Evidence map›Paper›PMID 29772686›Full record

ReviewInternational journal of molecular sciences2018

Inhibition of the CCL5/CCR5 Axis against the Progression of Gastric Cancer.

Donatella Aldinucci, Naike Casagrande

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing 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

87 citing papers in PubMed.

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  10. Inflammatory factors collaboratively linkFrontiers in immunology · 2025
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27 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

2 authors.

Donatella AldinucciDepartment of Molecular Oncology, CRO Aviano National Cancer Institute, via F. Gallini 2, I-33081 Aviano, Italy. daldinucci@cro.it.
Naike CasagrandeDepartment of Molecular Oncology, CRO Aviano National Cancer Institute, via F. Gallini 2, I-33081 Aviano, Italy. naike.casagrande@libero.it.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the progress made in molecular and clinical research, patients with advanced-stage gastric cancer (GC) have a bad prognosis and very low survival rates. Furthermore, it is challenging to find the complex molecular mechanisms that are involved in the development of GC, its progression, and its resistance to therapy. The interactions of chemokines, also known as chemotactic cytokines, with their receptors regulate immune and inflammatory responses. However, updated research demonstrates that cancer cells subvert the normal chemokine role, transforming them into fundamental constituents of the tumor microenvironment (TME) with tumor-promoting effects. C-C chemokine ligand 5 (CCL5) is a chemotactic cytokine, and its expression and secretion are regulated in T cells. C-C chemokine receptor type 5 (CCR5) is expressed in T cells, macrophages, other leukocytes, and certain types of cancer cells. The interaction between CCL5 and CCR5 plays an active role in recruiting leukocytes into target sites. This review summarizes recent information on the role of the CCL5 chemokine and its receptor CCR5 in GC cell proliferation, metastasis formation, and in the building of an immunosuppressive TME. Moreover, it highlights the development of new therapeutic strategies to inhibit the CCL5/CCR5 axis in different ways and their possible clinical relevance in the treatment of GC.

Indexed as

Signal TransductionAnimalsCCR5 Receptor AntagonistsCell Transformation, NeoplasticChemokine CCL5Disease ProgressionHumansMolecular Targeted TherapyReceptors, CCR5Stomach NeoplasmsTumor MicroenvironmentCCR5 Receptor AntagonistsChemokine CCL5Receptors, CCR5CCL5CCR5CCR5 antagonistsgastric cancerinvasiontumor microenvironment

Identifiers

PMID29772686
PMCPMC5983686

What OpenQuestion holds

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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.