Evidence map›Paper›PMID 27391078›Full record

ArticlePloS one2016

Mesenchymal Stem Cells (MSC) Regulate Activation of Granulocyte-Like Myeloid Derived Suppressor Cells (G-MDSC) in Chronic Myeloid Leukemia Patients.

Cesarina Giallongo, Alessandra Romano, Nunziatina Laura Parrinello, Piera La Cava, Maria Violetta Brundo, Vincenzo Bramanti, Fabio Stagno, Paolo Vigneri, Annalisa Chiarenza, Giuseppe Alberto Palumbo and 2 more

Abstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
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

33 citing papers in PubMed.

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  8. Biology and Therapeutic Properties of Mesenchymal Stem Cells in Leukemia.International journal of molecular sciences · 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

12 authors.

Cesarina GiallongoDivision of Hematology, A.O.U. Policlinico-OVE, Catania, University of Catania, Catania, Italy.
Alessandra RomanoDivision of Hematology, A.O.U. Policlinico-OVE, Catania, University of Catania, Catania, Italy.
Nunziatina Laura ParrinelloDivision of Hematology, A.O.U. Policlinico-OVE, Catania, University of Catania, Catania, Italy.
Piera La CavaDivision of Hematology, A.O.U. Policlinico-OVE, Catania, University of Catania, Catania, Italy.
Maria Violetta BrundoDepartment of Biological, Geological, and Environmental Sciences, University of Catania, Catania, Italy.
Vincenzo BramantiDepartment of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.
Fabio StagnoDivision of Hematology, A.O.U. Policlinico-OVE, Catania, University of Catania, Catania, Italy.
Paolo VigneriOncology, Department of Clinical and Experimental Medicine, University of Catania, Catania, Italy.
Annalisa ChiarenzaDivision of Hematology, A.O.U. Policlinico-OVE, Catania, University of Catania, Catania, Italy.
Giuseppe Alberto PalumboDivision of Hematology, A.O.U. Policlinico-OVE, Catania, University of Catania, Catania, Italy.
Daniele TibulloDivision of Hematology, A.O.U. Policlinico-OVE, Catania, University of Catania, Catania, Italy.
Francesco Di RaimondoDivision of Hematology, A.O.U. Policlinico-OVE, Catania, University of Catania, Catania, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is well known that mesenchymal stem cells (MSC) have a role in promotion of tumor growth, survival and drug-resistance in chronic myeloid leukemia (CML). Recent reports indicated that a subpopulation of myeloid cells, defined as granulocyte-like myeloid-derived suppressor cells (G-MDSC) is increased in these patients. So far, the role of MSC in MDSC expansion and activation into the BM microenvironment remains unexplored. To address this question, here we use a specific experimental model in vitro, co-culturing MSC with peripheral blood mononucleated cells (PBMC) from normal individuals, in order to generate MSC-educated G-MDSC. Although MSC of healthy donors (HD) and CML patients were able to generate the same amount of MDSC, only CML-MSC-educated G-MDSC exhibited suppressive ability on autologous T lymphocytes. In addition, compared with HD-MSC, CML-MSC over-expressed some immunomodulatory factors including TGFβ, IL6 and IL10, that could be involved in MDSC activation. CML-MSC-educated G-MDSC expressed higher levels of ARG1, TNFα, IL1β, COX2 and IL6 than G-MDSC isolated from co-culture with HD-MSC. Our data provide evidence that CML-MSC may play a critical role in tumor microenvironment by orchestrating G-MDSC activation and regulating T lymphocytes-mediated leukemia surveillance, thus contributing to CML immune escape.

Indexed as

Models, BiologicalTumor MicroenvironmentAdultAgedFemaleGranulocytesHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMesenchymal Stem CellsMiddle AgedNeoplasm ProteinsNeoplasm Proteins

Identifiers

PMID27391078
PMCPMC4938578

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Registered trials

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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.