Evidence map›Paper›PMID 27886105›Full record

ReviewInternational journal of molecular sciences2016

Pro-Tumoral Inflammatory Myeloid Cells as Emerging Therapeutic Targets.

Gabor J Szebeni, Csaba Vizler, Lajos I Nagy, Klara Kitajka, Laszlo G Puskas

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2016. 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
2.5field-weighted citation impact, top 11% 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, 52 citations in OpenAlex.

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  15. Infiltration of LPAR5Frontiers in immunology · 2022
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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

5 authors at 1 institution in 1 country.

Gabor J SzebeniAvidin Ltd., Also kikoto sor 11/D., H-6726 Szeged, Hungary. g.szebeni@avidinbiotech.com.
Csaba VizlerDepartment of Biochemistry, Biological Research Center, Hungarian Academy of Sciences, Temesvari krt. 62., H-6726 Szeged, Hungary. vizler.csaba@brc.mta.hu.
Lajos I NagyAvidin Ltd., Also kikoto sor 11/D., H-6726 Szeged, Hungary. lajos@avidinbiotech.com.
Klara KitajkaDepartment of Genetics, Biological Research Center, Hungarian Academy of Sciences, Temesvari krt. 62., H-6726 Szeged, Hungary. klarakitajka@gmail.com.
Laszlo G PuskasAvidin Ltd., Also kikoto sor 11/D., H-6726 Szeged, Hungary. laszlo@avidinbiotech.com.
Hungarian Academy of Sciences · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since the observation of Virchow, it has long been known that the tumor microenvironment constitutes the soil for the infiltration of inflammatory cells and for the release of inflammatory mediators. Under certain circumstances, inflammation remains unresolved and promotes cancer development. Here, we review some of these indisputable experimental and clinical evidences of cancer related smouldering inflammation. The most common myeloid infiltrate in solid tumors is composed of myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs). These cells promote tumor growth by several mechanisms, including their inherent immunosuppressive activity, promotion of neoangiogenesis, mediation of epithelial-mesenchymal transition and alteration of cellular metabolism. The pro-tumoral functions of TAMs and MDSCs are further enhanced by their cross-talk offering a myriad of potential anti-cancer therapeutic targets. We highlight these main pro-tumoral mechanisms of myeloid cells and give a general overview of their phenotypical and functional diversity, offering examples of possible therapeutic targets. Pharmacological targeting of inflammatory cells and molecular mediators may result in therapies improving patient condition and prognosis. Here, we review experimental and clinical findings on cancer-related inflammation with a major focus on creating an inventory of current small molecule-based therapeutic interventions targeting cancer-related inflammatory cells: TAMs and MDSCs.

Indexed as

Antineoplastic AgentsCell CommunicationCell MovementCytokinesEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansInflammationMacrophagesMolecular Targeted TherapyMyeloid-Derived Suppressor CellsNeoplasm ProteinsNeoplasmsNeovascularization, PathologicSmall Molecule LibrariesTumor MicroenvironmentAntineoplastic AgentsCytokinesNeoplasm ProteinsSmall Molecule Librariesinflammatory tumor microenvironmentmyeloid-derived suppressor cellstumor-associated macrophages

Identifiers

PMID27886105
PMCPMC5133952
OpenAlexW2554420728

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.