Evidence map›Paper›PMID 37451265›Full record

ArticleImmunity2023

Hypoxic niches attract and sequester tumor-associated macrophages and cytotoxic T cells and reprogram them for immunosuppression.

Anirudh Sattiraju, Sangjo Kang, Bruno Giotti, Zhihong Chen, Valerie J Marallano, Concetta Brusco, Aarthi Ramakrishnan, Li Shen, Alexander M Tsankov, Dolores Hambardzumyan and 2 more

Abstract read
In one paragraph

Article in Immunity, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
186citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

186 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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126 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Anirudh SattirajuNash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Sangjo KangNash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Bruno GiottiDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Zhihong ChenDepartment of Neurosurgery, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Oncological Sciences, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Valerie J MarallanoNash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Concetta BruscoNash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Aarthi RamakrishnanNash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Li ShenNash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Alexander M TsankovDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Dolores HambardzumyanDepartment of Neurosurgery, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Oncological Sciences, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Roland H FriedelNash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Neurosurgery, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Electronic address: roland.friedel@mssm.edu.
Hongyan ZouNash Family Department of Neuroscience, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Neurosurgery, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Electronic address: hongyan.zou@mssm.edu.

Funding

THE TISCH CANCER INSTITUTE - CANCER CENTER SUPPORT GRANTP30CA196521 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Ramon E Parsons · 2015 to 2026
$35.4M
Tumor-Associated Macrophages in Vasogenic Cerebral Edema in Brain TumorsR01NS100864 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI Dolores Hambardzumyan · 2017 to 2026
$5.4M
Plexin-B2 function in glioma invasion and glioma stem cell maintenanceR01NS092735 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI FRIEDEL, ROLAND HORST · 2016 to 2025
$4.1M
Dissect governing factors for tumor stem cell dormancy in biomimetic vascular/GBM modelR01NS107462 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI DAI, GUOHAO, FRIEDEL, ROLAND HORST · 2018 to 2022
$3.0M
Tracing Hypoxic State and Hypoxia Memory in Glioblastoma ProgressionR21NS125700 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI FRIEDEL, ROLAND HORST, ZOU, HONGYAN JENNY · 2022 to 2023
$465k
Functional Analysis of Hypoxia-Induced Genes in Promoting Malignant Growth of GlioblastomaF31NS124259 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MARALLANO, VALERIE · 2022 to 2023
$66k
NCI NIH HHS P30 CA196521NINDS NIH HHS F31 NS124259NINDS NIH HHS R01 NS092735NINDS NIH HHS R01 NS100864NINDS NIH HHS R01 NS107462NINDS NIH HHS R21 NS125700
6 · The paper itself

Abstract

Glioblastoma (GBM), a highly lethal brain cancer, is notorious for immunosuppression, but the mechanisms remain unclear. Here, we documented a temporospatial patterning of tumor-associated myeloid cells (TAMs) corresponding to vascular changes during GBM progression. As tumor vessels transitioned from the initial dense regular network to later scant and engorged vasculature, TAMs shifted away from perivascular regions and trafficked to vascular-poor areas. This process was heavily influenced by the immunocompetence state of the host. Utilizing a sensitive fluorescent UnaG reporter to track tumor hypoxia, coupled with single-cell transcriptomics, we revealed that hypoxic niches attracted and sequestered TAMs and cytotoxic T lymphocytes (CTLs), where they were reprogrammed toward an immunosuppressive state. Mechanistically, we identified chemokine CCL8 and cytokine IL-1β as two hypoxic-niche factors critical for TAM trafficking and co-evolution of hypoxic zones into pseudopalisading patterns. Therefore, perturbation of TAM patterning in hypoxic zones may improve tumor control.

Indexed as

GlioblastomaT-Lymphocytes, CytotoxicHumansImmunosuppression TherapyMacrophagesTumor-Associated MacrophagesTumor MicroenvironmentCCL8CTLscytotoxic T lymphocytesGBMIL-1βimmune landscapeimmunosuppressionTAMtumor-associated microglia/macrophagestumor hypoxiatumor vasculature

Identifiers

PMID37451265
PMCPMC10527169

What OpenQuestion holds

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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.