Evidence map›Paper›PMID 29703471›Full record

ReviewThrombosis research2018

The intersection of protein disulfide isomerase and cancer associated thrombosis.

Jack D Stopa, Jeffrey I Zwicker

Abstract readReview
In one paragraph

Review in Thrombosis research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Targeting thiol isomerase activity with zafirlukast to treat ovarian cancer from the bench to clinic.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  10. Extracellular Vesicles Linking Inflammation, Cancer and Thrombotic Risks.Frontiers in cell and developmental biology · 2022
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Novel Antiplatelet Therapies for Atherothrombotic Diseases.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Review
  17. Article
  18. 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

2 authors at 1 institution in 1 country.

Jack D StopaDivision of Hemostasis and Thrombosis, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
Jeffrey I ZwickerDivision of Hemostasis and Thrombosis, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States; Division of Hematology and Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States. Electronic address: jzwicker@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · US

Funding

PROGRAM IN BLOOD COAGULATION AND VASCULAR BIOLOGYT32HL007917 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Robert C Flaumenhaft · 1999 to 2026
$11.1M
Translational Research Skills DevelopmentU54HL112302 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI FURIE, BRUCE · 2012 to 2016
$11.1M
NHLBI NIH HHS T32 HL007917NHLBI NIH HHS U54 HL112302
6 · The paper itself

Abstract

The mechanisms underlying the hypercoagulability of cancer are complex and include the upregulation coagulation factors or procoagulant proteins, shedding of microparticles, and direct activation of vascular cells. Protein disulfide isomerase (PDI) is a thiol isomerase secreted from activated platelets and endothelial cells and plays a critical role in both platelet aggregation and fibrin generation. A number of potential intravascular targets of PDI have been identified including cell surface receptors (e.g. β-integrins and glycoprotein Ib), receptor ligands (e.g. fibrinogen and von Willebrand factor), serine proteases (e.g. cathepsin G and kallekrein-14), and coagulation factors (e.g. factor XI and factor V). Recent clinical studies demonstrated that a small molecule inhibitor of PDI, isoquercetin, decreases platelet-dependent thrombin generation and PDI activity in plasma following oral administration. This review explores the mechanistic overlap between the molecular drivers of cancer associated thrombosis and the potential roles PDI plays in mediating thrombosis. These molecular insights provide rationale for clinical trials targeting PDI to prevent thrombosis in cancer patients.

Indexed as

HumansNeoplasmsProtein Disulfide-IsomerasesThrombosisProtein Disulfide-IsomerasesAntithromboticsCancer associated thrombosisProtein disulfide isomerase

Identifiers

PMID29703471
PMCPMC5929485
OpenAlexW2802689457

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.