Evidence map›Paper›PMID 35865534›Full record

ReviewFrontiers in immunology2022

GM-CSF: A Double-Edged Sword in Cancer Immunotherapy.

Anil Kumar, Adeleh Taghi Khani, Ashly Sanchez Ortiz, Srividya Swaminathan

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
173citing papers in PubMed, 3 pooled it
18.4field-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

173 citing papers in PubMed, 3 syntheses or guidelines pooled it, 243 citations in OpenAlex.

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  16. Epitranscriptomic silencing of the ZC3H13/mJournal of experimental & clinical cancer research : CR · 2026
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113 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

4 authors at 2 institutions in 1 country.

Anil KumarDepartment of Systems Biology, Beckman Research Institute of City of Hope, Monrovia, CA, United States.
Adeleh Taghi KhaniDepartment of Systems Biology, Beckman Research Institute of City of Hope, Monrovia, CA, United States.
Ashly Sanchez OrtizDepartment of Systems Biology, Beckman Research Institute of City of Hope, Monrovia, CA, United States.
Srividya SwaminathanDepartment of Systems Biology, Beckman Research Institute of City of Hope, Monrovia, CA, United States.
Beckman Research InstituteCity of Hope · US

Funding

Transplant for Lymphoma:Therapy-Related LeukemiaP50CA107399 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI KWAK, LARRY W · 2004 to 2022
$35.5M
NCI NIH HHS P50 CA107399
6 · The paper itself

Abstract

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a cytokine that drives the generation of myeloid cell subsets including neutrophils, monocytes, macrophages, and dendritic cells in response to stress, infections, and cancers. By modulating the functions of innate immune cells that serve as a bridge to activate adaptive immune responses, GM-CSF globally impacts host immune surveillance under pathologic conditions. As with other soluble mediators of immunity, too much or too little GM-CSF has been found to promote cancer aggressiveness. While too little GM-CSF prevents the appropriate production of innate immune cells and subsequent activation of adaptive anti-cancer immune responses, too much of GM-CSF can exhaust immune cells and promote cancer growth. The consequences of GM-CSF signaling in cancer progression are a function of the levels of GM-CSF, the cancer type, and the tumor microenvironment. In this review, we first discuss the secretion of GM-CSF, signaling downstream of the GM-CSF receptor, and GM-CSF's role in modulating myeloid cell homeostasis. We then outline GM-CSF's anti-tumorigenic and pro-tumorigenic effects both on the malignant cells and on the non-malignant immune and other cells in the tumor microenvironment. We provide examples of current clinical and preclinical strategies that harness GM-CSF's anti-cancer potential while minimizing its deleterious effects. We describe the challenges in achieving the Goldilocks effect during administration of GM-CSF-based therapies to patients with cancer. Finally, we provide insights into how technologies that map the immune microenvironment spatially and temporally may be leveraged to intelligently harness GM-CSF for treatment of malignancies.

Indexed as

Granulocyte-Macrophage Colony-Stimulating FactorNeoplasmsCytokinesHumansImmunotherapyMonocytesReceptors, Granulocyte-Macrophage Colony-Stimulating FactorCytokinesGranulocyte-Macrophage Colony-Stimulating FactorReceptors, Granulocyte-Macrophage Colony-Stimulating Factoranti-tumor cytokinescancer treatmentGM-CSF (granulocyte-macrophage colony-stimulating factor)pro-tumor cytokinestumor immune microenvironment

Identifiers

PMID35865534
PMCPMC9294178
OpenAlexW4283808194

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.