Evidence map›Paper›PMID 29346400›Full record

ArticlePloS one2018

The mechanisms how heparin affects the tumor cell induced VEGF and chemokine release from platelets to attenuate the early metastatic niche formation.

Jan Moritz Ponert, Svenja Schwarz, Reza Haschemi, Jens Müller, Bernd Pötzsch, Gerd Bendas, Martin Schlesinger

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. AllergoOncology in Review: Harnessing Allergy in the Field of Oncology to Improve Patient Outcomes.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2026
    Review
  2. Targeting platelet-tumor cell interactions via thromboxane AExperimental hematology & oncology · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. Proteomics and its applications in breast cancer.American journal of cancer research · 2021
    Review
  7. Review
  8. Review
  9. Article
  10. Chemokines and Chemokine Receptors: Orchestrating Tumor Metastasization.International journal of molecular sciences · 2018
    Review
  11. Review
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

7 authors at 1 institution in 1 country.

Jan Moritz PonertDepartment of Pharmacy, Rheinische Friedrich-Wilhelms-University Bonn, Bonn, Germany.
Svenja SchwarzDepartment of Pharmacy, Rheinische Friedrich-Wilhelms-University Bonn, Bonn, Germany.
Reza HaschemiDepartment of Pharmacy, Rheinische Friedrich-Wilhelms-University Bonn, Bonn, Germany.
Jens MüllerInstitute for Experimental Hematology and Transfusion Medicine, University of Bonn Medical Centre, Bonn, Germany.
Bernd PötzschInstitute for Experimental Hematology and Transfusion Medicine, University of Bonn Medical Centre, Bonn, Germany.
Gerd BendasDepartment of Pharmacy, Rheinische Friedrich-Wilhelms-University Bonn, Bonn, Germany.
Martin SchlesingerDepartment of Pharmacy, Rheinische Friedrich-Wilhelms-University Bonn, Bonn, Germany.ORCID 0000-0001-8942-6136
University of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis is responsible for the majority of cancer associated fatalities. Tumor cells leaving the primary tumor and entering the blood flow immediately interact with platelets. Activated platelets contribute in different ways to cancer cell survival and proliferation, e.g. in formation of the early metastatic niche by release of different growth factors and chemokines. Here we show that a direct interaction between platelets and MV3 melanoma or MCF7 breast cancer cells induces platelet activation and a VEGF release in citrated plasma that cannot be further elevated by the coagulation cascade and generated thrombin. In contrast, the release of platelet-derived chemokines CXCL5 and CXCL7 depends on both, a thrombin-mediated platelet activation and a direct interaction between tumor cells and platelets. Preincubation of platelets with therapeutic concentrations of unfractionated heparin reduces the tumor cell initiated VEGF release from platelets. In contrast, tumor cell induced CXCL5 and CXCL7 release from platelets was not impacted by heparin pretreatment in citrated plasma. In defibrinated, recalcified plasma, on the contrary, heparin is able to reduce CXCL5 and CXCL7 release from platelets by thrombin inhibition. Our data indicate that different chemokines and growth factors in diverse platelet granules are released in tightly regulated processes by various trigger mechanisms. We show for the first time that heparin is able to reduce the mediator release induced by different tumor cells both in a contact and coagulation dependent manner.

Indexed as

beta-ThromboglobulinBlood CoagulationBlood PlateletsCell Line, TumorChemokine CXCL5HeparinHumansNeoplasm MetastasisPlatelet ActivationTumor MicroenvironmentVascular Endothelial Growth Factor Abeta-ThromboglobulinChemokine CXCL5HeparinPPBP protein, humanVascular Endothelial Growth Factor A

Identifiers

PMID29346400
PMCPMC5773218
OpenAlexW2789087673

What OpenQuestion holds

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LicenceCC BY
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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.