Evidence map›Paper›PMID 41857096›Full record

ArticleScientific reports2026

Exploring the dual role of extracellular vesicles in coagulation and immune modulation in glioblastoma.

Annabell Wolff, Grit Waitz, Philipp Kaps, Sonja Oehmcke-Hecht, Wendy Bergmann-Ewert, Björn Schneider, Katharina Richter, Charlotte Wagner, Ann-Sophie Becker, Anett Seifert and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

15 authors.

Annabell Wolff *Department of Internal Medicine - Clinic and Polyclinic for Hematology, Hemostaseology, Oncology, Stem Cell Therapy and Palliative Medicine, Rostock University Medical Center, University of Rostock, 18057, Rostock, Germany. annabell.wolff@med.uni-rostock.de.
Grit Waitz *Institute of Transfusion Medicine, Rostock University Medical Center, University of Rostock, 18057, Rostock, Germany.
Philipp KapsDepartment of Internal Medicine - Clinic and Polyclinic for Hematology, Hemostaseology, Oncology, Stem Cell Therapy and Palliative Medicine, Rostock University Medical Center, University of Rostock, 18057, Rostock, Germany.
Sonja Oehmcke-HechtInstitute of Medical Microbiology, Virology and Hygiene, Rostock University Medical Center, University of Rostock, 18057, Rostock, Germany.
Wendy Bergmann-EwertCore Facility for Cell Sorting & Cell Analysis, Rostock University Medical Centre, 18057, Rostock, Germany.
Björn SchneiderInstitute of Pathology, Rostock University Medical Center, University of Rostock, 18057, Rostock, Germany.
Katharina RichterDepartment of Internal Medicine - Clinic and Polyclinic for Hematology, Hemostaseology, Oncology, Stem Cell Therapy and Palliative Medicine, Rostock University Medical Center, University of Rostock, 18057, Rostock, Germany.
Charlotte WagnerDepartment of Internal Medicine - Clinic and Polyclinic for Hematology, Hemostaseology, Oncology, Stem Cell Therapy and Palliative Medicine, Rostock University Medical Center, University of Rostock, 18057, Rostock, Germany.
Ann-Sophie BeckerInstitute of Pathology, Rostock University Medical Center, University of Rostock, 18057, Rostock, Germany.
Anett SeifertDepartment of Internal Medicine - Clinic and Polyclinic for Hematology, Hemostaseology, Oncology, Stem Cell Therapy and Palliative Medicine, Rostock University Medical Center, University of Rostock, 18057, Rostock, Germany.
Daniel DubinskiDepartment of Neurosurgery, Rostock University Medical Center, University of Rostock, 18057, Rostock, Germany.
Thomas M FreimanDepartment of Neurosurgery, Rostock University Medical Center, University of Rostock, 18057, Rostock, Germany.
Thomas ThieleInstitute of Transfusion Medicine, Rostock University Medical Center, University of Rostock, 18057, Rostock, Germany.
Sascha Troschke-MeurerDepartment of Pediatric Oncology and Hematology, University Medicine Greifswald, 17475, Greifswald, Germany.
Claudia MaletzkiDepartment of Internal Medicine - Clinic and Polyclinic for Hematology, Hemostaseology, Oncology, Stem Cell Therapy and Palliative Medicine, Rostock University Medical Center, University of Rostock, 18057, Rostock, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma (GBM) is often complicated by venous thromboembolism (VTE), primarily driven by tissue factor (TF, F3) and podoplanin (PDPN). These factors promote local hypercoagulation and microthrombosis, thereby contributing to tumor progression by enhancing migration, invasion, and inflammation. Both TF and PDPN can be released via extracellular vesicles (EVs), which carry procoagulant and immunomodulatory cargo. We developed a translational workflow combining biobanked tumor samples, clinical data, ex vivo GBM cultures, and coagulation assays to investigate mechanisms of hypercoagulation. Intraoperative blood coagulation was profiled using ClotPro®. Gene expression of coagulation-related markers was analyzed in tumor tissues and cell lines, complemented by RNAseq-based profiling of coagulation–inflammation links. Functional coagulation assays included clotting time, platelet aggregation, and EV-based analysis of prothrombotic and immunomodulatory activity. Peripheral coagulation in GBM patients was largely unaltered. However, tumor tissues consistently showed high F3 and PDPN expression and markedly low tissue factor pathway inhibitor (TFPI) levels (p < 0.001), indicating a shift toward a procoagulant phenotype. Patient-derived GBM cell lines showed variable TF and PDPN expression, which correlated with clotting potential. Distinct procoagulant mechanisms were observed, with some cells engaging both TF-mediated thrombin generation and PDPN-driven platelet activation. EVs isolated from GBM patient plasma and culture media showed similar procoagulant characteristics, with activity proportional to TF expression, and immune-modulating effects. Notably, GBM-derived EVs modulated microglial behavior, induced senescence, and triggered immune polarization in a cell line-dependent manner, likely contributing to tumor microenvironment remodeling. GBM-associated hypercoagulability is shaped by heterogeneous tumor-intrinsic pathways and EV-mediated mechanisms. The dual role of EVs in promoting coagulation and modulating immune responses provides a mechanistic framework for further studies investigating EVs as potential biomarkers and therapeutic targets relevant to future thromboprophylactic strategies in GBM patients.

Indexed as

Blood CoagulationBrain NeoplasmsExtracellular VesiclesGlioblastomaImmunomodulationCell Line, TumorFemaleHumansLipoproteinsMaleMembrane GlycoproteinsPodoplaninThromboplastinVenous Thromboembolismlipoprotein-associated coagulation inhibitorLipoproteinsMembrane GlycoproteinsPDPN protein, humanPodoplaninThromboplastinExtracellular vesicleGlioblastomaHypercoagulationImmune modulationSenescence

Identifiers

PMID41857096
PMCPMC13004914

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.