Evidence map›Paper›PMID 38022534›Full record

ReviewFrontiers in immunology2023

Cancer-associated mesenchymal stem/stromal cells: role in progression and potential targets for therapeutic approaches.

Ali Hazrati, Kosar Malekpour, Zahra Mirsanei, Arezou Khosrojerdi, Nasim Rahmani-Kukia, Neda Heidari, Ardeshir Abbasi, Sara Soudi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

16 citing papers in PubMed, 16 citations in OpenAlex.

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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

8 authors at 6 institutions in 1 country.

Ali HazratiDepartment of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Kosar MalekpourDepartment of Immunology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Zahra MirsaneiDepartment of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Arezou KhosrojerdiInfectious Diseases Research Center, Birjand University of Medical Sciences, Birjand, Iran.
Nasim Rahmani-KukiaDepartment of Biochemistry, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Neda HeidariDepartment of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Ardeshir AbbasiDepartment of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Sara SoudiDepartment of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Shahid Beheshti University of Medical Sciences · IRTarbiat Modares University · IRBirjand University of Medical Sciences · IRIran University of Medical Sciences · IRShiraz University of Medical Sciences · IRTehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignancies contain a relatively small number of Mesenchymal stem/stromal cells (MSCs), constituting a crucial tumor microenvironment (TME) component. These cells comprise approximately 0.01-5% of the total TME cell population. MSC differentiation potential and their interaction with the tumor environment enable these cells to affect tumor cells' growth, immune evasion, metastasis, drug resistance, and angiogenesis. This type of MSC, known as cancer-associated mesenchymal stem/stromal cells (CA-MSCs (interacts with tumor/non-tumor cells in the TME and affects their function by producing cytokines, chemokines, and various growth factors to facilitate tumor cell migration, survival, proliferation, and tumor progression. Considering that the effect of different cells on each other in the TME is a multi-faceted relationship, it is essential to discover the role of these relationships for targeting in tumor therapy. Due to the immunomodulatory role and the tissue repair characteristic of MSCs, these cells can help tumor growth from different aspects. CA-MSCs indirectly suppress antitumor immune response through several mechanisms, including decreasing dendritic cells (DCs) antigen presentation potential, disrupting natural killer (NK) cell differentiation, inducing immunoinhibitory subsets like tumor-associated macrophages (TAMs) and Treg cells, and immune checkpoint expression to reduce effector T cell antitumor responses. Therefore, if these cells can be targeted for treatment so that their population decreases, we can hope for the treatment and improvement of the tumor conditions. Also, various studies show that CA-MSCs in the TME can affect other vital aspects of a tumor, including cell proliferation, drug resistance, angiogenesis, and tumor cell invasion and metastasis. In this review article, we will discuss in detail some of the mechanisms by which CA-MSCs suppress the innate and adaptive immune systems and other mechanisms related to tumor progression.

Indexed as

Mesenchymal Stem CellsNeoplasmsCell DifferentiationCytokinesHumansImmunityTumor MicroenvironmentCytokinesangiogenesiscancerimmunosuppressionmetastasisMSCstumor growth

Identifiers

PMID38022534
PMCPMC10655012
OpenAlexW4388294758

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.