Evidence map›Paper›PMID 34831416›Full record

ReviewCells2021

Macrophage Reprogramming and Cancer Therapeutics: Role of iNOS-Derived NO.

Khosrow Kashfi, Jasmine Kannikal, Niharika Nath

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed, 2 pooled it
11.6field-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

135 citing papers in PubMed, 2 syntheses or guidelines pooled it, 205 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Sulfated galactans fromiScience · 2026
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  10. Mature-StageInternational journal of molecular sciences · 2026
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  14. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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  18. Article
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75 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

3 authors at 2 institutions in 1 country.

Khosrow KashfiDepartment of Molecular, Cellular, and Biomedical Sciences, Sophie Davis School of Biomedical Education, City University of New York School of Medicine, New York, NY 10031, USA.ORCID 0000-0002-4060-7283
Jasmine KannikalDepartment of Biological and Chemical Sciences, College of Arts and Sciences, New York Institute of Technology, New York, NY 10023, USA.
Niharika NathDepartment of Biological and Chemical Sciences, College of Arts and Sciences, New York Institute of Technology, New York, NY 10023, USA.
New York Institute of Technology · USThe Graduate Center, CUNY · US

Funding

MIDARP at CCNYR24DA018055 · NIDA · CITY COLLEGE OF NEW YORK · PI FRIEDMAN, EITAN · 2005 to 2010
$2.2M
Delivery of H2S: Supramolecular and Enzyme-Triggered Strategies for Controlled ReleaseR01GM123508 · NIGMS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI MATSON, JOHN B · 2017 to 2021
$1.6M
NIDA NIH HHS R24 DA018055NIGMS NIH HHS R01 GM123508
6 · The paper itself

Abstract

Nitric oxide and its production by iNOS is an established mechanism critical to tumor promotion or suppression. Macrophages have important roles in immunity, development, and progression of cancer and have a controversial role in pro- and antitumoral effects. The tumor microenvironment consists of tumor-associated macrophages (TAM), among other cell types that influence the fate of the growing tumor. Depending on the microenvironment and various cues, macrophages polarize into a continuum represented by the M1-like pro-inflammatory phenotype or the anti-inflammatory M2-like phenotype; these two are predominant, while there are subsets and intermediates. Manipulating their plasticity through programming or reprogramming of M2-like to M1-like phenotypes presents the opportunity to maximize tumoricidal defenses. The dual role of iNOS-derived NO also influences TAM activity by repolarization to tumoricidal M1-type phenotype. Regulatory pathways and immunomodulation achieve this through miRNA that may inhibit the immunosuppressive tumor microenvironment. This review summarizes the classical physiology of macrophages and polarization, iNOS activities, and evidence towards TAM reprogramming with current information in glioblastoma and melanoma models, and the immunomodulatory and therapeutic options using iNOS or NO-dependent strategies.

Indexed as

Cellular ReprogrammingAnimalsCell PlasticityHumansMacrophagesNeoplasmsNitric OxideNitric Oxide Synthase Type IINitric OxideNitric Oxide Synthase Type IIarginasecancer progressioniNOSM1M2miRNAnitric oxidetumor-associated macrophage

Identifiers

PMID34831416
PMCPMC8624911
OpenAlexW3213416797

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.