Evidence map›Paper›PMID 36900379›Full record

ArticleCancers2023

Urokinase-Type Plasminogen Activator Receptor (uPAR) Cooperates with Mutated

Luogen Peng, Yuchan Li, Sha Yao, Jochen Gaedcke, Victor M Baart, Cornelis F M Sier, Albrecht Neesse, Volker Ellenrieder, Hanibal Bohnenberger, Frieder Fuchs and 3 more

Open access · goldFull text read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.8field-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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Canon enables causal inference of downstream genes in single-cell CRISPR studies via instrumental variable analysis.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

13 authors at 5 institutions in 3 countries.

Luogen PengInstitute of Pathology, University Medical Center Göttingen, University of Göttingen, 37075 Göttingen, Germany.ORCID 0000-0001-8181-0467
Yuchan LiInstitute of Pathology, University Medical Center Göttingen, University of Göttingen, 37075 Göttingen, Germany.
Sha YaoInstitute of Pathology, University Medical Center Göttingen, University of Göttingen, 37075 Göttingen, Germany.
Jochen GaedckeDepartment of General, Visceral and Pediatric Surgery, University Medical Center Göttingen, 37075 Göttingen, Germany.ORCID 0000-0002-6130-5874
Victor M BaartDepartment of Surgery, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.
Cornelis F M SierDepartment of Surgery, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.ORCID 0000-0002-4337-2758
Albrecht NeesseDepartment of Gastroenterology and Gastrointestinal Oncology, University Medical Center Göttingen, 37075 Göttingen, Germany.
Volker EllenriederDepartment of Gastroenterology and Gastrointestinal Oncology, University Medical Center Göttingen, 37075 Göttingen, Germany.
Hanibal BohnenbergerInstitute of Pathology, University Medical Center Göttingen, University of Göttingen, 37075 Göttingen, Germany.ORCID 0000-0003-1038-1030
Frieder FuchsInstitute of Pathology, University Medical Center Göttingen, University of Göttingen, 37075 Göttingen, Germany.ORCID 0000-0001-7075-5378
Julia KitzInstitute of Pathology, University Medical Center Göttingen, University of Göttingen, 37075 Göttingen, Germany.
Philipp StröbelInstitute of Pathology, University Medical Center Göttingen, University of Göttingen, 37075 Göttingen, Germany.ORCID 0000-0002-8528-8060
Stefan KüfferInstitute of Pathology, University Medical Center Göttingen, University of Göttingen, 37075 Göttingen, Germany.ORCID 0000-0001-8443-601X
Universitätsmedizin Göttingen · DELeiden University Medical Center · NLCentral South University · CNChangsha Central Hospital · CNUniversity of Cologne · DE

Funding

Deutsche Forschungsgemeinschaft KFO5002Hunan Provincial Health Committee Foundation of China D202302087111
6 · The paper itself

Abstract

backgroundPancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal cancers. Given the currently limited therapeutic options, the definition of molecular subgroups with the development of tailored therapies remains the most promising strategy. Patients with high-level gene amplification of urokinase plasminogen activator receptor (

methodsA total of 67 PDAC samples with clinical follow-up and TCGA gene expression data from 316 patients were used for prognostic correlations. Gene silencing by CRISPR/Cas9, as well as transfection of

resultsHigh levels of uPAR were correlated with significantly shorter survival in PDAC, especially in the subgroup of HNF1A-positive exocrine-like tumors. uPAR knockout by CRISPR/Cas9 resulted in activation of FAK, CDC42, and p38, upregulation of epithelial makers, decreased cell growth and motility, and resistance against gemcitabine that could be reversed by re-expression of uPAR. Silencing of

conclusionsActivation of uPAR is a potent negative prognostic factor in PDAC. uPAR and KRAS cooperate in switching the tumor from a dormant epithelial to an active mesenchymal state, which likely explains the poor prognosis of PDAC with high uPAR. At the same time, the active mesenchymal state is more vulnerable to gemcitabine. Strategies targeting either KRAS or uPAR should consider this potential tumor-escape mechanism.

Indexed as

dormancyERKFAKgemcitabineKRASMEKpancreatic canceruPAR

Identifiers

PMID36900379
PMCPMC10000455
OpenAlexW4323314926

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read32
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.