute, Philadelphia, PA, 19104, USA.
Maria Cecília Oliveira-Nunes *Immunology, Microenvironment and Metastasis Program, The Wistar Institute, Philadelphia, PA, 19104, USA.ORCID 0000-0002-4630-3918
Ke XuMD/PhD Program, Boston University School of Medicine, Boston, MA, 02215, USA.ORCID 0000-0003-2628-2061
Andrew KossenkovGene Expression & Regulation Program, The Wistar Institute, Philadelphia, PA, 19104, USA.
Benjamin C ReinerDepartment of Psychiatry, Perelman School of Medicine, The University of Pennsylvania, Philadelphia, PA, 19104, USA.ORCID 0000-0001-7796-587X
Richard C CristDepartment of Psychiatry, Perelman School of Medicine, The University of Pennsylvania, Philadelphia, PA, 19104, USA.
James HaydenImaging Shared Resource, The Wistar Institute, Philadelphia, PA, 19104, USA.ORCID 0000-0002-5491-2975
Qing ChenImmunology, Microenvironment and Metastasis Program, The Wistar Institute, Philadelphia, PA, 19104, USA. qichen@wistar.org.
The Wistar Institute · USUniversity of Pennsylvania · USBoston University · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
TRAINING PROGRAM IN BASIC CANCER RESEARCHT32CA009171 · NCI · WISTAR INSTITUTE · PI Alessandro Gardini · 1985 to 2026
$15.3M
Targeted Combination Therapy for MelanomaP50CA174523 · NCI · WISTAR INSTITUTE · PI HERLYN, MEENHARD F · 2014 to 2018
$11.1M
Understanding PPARgamma signaling in melanoma brain metastasisR01CA241490 · NCI · WISTAR INSTITUTE · PI CHEN, QING · 2020 to 2024
$2.0M
Integrative Approach to Comprehensive Analysis of High Throughput Data on a Cancer Center LevelR50CA211199 · NCI · WISTAR INSTITUTE · PI Andrew V Kossenkov · 2016 to 2026
$1.6M
NCI NIH HHS P30 CA010815NCI NIH HHS P50 CA174523NCI NIH HHS R01 CA241490NCI NIH HHS R50 CA211199NCI NIH HHS T32 CA009171
6 · The paper itself

Abstract

Cancer metastasis to the brain is a significant clinical problem. Metastasis is the consequence of favorable interactions between invaded cancer cells and the microenvironment. Here, we demonstrate that cancer-activated astrocytes create a sustained low-level activated type I interferon (IFN) microenvironment in brain metastatic lesions. We further confirm that the IFN response in astrocytes facilitates brain metastasis. Mechanistically, IFN signaling in astrocytes activates C-C Motif Chemokine Ligand 2 (CCL2) production, which further increases the recruitment of monocytic myeloid cells. The correlation between CCL2 and monocytic myeloid cells is confirmed in clinical brain metastasis samples. Lastly, genetically or pharmacologically inhibiting C-C Motif Chemokine Receptor 2 (CCR2) reduces brain metastases. Our study clarifies a pro-metastatic effect of type I IFN in the brain even though IFN response has been considered to have anti-tumor effects. Moreover, this work expands our understandings on the interactions between cancer-activated astrocytes and immune cells in brain metastasis.

Indexed as

Brain NeoplasmsInterferon Type IAstrocytesChemokine CCL2HumansMyeloid CellsReceptors, CCR2Tumor MicroenvironmentChemokine CCL2Interferon Type IReceptors, CCR2

Identifiers

PMID37149684
PMCPMC10163863
OpenAlexW4372306523

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.