Evidence map›Paper›PMID 31337034›Full record

ReviewCells2019

Novel Aspects of Extracellular Vesicles as Mediators of Cancer-Associated Thrombosis.

Vitor H Almeida, Araci M R Rondon, Tainá Gomes, Robson Q Monteiro

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Unmet Needs and Challenges in Cancer-Associated Venous Thromboembolism.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Exomap1 mouse: A transgenic model forExtracellular vesicle · 2023
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. A crucial exosome-related gene pair (Frontiers in immunology · 2023
    Article
  16. Article
  17. Review
  18. Review
  19. Extracellular Vesicles and Thrombogenicity in Atrial Fibrillation.International journal of molecular sciences · 2022
    Review
  20. Article
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

4 authors at 1 institution in 1 country.

Vitor H AlmeidaInstitute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, 21941-160 Rio de Janeiro, Brazil.ORCID 0000-0002-2789-7116
Araci M R RondonInstitute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, 21941-160 Rio de Janeiro, Brazil.ORCID 0000-0002-2703-8805
Tainá GomesInstitute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, 21941-160 Rio de Janeiro, Brazil.ORCID 0000-0003-3987-2490
Robson Q MonteiroInstitute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, 21941-160 Rio de Janeiro, Brazil. robsonqm@bioqmed.ufrj.br.ORCID 0000-0002-5260-2332
Universidade Federal do Rio de Janeiro · BR

Funding

Lacrimal Gland Repair Using Progenitor CellsR01EY026202 · NEI · SCRIPPS RESEARCH INSTITUTE, THE · PI MAKARENKOVA, HELEN P. · 2016 to 2025
$5.2M
6 · The paper itself

Abstract

The establishment of prothrombotic states during cancer progression is well reported but the precise mechanisms underlying this process remain elusive. A number of studies have implicated the presence of the clotting initiator protein, tissue factor (TF), in circulating tumor-derived extracellular vesicles (EVs) with thrombotic manifestations in certain cancer types. Tumor cells, as well as tumor-derived EVs, may activate and promote platelet aggregation by TF-dependent and independent pathways. Cancer cells and their secreted EVs may also facilitate the formation of neutrophil extracellular traps (NETs), which may contribute to thrombus development. Alternatively, the presence of polyphosphate (polyP) in tumor-derived EVs may promote thrombosis through a TF-independent route. We conclude that the contribution of EVs to cancer coagulopathy is quite complex, in which one or more mechanisms may take place in a certain cancer type. In this context, strategies that could attenuate the crosstalk between the proposed pro-hemostatic routes could potentially reduce cancer-associated thrombosis.

Indexed as

NeoplasmsPlatelet AggregationThrombosisAnimalsCell Line, TumorExtracellular TrapsExtracellular VesiclesHumansNeutrophilsPolyphosphatesThromboplastinPolyphosphatesThromboplastincancerexosomesextracellular vesiclesmicrovesiclesneutrophil extracellular trapsneutrophilsplateletspolyphosphatethrombosistissue factor

Identifiers

PMID31337034
PMCPMC6679024
OpenAlexW2961900645

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.