Evidence map›Paper›PMID 32001555›Full record

ArticleGut2020

SUMO pathway inhibition targets an aggressive pancreatic cancer subtype.

Alexander Biederstädt, Zonera Hassan, Christian Schneeweis, Markus Schick, Lara Schneider, Alexander Muckenhuber, Yingfen Hong, Gerrit Siegers, Lisa Nilsson, Matthias Wirth and 17 more

Open access · hybridAbstract read
In one paragraph

Article in Gut, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

73 citing papers in PubMed, 99 citations in OpenAlex.

  1. Trial
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  5. Aberrant SUMOylation Restricts the Targetable Cancer Immunopeptidome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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13 more citing papers are in PubMed but not listed here.

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

27 authors at 8 institutions in 3 countries.

Alexander BiederstädtMedical Clinic and Policlinic III, Klinikum rechts der Isar, Technical University Munich, München, Germany.
Zonera HassanMedical Clinic and Polyclinic II, Klinikum rechts der Isar, Technical University Munich, München, Germany.ORCID 0000-0002-8485-1958
Christian SchneeweisMedical Clinic and Polyclinic II, Klinikum rechts der Isar, Technical University Munich, München, Germany.
Markus SchickDepartment of Hematology, Oncology and Tumor Immunology, Campus Benjamin Franklin, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Lara SchneiderCenter for Bioinformatics, Saarland Informatics Campus, Saarland University, Saarbrücken, Germany.
Alexander MuckenhuberInstitute of Pathology, Technical University Munich, München, Germany.
Yingfen HongMedical Clinic and Policlinic III, Klinikum rechts der Isar, Technical University Munich, München, Germany.
Gerrit SiegersMedical Clinic and Policlinic III, Klinikum rechts der Isar, Technical University Munich, München, Germany.
Lisa NilssonDepartment of Surgery, Sahlgrenska Cancer Center, Gothenburg University, Gothenburg, Sweden.
Matthias WirthDepartment of Hematology, Oncology and Tumor Immunology, Campus Benjamin Franklin, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Zahra DantesMedical Clinic and Polyclinic II, Klinikum rechts der Isar, Technical University Munich, München, Germany.
Katja SteigerInstitute of Pathology, Technical University Munich, München, Germany.
Kathrin SchunckGoethe University, Medical School, Institute of Biochemistry II, Frankfurt, Germany.
Steve LangstonOncology Drug Discovery Unit, Takeda Pharmaceuticals International Co, Cambridge, Massachusetts, USA.
H-P LenhofCenter for Bioinformatics, Saarland Informatics Campus, Saarland University, Saarbrücken, Germany.
Andrea ColuccioMedical Clinic and Polyclinic II, Klinikum rechts der Isar, Technical University Munich, München, Germany.
Felix OrbenMedical Clinic and Polyclinic II, Klinikum rechts der Isar, Technical University Munich, München, Germany.
Jolanta SlawskaMedical Clinic and Policlinic III, Klinikum rechts der Isar, Technical University Munich, München, Germany.
Anna SchergerMedical Clinic and Policlinic III, Klinikum rechts der Isar, Technical University Munich, München, Germany.
Dieter SaurGerman Cancer Research Center (DKFZ) and German Cancer Consortium (DKTK), Heidelberg, Germany.
Stefan MüllerGoethe University, Medical School, Institute of Biochemistry II, Frankfurt, Germany.
Roland RadGerman Cancer Research Center (DKFZ) and German Cancer Consortium (DKTK), Heidelberg, Germany.
Wilko WeichertInstitute of Pathology, Technical University Munich, München, Germany.
Jonas NilssonDepartment of Surgery, Sahlgrenska Cancer Center, Gothenburg University, Gothenburg, Sweden.
Maximilian ReichertMedical Clinic and Polyclinic II, Klinikum rechts der Isar, Technical University Munich, München, Germany.ORCID 0000-0002-8611-5639
Günter SchneiderMedical Clinic and Polyclinic II, Klinikum rechts der Isar, Technical University Munich, München, Germany guenter.schneider@tum.de ulrich.keller@charite.de.ORCID 0000-0003-1840-4508
Ulrich KellerDepartment of Hematology, Oncology and Tumor Immunology, Campus Benjamin Franklin, Charité - Universitätsmedizin Berlin, Berlin, Germany guenter.schneider@tum.de ulrich.keller@charite.de.ORCID 0000-0002-8485-1958
TUM Klinikum · DEGerman Cancer Research Center · DECharité - Universitätsmedizin Berlin · DEGoethe University Frankfurt · DESaarland University · DESahlgrenska University Hospital · SETakeda (United States) · USTechnical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivePancreatic ductal adenocarcinoma (PDAC) still carries a dismal prognosis with an overall 5-year survival rate of 9%. Conventional combination chemotherapies are a clear advance in the treatment of PDAC; however, subtypes of the disease exist, which exhibit extensive resistance to such therapies. Genomic MYC amplifications represent a distinct subset of PDAC with an aggressive tumour biology. It is clear that hyperactivation of MYC generates dependencies that can be exploited therapeutically. The aim of the study was to find and to target MYC-associated dependencies.

designWe analysed human PDAC gene expression datasets. Results were corroborated by the analysis of the small ubiquitin-like modifier (SUMO) pathway in a large PDAC cohort using immunohistochemistry. A SUMO inhibitor was used and characterised using human and murine two-dimensional, organoid and in vivo models of PDAC.

resultsWe observed that MYC is connected to the SUMOylation machinery in PDAC. Components of the SUMO pathway characterise a PDAC subtype with a dismal prognosis and we provide evidence that hyperactivation of MYC is connected to an increased sensitivity to pharmacological SUMO inhibition.

conclusionSUMO inhibitor-based therapies should be further developed for an aggressive PDAC subtype.

Indexed as

AgedAnimalsApoptosisCarcinoma, Pancreatic DuctalCell Line, TumorCell ProliferationEnzyme InhibitorsEstersFemaleGene AmplificationGene ExpressionHumansMaleMiceMiddle AgedNeoplasm TransplantationEnzyme InhibitorsEstersML-792MYC protein, humanMyc protein, mouseProto-Oncogene Proteins c-mycPyrazolesPyrimidinesSAE1 protein, humanSmall Ubiquitin-Related Modifier ProteinsSulfonic AcidsSUMO-1 ProteinSUMO1 protein, humanSUMO2 protein, humanSUMO3 protein, humanUbiquitin-Activating EnzymesUbiquitin-Conjugating EnzymesUbiquitin-Conjugating Enzyme UBC9Ubiquitinscancerpancreatic cancer

Identifiers

PMID32001555
PMCPMC7398468
OpenAlexW3003760629

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

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.