Evidence map›Paper›PMID 31327867›Full record

ReviewBritish journal of cancer2019

The relationship between pancreatic cancer and hypercoagulability: a comprehensive review on epidemiological and biological issues.

Elena Campello, Anton Ilich, Paolo Simioni, Nigel S Key

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in British journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 5 pooled it
10.9field-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

87 citing papers in PubMed, 5 syntheses or guidelines pooled it, 140 citations in OpenAlex.

  1. Pooled it
  2. Stroke risk in cancer survivors: A meta-analysis and meta regression.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
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  6. Can thromboprophylaxis build a link for cancer patients undergoing surgical and/or chemotherapy treatment? The MeTHOS cohort study.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2022
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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

4 authors at 2 institutions in 2 countries.

Elena CampelloThrombotic and Haemorrhagic Disease Unit, Department of Medicine, University of Padova, Padova, Italy.
Anton IlichDivision of Haematology/Oncology, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Paolo SimioniThrombotic and Haemorrhagic Disease Unit, Department of Medicine, University of Padova, Padova, Italy.
Nigel S KeyDivision of Haematology/Oncology, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. nigel_key@med.unc.edu.
University of North Carolina at Chapel Hill · USUniversity of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has long been recognised that pancreatic cancer induces a hypercoagulable state that may lead to clinically apparent thrombosis. Although the relationship between pancreatic cancer and hypercoagulability is well described, the underlying pathological mechanism(s) and the interplay between these pathways remain a matter of intensive study. This review summarises existing data on epidemiology and pathogenesis of thrombotic complications in pancreatic cancer with a particular emphasis on novel pathophysiological pathways. Pancreatic cancer is characterised by high tumoural expression of tissue factor, activation of leukocytes with the release of neutrophil extracellular traps, the dissemination of tumour-derived microvesicles that promote hypercoagulability and increased platelet activation. Furthermore, other coagulation pathways probably contribute to these processes, such as those that involve heparanase, podoplanin and hypofibrinolysis. In the era in which heparin and its derivatives-the currently recommended therapy for cancer-associated thrombosis-might be superseded by direct oral anticoagulants, novel data from mouse models of cancer-associated thrombosis suggest the possibility of future personalised therapeutic approaches. In this dynamic era for cancer-associated thrombosis, the discovery of novel prothrombotic and proinflammatory mechanisms will potentially uncover pharmacological targets to prevent and treat thrombosis without adversely affecting haemostasis.

Indexed as

AnimalsAnticoagulantsAntithrombin IIICell-Derived MicroparticlesDisease Models, AnimalExtracellular TrapsFactor VIIIFactor Xa InhibitorsFibrin Fibrinogen Degradation ProductsFibrinogenFibrinolysisGlucuronidaseHeparanaseHeparinHumansLeukocytesAnticoagulantsAntithrombin IIIFactor VIIIFactor Xa InhibitorsFibrin Fibrinogen Degradation Productsfibrin fragment DFibrinogenGlucuronidaseHeparanaseHeparinMembrane GlycoproteinsPDPN protein, humanPodoplaninProtein CThromboplastin

Identifiers

PMID31327867
PMCPMC6738049
OpenAlexW2964286623

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.