Evidence map›Paper›PMID 34789568›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

CRISPR-SID: Identifying EZH2 as a druggable target for desmoid tumors via in vivo dependency mapping.

Thomas Naert, Dieter Tulkens, Tom Van Nieuwenhuysen, Joanna Przybyl, Suzan Demuynck, Matt van de Rijn, Mushriq Al-Jazrawe, Benjamin A Alman, Paul J Coucke, Kim De Leeneer and 4 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Deep learning in CRISPR-Cas systems: a review of recent studies.Frontiers in bioengineering and biotechnology · 2023
    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

14 authors at 5 institutions in 3 countries.

Thomas NaertDepartment of Biomedical Molecular Biology, Ghent University, Ghent 9052, Belgium.
Dieter TulkensDepartment of Biomedical Molecular Biology, Ghent University, Ghent 9052, Belgium.
Tom Van NieuwenhuysenDepartment of Biomedical Molecular Biology, Ghent University, Ghent 9052, Belgium.
Joanna PrzybylDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305.
Suzan DemuynckDepartment of Biomedical Molecular Biology, Ghent University, Ghent 9052, Belgium.
Matt van de RijnDepartment of Pathology, Stanford University School of Medicine, Stanford, CA 94305.
Mushriq Al-JazraweDepartment of Cell Biology, Duke University School of Medicine, Durham, NC 12422.
Benjamin A AlmanDepartment of Cell Biology, Duke University School of Medicine, Durham, NC 12422.
Paul J CouckeCenter for Medical Genetics, Ghent University, Ghent 9000, Belgium.
Kim De LeeneerCenter for Medical Genetics, Ghent University, Ghent 9000, Belgium.
Christian VanhoveDepartment of Electronics and Information Systems, Ghent University, Ghent 9000, Belgium.ORCID 0000-0002-3988-5980
Savvas N SavvidesVIB Center for Inflammation Research, VIB, Ghent 9052, Belgium.ORCID 0000-0003-3420-5947
David CreytensCancer Research Institute Ghent (CRIG), Ghent University, Ghent 9000, Belgium.
Kris VleminckxDepartment of Biomedical Molecular Biology, Ghent University, Ghent 9052, Belgium; kris.vleminckx@irc.ugent.be.ORCID 0000-0002-9666-4105
Ghent University · BEGhent University Hospital · BEDuke University · USMcGill University Health Centre · CAStanford University · US

Funding

Women's Cancer Research ProgramP30CA014236 · NCI · DUKE UNIVERSITY · PI DONNA NIEDZWIECKI · 1985 to 2026
$174.8M
NCI NIH HHS P30 CA014236
6 · The paper itself

Abstract

Cancer precision medicine implies identification of tumor-specific vulnerabilities associated with defined oncogenic pathways. Desmoid tumors are soft-tissue neoplasms strictly driven by Wnt signaling network hyperactivation. Despite this clearly defined genetic etiology and the strict and unique implication of the Wnt/β-catenin pathway, no specific molecular targets for these tumors have been identified. To address this caveat, we developed fast, efficient, and penetrant genetic

Indexed as

Clustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Cas SystemsAbdominal NeoplasmsAdenomatous Polyposis ColiAnimalsbeta CateninCarcinogenesisCell Line, TumorCyclic AMP Response Element-Binding ProteinDesmoid TumorsEnhancer of Zeste Homolog 2 ProteinGene EditingGene Expression Regulation, NeoplasticHumansNeoplasm ProteinsNerve Tissue Proteinsbeta CateninCREB3L1 protein, humanCTNNB1 protein, humanCyclic AMP Response Element-Binding ProteinEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanNeoplasm ProteinsNerve Tissue ProteinsPolycomb Repressive Complex 2SUZ12 protein, humanTranscription FactorsAPCcancer dependencydesmoid tumorEZH2Xenopus

Identifiers

PMID34789568
PMCPMC8617425
OpenAlexW3214304248

What OpenQuestion holds

Textmetadata
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.