Evidence map›Paper›PMID 42149304›Full record

Observational studyJournal of thrombosis and thrombolysis2026

Platelet FcɣRIIa: a novel biomarker of risk for thromboembolism and death in cancer.

Chris E Holmes, George A Davis, Heidi S Taatjes-Sommer, Naomi E Sai-Hardebeck, Peter W Callas, Ikechukwu Chidobem, Ryan Thomas, David J Schneider

Registry-linked trialAbstract readObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in Journal of thrombosis and thrombolysis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05240508 (Platelet FcGammaRIIa and Risk of Venous Thromboembolism in Cancer), which is not on this map. Not yet cited in PubMed.

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

NCT05240508 unknown statusnot on this map

Platelet FcGammaRIIa and Risk of Venous Thromboembolism in Cancer

TypeobservationalSponsorUniversity of VermontRan2022 to 2024Enrolled600ConditionsVenous Thromboembolism
3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Chris E HolmesDepartment of Medicine, Division of Hematology and Oncology, University of Vermont Cancer Center, Burlington, VT, USA.
George A DavisDepartment of Medicine, Division of Hematology and Oncology, University of Vermont Cancer Center, Burlington, VT, USA.
Heidi S Taatjes-SommerDepartment of Medicine, Cardiovascular Research Institute, Burlington, VT, USA.
Naomi E Sai-HardebeckDepartment of Medicine, Cardiovascular Research Institute, Burlington, VT, USA.
Peter W CallasBiomedical Statistics Research Core, The University of Vermont, Burlington, VT, USA.
Ikechukwu ChidobemDepartment of Medicine, Division of Hematology and Oncology, University of Vermont Cancer Center, Burlington, VT, USA.
Ryan ThomasDepartment of Medicine, Division of Hematology and Oncology, University of Vermont Cancer Center, Burlington, VT, USA.
David J SchneiderDepartment of Medicine, Cardiovascular Research Institute, Burlington, VT, USA. david.schneider@med.uvm.edu.

Funding

NIH R21 20231130NIH HHS R21 20231130
6 · The paper itself

Abstract

Cancer is associated with arterial and venous thrombotic events (ATE/VTE). Platelet FcγRIIa (pFCG) impacts platelet activation that contributes to ATE/VTE. Recurrent myocardial infarction (MI) and death are predicted by pFCG in patients with MI. Crosstalk between platelets and malignant cells that may promote cell invasion and cancer progression is mediated by pFCG. The objective is to determine whether pFCG (high vs. low) identifies cancer patients at greater risk of thrombosis and death. Ambulatory patients with cancer (n = 219) initiating cancer directed therapy were enrolled in a prospective translational study. The pFCG test was performed at study initiation and used flow cytometry to quantify mean fluorescence intensity that was translated to molecules of FCG/platelet. Outcomes of VTE/ATE and all cause death were abstracted from the Electronic Health Record at least 6 months after enrollment. Hazard ratios (HR) were analyzed with Kaplan-Meier analysis. Risk of the composite endpoint (ATE/VTE/death) was increased in patients with high pFCG (HR 1.9, 95% confidence interval [CI] 1.1-3.2, p = 0.02). A consistent non-significant trend for increased composite of ATE/VTE was associated with high pFCG (HR 1.7, 95% CI 0.8-3.3, p = 0.14). High pFCG identified patients at greater risk of all-cause death (HR 2.5, 95% CI 1.3-5.0, p = 0.009). Among patients who died (n = 50), ATE/VTE was a cause of death in 4 (8%) and temporally not associated with death in 19 (38%). The pFCG test identifies cancer patients at greater risk of death and could predict risk of thromboembolism. Additional studies are warranted to evaluate this novel biomarker of risk. Clinical trial registration: NCT05240508.

Indexed as

Blood PlateletsNeoplasmsReceptors, IgGThromboembolismAgedBiomarkersFemaleHumansMaleMiddle AgedProspective StudiesRisk FactorsBiomarkersFc gamma receptor IIAReceptors, IgGBiomarkerCancerPlateletPrognosisVenous thromboembolism

Identifiers

PMID42149304
PMCPMC13447332

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Registered trials

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.