Evidence map›Paper›PMID 41161002›Full record

ArticleBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2025

Co-treatment of ticagrelor and anti-PD-1 immunotherapy in tumor-associated macrophages reduces pancreatic cancer cell growth and migration through the TGF-β1/Smad2 pathway.

Ying Kang, Emmanuel Boadi Amoafo, Philomena Entsie, Buddhadev Layek, Paul M Grandgenett, Michael A Hollingsworth, Marina Pasca di Magliano, Elisabetta Liverani

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2025. 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
–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

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.

Ying KangDepartment of Pharmaceutical Sciences, School of Pharmacy, College of Health and Human Sciences, North Dakota State University, Fargo, ND, USA.
Emmanuel Boadi AmoafoDepartment of Pharmaceutical Sciences, School of Pharmacy, College of Health and Human Sciences, North Dakota State University, Fargo, ND, USA.
Philomena EntsieDepartment of Pharmaceutical Sciences, School of Pharmacy, College of Health and Human Sciences, North Dakota State University, Fargo, ND, USA.
Buddhadev LayekDepartment of Pharmaceutical Sciences, School of Pharmacy, College of Health and Human Sciences, North Dakota State University, Fargo, ND, USA.
Paul M GrandgenettEppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Michael A HollingsworthEppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Marina Pasca di MaglianoDepartment of Surgery, The University of Michigan Medical School, Ann Arbor, Michigan, USA; Rogel Cancer Center, USA; Department of Cell and Developmental Biology, The University of Michigan Medical School, Ann Arbor, Michigan, USA.
Elisabetta LiveraniDepartment of Pharmaceutical Sciences, School of Pharmacy, College of Health and Human Sciences, North Dakota State University, Fargo, ND, USA. Electronic address: elisabetta.liverani@ndsu.edu.

Funding

Targeting CLEC-2/podoplanin as a therapeutic strategy for pancreatic cancerP20GM109024 · NORTH DAKOTA STATE UNIVERSITY · 2025 to 2025
$1.9M
Pancreatic Cancer Detection ConsortiumU01CA210240 · UNIVERSITY OF NEBRASKA MEDICAL CENTER · 2025 to 2025
$818k
NCI NIH HHS U01 CA210240NIGMS NIH HHS P20 GM109024
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is the third primary cause of cancer-related mortality in the US. PDAC is associated with an immunosuppressive tumor microenvironment (TME) that restricts the effectiveness of immunotherapies. Immunosuppressive tumor-associated macrophages (TAMs), the most abundant cell type in TME, express immune checkpoint ligands, including programmed cell death protein 1 (PD-1) ligand 1 (PD-L1). Targeting PD-1/PD-L1 alone has no effect in PDAC, highlighting the need for combination approaches. P2Y

Indexed as

Carcinoma, Pancreatic DuctalImmune Checkpoint InhibitorsPancreatic NeoplasmsProgrammed Cell Death 1 ReceptorSmad2 ProteinTicagrelorTransforming Growth Factor beta1Tumor-Associated MacrophagesB7-H1 AntigenCell Line, TumorCell MovementCell ProliferationHumansImmunotherapySignal TransductionTumor MicroenvironmentB7-H1 AntigenImmune Checkpoint InhibitorsPDCD1 protein, humanProgrammed Cell Death 1 ReceptorSmad2 ProteinSMAD2 protein, humanTGFB1 protein, humanTicagrelorTransforming Growth Factor beta1P2Y(12)PD-1PDACPD-L1TMETumor-associated macrophages

Identifiers

PMID41161002
PMCPMC12915496

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.