Evidence map›Paper›PMID 32943450›Full record

ArticleJournal for immunotherapy of cancer2020

Enhanced lipid biosynthesis in human tumor-induced macrophages contributes to their protumoral characteristics.

Katrin Rabold, Anna Aschenbrenner, Christoph Thiele, Collins K Boahen, Alexander Schiltmans, Johannes W A Smit, Joachim L Schultze, Mihai G Netea, Gosse J Adema, Romana T Netea-Maier

Open access · goldAbstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2020. 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
2.5field-weighted citation impact, top 9% 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.

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  19. Metabolic Reprogramming in Thyroid Cancer.Endocrinology and metabolism (Seoul, Korea) · 2024
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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

10 authors at 2 institutions in 2 countries.

Katrin RaboldDepartment of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands katrin.rabold@radboudumc.nl.ORCID 0000-0002-4175-3370
Anna AschenbrennerDepartment of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands.
Christoph ThieleBiochemistry and Cell Biology of Lipids, Life and Medical Sciences Institute (LIMES), Bonn, Germany.
Collins K BoahenDepartment of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands.
Alexander SchiltmansDepartment of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands.
Johannes W A SmitDepartment of Internal Medicine, Division of Endocrinology, Radboud University Medical Center, Nijmegen, The Netherlands.
Joachim L SchultzeDepartment for Genomics & Immunoregulation, Life and Medical Sciences Institute (LIMES), Bonn, Germany.
Mihai G NeteaDepartment of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands.
Gosse J Adema *Radiotherapy & OncoImmunology Laboratory, Department of Radiation Oncology, Radboud Institute for Molecular Life Sciences, Nijmegen, The Netherlands.ORCID 0000-0002-6750-1665
Romana T Netea-Maier *Department of Internal Medicine, Division of Endocrinology, Radboud University Medical Center, Nijmegen, The Netherlands.
Radboud University Nijmegen · NLLife & Brain (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumor-associated macrophages (TAMs) are key components of the tumor microenvironment (TME) in non-medullary thyroid carcinoma (TC) and neuroblastoma (NB), being associated with a poor prognosis for patients. However, little is known about how tumors steer the specific metabolic phenotype and function of TAMs.

methodsIn a human coculture model, transcriptome, metabolome and lipidome analysis were performed on TC-induced and NB-induced macrophages. The metabolic shift was correlated to functional readouts, such as cytokine production and reactive oxygen species (ROS) production, including pharmacological inhibition of metabolic pathways.

resultsBased on transcriptome and metabolome analysis, we observed a strong upregulation of lipid biosynthesis pathways in TAMs. Subsequently, lipidome analysis revealed that tumor-induced macrophages have an increased total lipid content and enriched levels of intracellular lipids, especially phosphoglycerides and sphingomyelins. Strikingly, this metabolic shift in lipid synthesis contributes to their protumoral functional characteristics: blocking key enzymes of lipid biosynthesis in the tumor-induced macrophages reversed the increased inflammatory cytokines and the capacity to produce ROS, two well-known protumoral factors in the TME.

conclusionsTaken together, our data show that tumor cells can stimulate lipid biosynthesis in macrophages to induce protumoral cytokine and ROS responses and advocate lipid biosynthesis as a potential therapeutic target to reprogram the TME.

Indexed as

HumansLipid MetabolismMetabolomicsNeoplasmsTumor-Associated MacrophagesTumor Microenvironmentmetabolic networks and pathwaysneuroblastomatumor microenvironment

Identifiers

PMID32943450
PMCPMC7500191
OpenAlexW3087253698

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.