Evidence map›Paper›PMID 31119318›Full record

ArticleCancer immunology, immunotherapy : CII2019

Metabolic remodeling contributes towards an immune-suppressive phenotype in glioblastoma.

Pravin Kesarwani, Antony Prabhu, Shiva Kant, Prakash Chinnaiyan

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

45 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
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  7. Interactions between glioblastoma and myeloid cells.Frontiers in cell and developmental biology · 2025
    Review
  8. Article
  9. Review
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  12. Review
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  14. Article
  15. Article
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  17. Expression and Prognostic Role of PANK1 in Glioma.Combinatorial chemistry & high throughput screening · 2024
    Article
  18. Review
  19. Review
  20. Review
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

4 authors at 1 institution in 1 country.

Pravin KesarwaniDepartment of Radiation Oncology, Beaumont Health, 3811 West Thirteen Mile Road, Royal Oak, MI, 48073, USA.
Antony PrabhuDepartment of Radiation Oncology, Beaumont Health, 3811 West Thirteen Mile Road, Royal Oak, MI, 48073, USA.
Shiva KantDepartment of Radiation Oncology, Beaumont Health, 3811 West Thirteen Mile Road, Royal Oak, MI, 48073, USA.
Prakash ChinnaiyanDepartment of Radiation Oncology, Beaumont Health, 3811 West Thirteen Mile Road, Royal Oak, MI, 48073, USA. prakash.chinnaiyan@beaumont.edu.
Beaumont Health · US

Funding

Developing therapeutic strategies to elicit metabolic synthetic lethality in glioblastomaR01NS110838 · NINDS · WILLIAM BEAUMONT HOSPITAL RESEARCH INST · PI CHINNAIYAN, PRAKASH · 2020 to 2024
$1.7M
Biologic consequence and therapeuticimplications of cysteine catabolism in glioblastomaR21NS090087 · NINDS · WILLIAM BEAUMONT HOSPITAL RESEARCH INST · PI CHINNAIYAN, PRAKASH · 2016 to 2017
$418k
American Cancer Society RSG-11-029-01Bankhead-Coley Foundation Bankhead-Coley Cancer Research ProgramBankhead-Coley Foundation Cancer Research Seed Grant from BeaumontNINDS NIH HHS R01 NS110838NINDS NIH HHS R21 NS090087NINDS NIH HHS R21NS090087
6 · The paper itself

Abstract

Glioblastoma (GBM) is one of the most aggressive tumors. Numerous studies in the field of immunotherapy have focused their efforts on identifying various pathways linked with tumor-induced immunosuppression. Recent research has demonstrated that metabolic reprogramming in a tumor can contribute towards immune tolerance. To begin to understand the interface between metabolic remodeling and the immune-suppressive state in GBM, we performed a focused, integrative analysis coupling metabolomics with gene-expression profiling in patient-derived GBM (n = 80) and compared them to low-grade astrocytoma (LGA; n = 28). Metabolic intermediates of tryptophan, arginine, prostaglandin, and adenosine emerged as immuno-metabolic nodes in GBM specific to the mesenchymal and classical molecular subtypes of GBM. Integrative analyses emphasized the importance of downstream metabolism of several of these metabolic pathways in GBM. Using CIBERSORT to analyze immune components from the transcriptional profiles of individual tumors, we demonstrated that tryptophan and adenosine metabolism resulted in an accumulation of Tregs and M2 macrophages, respectively, and was recapitulated in mouse models. Furthermore, we extended these findings to preclinical models to determine their potential utility in defining the biologic and/or immunologic consequences of the identified metabolic programs. Collectively, through integrative analysis, we uncovered multifaceted ways by which metabolic reprogramming may contribute towards immune tolerance in GBM, providing the framework for further investigations designed to determine the specific immunologic consequence of these metabolic programs and their therapeutic potential.

Indexed as

AdenosineAdultAnimalsBrainBrain NeoplasmsCell Line, TumorGene Expression ProfilingGlioblastomaHumansMacrophagesMetabolic Networks and PathwaysMetabolomeMetabolomicsMiceMice, Inbred C57BLT-Lymphocytes, RegulatoryAdenosineTryptophanAdenosineArginaseGlioblastomaImmune metabolismProstaglandinTryptophan

Identifiers

PMID31119318
PMCPMC6586493
OpenAlexW2945800362

What OpenQuestion holds

Textmetadata
LicenceTDM
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.