Evidence map›Paper›PMID 42676425›Full record

ArticleFrontiers in immunology2026

Plectin promotes an aggressive phenotype and represses cytotoxic T cell activity in pancreatic cancer.

Cody L Wolf, Roxanne K Ruiz, Sokchea Khou, Robert Cornelison, Edward B Stelow, Karl M Kowalewski, Matthew J Lazzara, Amanda Poissonnier, Lisa M Coussens, Kimberly A Kelly

Abstract read
In one paragraph

Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Cody L Wolf *Department of Biomedical Engineering, University of Virginia, Charlottesville, VA, United States.
Roxanne K Ruiz *Department of Biomedical Engineering, University of Virginia, Charlottesville, VA, United States.
Sokchea Khou *Department of Cell, Developmental, & Cancer Biology, Oregon Health and Science University, Portland, OR, United States.
Robert CornelisonDepartment of Experimental Pathology, University of Virginia, Charlottesville, VA, United States.
Edward B StelowDepartment of Experimental Pathology, University of Virginia, Charlottesville, VA, United States.
Karl M KowalewskiDepartment of Chemical Engineering, University of Virginia, Charlottesville, VA, United States.
Matthew J LazzaraDepartment of Biomedical Engineering, University of Virginia, Charlottesville, VA, United States.
Amanda PoissonnierDepartment of Cell, Developmental, & Cancer Biology, Oregon Health and Science University, Portland, OR, United States.
Lisa M CoussensDepartment of Cell, Developmental, & Cancer Biology, Oregon Health and Science University, Portland, OR, United States.
Kimberly A Kelly *Department of Biomedical Engineering, University of Virginia, Charlottesville, VA, United States.

Funding

Women's Oncology Program - WONP30CA044579 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Thomas P. Loughran · 1987 to 2026
$72.1M
Understanding the origins of rapid recurrence of pancreatic cancer after resectionP30CA069533 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI Luiz Eduardo Bertassoni · 1997 to 2026
$60.5M
Biotechnology Training ProgramT32GM136615 · NIGMS · UNIVERSITY OF VIRGINIA · PI Silvia Salinas Blemker, Kimberly A. Kelly · 2020 to 2026
$3.4M
Comparative analysis between patient-derived models of pancreatic ductal adenocarcinomas and matched tumor specimensU01CA224012 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI BRODY, JONATHAN, COUSSENS, LISA M. · 2019 to 2023
$2.9M
Optimal control models of epithelial-mesenchymal transition for the design of pancreas cancer combination therapyU01CA243007 · NCI · UNIVERSITY OF VIRGINIA · PI LAZZARA, MATTHEW J · 2019 to 2023
$2.5M
NCI NIH HHS P30 CA044579NCI NIH HHS P30 CA069533NCI NIH HHS U01 CA224012NCI NIH HHS U01 CA243007NIGMS NIH HHS T32 GM136615
6 · The paper itself

Abstract

Background: Pancreatic adenocarcinoma (PDAC) is an abysmal disease with poor clinical outcomes, largely due to limited life-extending treatments. Notably, PDAC displays a T cell-suppressive tumor microenvironment, and the underlying molecular mechanisms that lead to this phenotype remain poorly understood. Methods: Utilizing the TCGA-PAAD dataset, tumor samples were separated by PLEC expression to evaluate patient survival, and pathway analyses associated with increased tumorigenesis. Evaluation of immune infiltration and subsequent immune deconvolution was performed using tidyestimate and CIBERSORTx R packages and immunohistochemistry (IHC) from human PDAC samples was performed to analyze PLEC expression and immune cell infiltration. Single-cell RNA-seq (scRNA-seq) analysis from 229 PDAC patients was analyzed to investigate signaling dynamics and immune cell infiltration in PLEC Results: Our studies revealed that high plectin expression results in an overall worse survival associated with activation of pro-tumorigenic pathways and decreased anti-tumor immune signature in PDAC patients. Analysis via GSEA indicates PLEC Discussion: Our findings identify plectin as a biomarker of aggressive disease in PDAC, with high plectin expression associated with decreased T cell infiltration, and anti-CSP treatment reinstates antitumor immunity and decreases tumor volume

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsPlectinT-Lymphocytes, CytotoxicAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansLymphocytes, Tumor-InfiltratingMicePhenotypeTumor MicroenvironmentPLEC protein, humanPlectincancer immunologypancreatic cancerplectintherapeutic targettumor microenvironment

Identifiers

PMID42676425
PMCPMC13526953

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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.