Evidence map›Paper›PMID 25988873›Full record

ReviewJournal of thrombosis and haemostasis : JTH2015

Venous thrombosis and cancer: from mouse models to clinical trials.

Y Hisada, J E Geddings, C Ay, N Mackman

Open access · greenAbstract readReview
In one paragraph

Review in Journal of thrombosis and haemostasis : JTH, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
12.8field-weighted citation impact, top 1% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
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  11. Article
  12. Circulating Tumor Cells and Cancer-Associated Venous Thrombosis: A Missing Link.Arteriosclerosis, thrombosis, and vascular biology · 2023
    Article
  13. Article
  14. Review
  15. Article
  16. Observational
  17. Review
  18. Extracellular Vesicles Linking Inflammation, Cancer and Thrombotic Risks.Frontiers in cell and developmental biology · 2022
    Review
  19. Review
  20. Review

7 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

4 authors at 2 institutions in 3 countries.

Y HisadaDivision of Hematology and Oncology, Department of Medicine, Thrombosis and Hemostasis Program, UNC McAllister Heart Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
J E GeddingsDepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
C AyDepartment of Medicine I, Medical University of Vienna, Vienna, Austria.ORCID http://orcid.org/0000-0003-2607-9717
N MackmanDivision of Hematology and Oncology, Department of Medicine, Thrombosis and Hemostasis Program, UNC McAllister Heart Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
University of North Carolina at Chapel Hill · USMedical University of Vienna · AT

Funding

Research Training in Hematology at UNC Chapel HillT32HL007149 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Nigel S. Key · 1985 to 2026
$8.6M
Mechanisms of Venous Thromboembolism in CancerR01HL095096 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KEY, NIGEL S., MACKMAN, NIGEL · 2008 to 2012
$2.6M
Microparticle Docking in Pancreatic Cancer Induced VTEF30HL117546 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI GEDDINGS, JULIA E · 2013 to 2016
$139k
NHLBI NIH HHS F30 HL117546NHLBI NIH HHS F30HL117546NHLBI NIH HHS HL095096NHLBI NIH HHS R01 HL095096NHLBI NIH HHS T32 HL007149
6 · The paper itself

Abstract

Cancer patients have a ~4 fold increased risk of venous thromboembolism (VTE) compared with the general population and this is associated with significant morbidity and mortality. This review summarizes our current knowledge of VTE and cancer, from mouse models to clinical studies. Notably, the risk of VTE varies depending on the type and stage of cancer. For instance, pancreatic and brain cancer patients have a higher risk of VTE than breast and prostate cancer patients. Moreover, patients with metastatic disease have a higher risk than those with localized tumors. Tumor-derived procoagulant factors and growth factors may directly and indirectly enhance VTE. For example, increased levels of circulating tumor-derived, tissue factor-positive microvesicles may trigger VTE. In a mouse model of ovarian cancer, tumor-derived IL-6 and hepatic thrombopoietin have been linked to increased platelet production and thrombosis. In addition, mouse models of mammary and lung cancer showed that tumor-derived granulocyte colony-stimulating factor causes neutrophilia and activation of neutrophils. Activated neutrophils can release neutrophil extracellular traps (NETs) that enhance thrombosis. Cell-free DNA in the blood derived from cancer cells, NETs and treatment with cytotoxic drugs can activate the clotting cascade. These studies suggest that there are multiple mechanisms for VTE in patients with different types of cancer. Preventing and treating VTE in cancer patients is challenging; the current recommendations are to use low-molecular-weight heparin. Understanding the underlying mechanisms may allow the development of new therapies to safely prevent VTE in cancer patients.

Indexed as

Blood CoagulationAnimalsAnticoagulantsDisease Models, AnimalFibrinolytic AgentsHumansMiceNeoplasmsPrognosisRisk AssessmentRisk FactorsVenous ThrombosisAnticoagulantsFibrinolytic Agentscancerleukocytesplateletsthrombosistissue factor

Identifiers

PMID25988873
PMCPMC4773200
OpenAlexW1696065146

What OpenQuestion holds

Textmetadata
LicenceTDM
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.