Evidence map›Paper›PMID 29946821›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2018

TLR4 and RAGE conversely mediate pro-inflammatory S100A8/9-mediated inhibition of proliferation-linked signaling in myeloproliferative neoplasms.

Marijana Kovačić, Olivera Mitrović-Ajtić, Bojana Beleslin-Čokić, Dragoslava Djikić, Tijana Subotički, Miloš Diklić, Danijela Leković, Mirjana Gotić, Pascal Mossuz, Vladan P Čokić

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

39 citing papers in PubMed, 59 citations in OpenAlex.

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  11. S100A8/A9Cell death & disease · 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

10 authors at 4 institutions in 2 countries.

Marijana KovačićDepartment of Molecular Oncology, Institute for Medical Research, University of Belgrade, Dr. Subotica 4, Belgrade, 11129, Serbia.
Olivera Mitrović-AjtićDepartment of Molecular Oncology, Institute for Medical Research, University of Belgrade, Dr. Subotica 4, Belgrade, 11129, Serbia.
Bojana Beleslin-ČokićClinic for Endocrinology, Diabetes and Metabolic Diseases, Genetic laboratory, Clinical Center of Serbia, Belgrade, Serbia.
Dragoslava DjikićDepartment of Molecular Oncology, Institute for Medical Research, University of Belgrade, Dr. Subotica 4, Belgrade, 11129, Serbia.
Tijana SubotičkiDepartment of Molecular Oncology, Institute for Medical Research, University of Belgrade, Dr. Subotica 4, Belgrade, 11129, Serbia.
Miloš DiklićDepartment of Molecular Oncology, Institute for Medical Research, University of Belgrade, Dr. Subotica 4, Belgrade, 11129, Serbia.
Danijela LekovićClinic of Hematology, Clinical Center of Serbia, Belgrade, Serbia.
Mirjana GotićClinic of Hematology, Clinical Center of Serbia, Belgrade, Serbia.
Pascal MossuzDépartement d'Hématologie, Institut de Biologie et Pathologie, CHU Grenoble, Grenoble, France.
Vladan P ČokićDepartment of Molecular Oncology, Institute for Medical Research, University of Belgrade, Dr. Subotica 4, Belgrade, 11129, Serbia. vl@imi.bg.ac.rs.ORCID http://orcid.org/0000-0002-0362-1449
University of Belgrade · RSCentar za Promociju Nauke · RSCenter for Health, Exercise and Sport Sciences · RSCentre Hospitalier Universitaire de Grenoble · FR

Funding

Serbian Ministry of Education, Science and Technological Development OI175053
6 · The paper itself

Abstract

purposePreviously, the family of S100A proteins has been found to be associated with inflammation and myelopoiesis and to be able to induce or support myeloproliferation during chronic inflammation. Here, we studied the inflammatory myeloid-related proteins S100A4, S100A8, S100A9 and S100A12 in myeloproliferative neoplasms (MPNs) in order to assess the involvement of chronic inflammation in the pathogenesis of MPN.

methodsWe analyzed the S100A4, S100A8, S100A9 and S100A12 mRNA and protein levels in the bone marrow and circulation of 140 patients with MPN and 15 healthy controls using Western blotting, microarray-based mRNA expression profiling and ELISA assays, respectively. In addition we performed functional studies on the proliferation-related AKT and ERK1/2 signaling pathways in MPN-derived granulocytes using Western blotting and proteomic analyses.

resultsWe found that the S100A mRNA levels were increased in MPN patient-derived circulatory CD34

conclusionsFrom our data we conclude that the S100A8 and S100A9 granulocyte and plasma levels are increased in MPN patients, along with inflammation markers, depending on their JAK2V617F mutation allele burden. We also found that S100A8/9-mediated inhibition of the proliferation-related AKT and ERK1/2 signaling pathways can be decreased by CALR mutation-dependent TLR4 blocking and increased by RAGE inhibition in MPN.

Indexed as

AdultAgedAged, 80 and overBlotting, WesternCalgranulin ACalgranulin BCell ProliferationFemaleHumansImmunohistochemistryInterleukin-8MaleMiddle AgedMyeloproliferative DisordersReceptor for Advanced Glycation End ProductsSignal TransductionCalgranulin ACalgranulin BInterleukin-8Receptor for Advanced Glycation End ProductsS100A8 protein, humanS100A9 protein, humanTLR4 protein, humanToll-Like Receptor 4AKT signalingERK1/2 signalingInflammationMyeloproliferative neoplasmS100A proteins

Identifiers

PMID29946821
PMCPMC12995227
OpenAlexW2810569452

What OpenQuestion holds

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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.