Evidence map›Paper›PMID 40658336›Full record

ArticleJournal of thrombosis and thrombolysis2025

Clot formation, structure, and fibrinolysis of plasma from pancreatic cancer patients.

Rebecca A Risman, Noam Milman, Hajer Ali Sinan, Valerie Tutwiler

Abstract read
In one paragraph

Article in Journal of thrombosis and thrombolysis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Thrombosis in patients with cancer: challenges and advances.Journal of thrombosis and thrombolysis · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Rebecca A RismanDepartment of Biomedical Engineering, Rutgers University, New Brunswick, USA.
Noam MilmanDepartment of Biomedical Engineering, Rutgers University, New Brunswick, USA.
Hajer Ali SinanDepartment of Biomedical Engineering, Rutgers University, New Brunswick, USA.
Valerie TutwilerDepartment of Biomedical Engineering, Rutgers University, New Brunswick, USA. valerie.tutwiler@rutgers.edu.

Funding

Rutgers Biotechnology Training ProgramT32GM135141 · NIGMS · RUTGERS, THE STATE UNIV OF N.J. · PI ANN M. STOCK, Martin L Yarmush · 2020 to 2026
$3.5M
Systematic multidisciplinary approach to study traumatic bleeding as a complex structural and biomechanical problemR00HL148646 · NHLBI · RUTGERS, THE STATE UNIV OF N.J. · PI TUTWILER, VALERIE · 2020 to 2022
$747k
National Science Foundation CMMI-2332978New Jersey Commission on Cancer Research COCR22PRF010New Jersey Commission on Spinal Cord Research CSCR23IRG005New Jersey Health Foundation PC 140-24NHLBI NIH HHS R00 HL148646NIGMS NIH HHS T32 GM135141NIH HHS R00HL148646-01NIH HHS T32 GM135141
6 · The paper itself

Abstract

Pancreatic cancer (PC) has the highest risk of venous thromboembolisms amongst all cancer types. If not degraded through a process known as fibrinolysis, thrombi will continue to restrict blood flow and the transport of nutrients to downstream organs, which can lead to heart attack or stroke. While PC patients are known to be hypercoagulable and thus have an elevated thrombosis risk, the mechanism behind this behavior is not fully understood. We aimed to characterize alterations in clotting and fibrinolytic profiles in PC patients compared to healthy controls. Human blood plasma was collected from PC patients and healthy donor controls following institutional review board approval. We used kinetic turbidity to define the rates/timing of blood clot formation/degradation. Confocal and scanning electron microscopy were used to probe the effect PC has on fibrin network structure. Concentrations of proteins for clotting/fibrinolytic pathways were measured using ELISAs. PC patients were hypercoagulable compared to healthy donors with heightened fibrinogen concentration. A subset of patients were hypofibrinolytic, while most had similar fibrinolytic profiles to healthy. A comprehensive analysis revealed that delayed lysis in this subset was only present in patients with diabetes and/or COVID-19 due delayed clotting and, notably, elevated plasminogen activator inhibitor (PAI-1). In the general PC population, an extended PTT correlated with thicker fiber diameters while faster clotting resulted in smaller network pore size but was not correlated with lysis rate. Healthy, pooled plasma spiked with relevant concentrations of PAI-1 showed no difference in clot structure and comparable delays in lysis to patients. PAI-1, rather than network structure or other clotting/fibrinolytic factors, played a more significant role in hypofibrinolysis. PAI-1 inhibitors could be a prospective target for development of improved therapeutics to prevent restricted fibrinolysis.

Indexed as

Blood CoagulationFibrinolysisPancreatic NeoplasmsThrombosisAdultAgedCase-Control StudiesCOVID-19FemaleFibrinHumansMaleMiddle AgedPlasminogen Activator Inhibitor 1FibrinPlasminogen Activator Inhibitor 1SERPINE1 protein, humanFibrinFibrinogenFibrinolysisPancreatic cancerPlasminogen activator inhibitor 1Thrombosis

Identifiers

PMID40658336
PMCPMC12740958

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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.