Evidence map›Paper›PMID 34112755›Full record

ArticleNature communications2021

Targeting monoamine oxidase A-regulated tumor-associated macrophage polarization for cancer immunotherapy.

Yu-Chen Wang, Xi Wang, Jiaji Yu, Feiyang Ma, Zhe Li, Yang Zhou, Samuel Zeng, Xiaoya Ma, Yan-Ruide Li, Adam Neal and 6 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed, 1 pooled it
8.8field-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

105 citing papers in PubMed, 1 synthesis or guideline pooled it, 151 citations in OpenAlex.

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  8. COX5A induces M2 macrophage polarization in chronic rhinosinusitis with nasal polyps through ROS generation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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45 more citing papers are in PubMed but not listed here.

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

16 authors at 1 institution in 1 country.

Yu-Chen WangDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, USA.
Xi WangDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, USA.
Jiaji YuDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, USA.
Feiyang MaDepartment of Molecular, Cell and Developmental Biology, and Institute for Genomics and Proteomics, University of California, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0002-6260-0787
Zhe LiDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, USA.
Yang ZhouDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, USA.
Samuel ZengDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, USA.
Xiaoya MaDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, USA.
Yan-Ruide LiDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, USA.
Adam NealEli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California, Los Angeles, CA, USA.
Jie HuangDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, USA.
Angela ToDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, USA.
Nicole ClarkeDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, USA.
Sanaz MemarzadehEli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California, Los Angeles, CA, USA.
Matteo PellegriniDepartment of Molecular, Cell and Developmental Biology, and Institute for Genomics and Proteomics, University of California, Los Angeles, CA, USA.
Lili YangDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA, USA. liliyang@ucla.edu.ORCID http://orcid.org/0000-0001-6568-0404
University of California, Los Angeles · US

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
UCLA-Caltech Medical Scientist Training ProgramT32GM008042 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI AJIJOLA, OLUJIMI A, DAWSON, DAVID WAYNE · 1985 to 2023
$29.9M
UCLA SPORE in Brain CancerP50CA211015 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Yvonne Yu-Hsuan Chen · 2017 to 2026
$25.2M
UCLA Tumor Immunology Training ProgramT32CA009120 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Steven M. Dubinett, MICHAEL A TEITELL · 1985 to 2026
$10.3M
NCI NIH HHS P30 CA016042NCI NIH HHS P50 CA211015NCI NIH HHS T32 CA009120NIGMS NIH HHS T32 GM008042
6 · The paper itself

Abstract

Targeting tumor-associated macrophages (TAMs) is a promising strategy to modify the immunosuppressive tumor microenvironment and improve cancer immunotherapy. Monoamine oxidase A (MAO-A) is an enzyme best known for its function in the brain; small molecule MAO inhibitors (MAOIs) are clinically used for treating neurological disorders. Here we observe MAO-A induction in mouse and human TAMs. MAO-A-deficient mice exhibit decreased TAM immunosuppressive functions corresponding with enhanced antitumor immunity. MAOI treatment induces TAM reprogramming and suppresses tumor growth in preclinical mouse syngeneic and human xenograft tumor models. Combining MAOI and anti-PD-1 treatments results in synergistic tumor suppression. Clinical data correlation studies associate high intratumoral MAOA expression with poor patient survival in a broad range of cancers. We further demonstrate that MAO-A promotes TAM immunosuppressive polarization via upregulating oxidative stress. Together, these data identify MAO-A as a critical regulator of TAMs and support repurposing MAOIs for TAM reprogramming to improve cancer immunotherapy.

Indexed as

AnimalsCell Line, TumorDrug SynergismFemaleGene Expression Regulation, NeoplasticHumansImmunotherapyKaplan-Meier EstimateLymphomaMelanomaMiceMice, Inbred C57BLMonoamine OxidaseMonoamine Oxidase InhibitorsNeoplasmsOvarian NeoplasmsMonoamine OxidaseMonoamine Oxidase InhibitorsPdcd1 protein, mouseProgrammed Cell Death 1 ReceptorReactive Oxygen Species

Identifiers

PMID34112755
PMCPMC8192781
OpenAlexW3167313437

What OpenQuestion holds

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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.