Evidence map›Paper›PMID 33071285›Full record

ReviewBritish journal of cancer2021

The SUMO pathway in pancreatic cancer: insights and inhibition.

Christian Schneeweis, Zonera Hassan, Markus Schick, Ulrich Keller, Günter Schneider

Open access · hybridAbstract readReview
In one paragraph

Review in British journal of cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Unveiling the resistance to therapies in pancreatic ductal adenocarcinoma.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. The Role of SUMO E3 Ligases in Signaling Pathway of Cancer Cells.International journal of molecular sciences · 2022
    Review
  18. Article
  19. Article
  20. Review
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

5 authors at 3 institutions in 2 countries.

Christian Schneeweis *Medical Clinic and Polyclinic II, Klinikum rechts der Isar, Technical University Munich, 81675, München, Germany.
Zonera Hassan *Medical Clinic and Polyclinic II, Klinikum rechts der Isar, Technical University Munich, 81675, München, Germany.ORCID http://orcid.org/0000-0002-7981-8328
Markus SchickDepartment of Hematology, Oncology and Tumor Immunology, Campus Benjamin Franklin, Charité - Universitätsmedizin Berlin, Hindenburgdamm 30, 12203, Berlin, Germany.
Ulrich KellerDepartment of Hematology, Oncology and Tumor Immunology, Campus Benjamin Franklin, Charité - Universitätsmedizin Berlin, Hindenburgdamm 30, 12203, Berlin, Germany. ulrich.keller@charite.de.
Günter SchneiderMedical Clinic and Polyclinic II, Klinikum rechts der Isar, Technical University Munich, 81675, München, Germany. guenter.schneider@tum.de.ORCID http://orcid.org/0000-0003-1840-4508
German Cancer Research Center · DETUM Klinikum · DECharité - Universitätsmedizin Berlin · DE

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) SCHN 959/3-1Deutsche Forschungsgemeinschaft (German Research Foundation) SFB1335/P2Deutsche Forschungsgemeinschaft (German Research Foundation) SFB 824/C3Deutsche Forschungsgemeinschaft (German Research Foundation) SFB 824/C9Wilhelm Sander-Stiftung (Wilhelm Sander Foundation) 2017.048.2
6 · The paper itself

Abstract

An urgent medical need to develop novel treatment strategies for patients with pancreatic ductal adenocarcinoma (PDAC) exists. However, despite various efforts in the histopathological and molecular subtyping of PDAC, novel targeted or specific therapies have not been established. Posttranslational modifications (PTMs) with ubiquitin-like proteins, including small ubiquitin-like modifiers (SUMOs), mediate numerous processes that can contribute to the fitness and survival of cancer cells. The contribution of SUMOylation to transcriptional control, DNA repair pathways, mitotic progression, and oncogenic signalling has been described. Here we review functions of the SUMO pathway in PDAC, with a special focus on its connection to an aggressive subtype of the disease characterised by high MYC activity, and discuss SUMOylation inhibitors under development for precise PDAC therapies.

Indexed as

Protein Processing, Post-TranslationalCarcinoma, Pancreatic DuctalCell SurvivalCysteine EndopeptidasesDNA RepairEnzyme InhibitorsHumansMitosisPancreatic NeoplasmsPoly-ADP-Ribose Binding ProteinsPromyelocytic Leukemia ProteinProtein Inhibitors of Activated STATProto-Oncogene Proteins c-mycSignal TransductionSmall Ubiquitin-Related Modifier ProteinsSUMO-1 ProteinCysteine EndopeptidasesEnzyme InhibitorsMYC protein, humanPIAS4 protein, humanPML protein, humanPoly-ADP-Ribose Binding ProteinsPromyelocytic Leukemia ProteinProtein Inhibitors of Activated STATProto-Oncogene Proteins c-mycSENP1 protein, humanSmall Ubiquitin-Related Modifier ProteinsSUMO-1 ProteinUbiquitin-Conjugating EnzymesUbiquitin-Conjugating Enzyme UBC9Ubiquitins

Identifiers

PMID33071285
PMCPMC7851129
OpenAlexW3092869390

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.