Evidence map›Paper›PMID 31739488›Full record

ArticleInternational journal of molecular sciences2019

CRISPR/Cas9-Mediated Knock-Out of Kras

Eva Lentsch, Lifei Li, Susanne Pfeffer, Arif B Ekici, Leila Taher, Christian Pilarsky, Robert Grützmann

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
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  7. Review
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  9. Article
  10. Precise Gene Knock-In Tools with Minimized Risk of DSBs: A Trend for Gene Manipulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  11. Targeted disruption of theActa biochimica et biophysica Sinica · 2024
    Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Nucleic Acid-Based Approaches to Tackle KRAS Mutant Cancers.International journal of molecular sciences · 2023
    Review
  17. Review
  18. Review
  19. Oncogenic dependency plays a dominant role in the immune response to cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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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

7 authors at 1 institution in 1 country.

Eva LentschDepartment of Surgery, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany.ORCID 0000-0002-5110-0082
Lifei LiDivision of Bioinformatics, Department of Biology, Friedrich-Alexander Universität Erlangen-Nürnberg (FAU), 91054 Erlangen, Germany.
Susanne PfefferDepartment of Surgery, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany.
Arif B EkiciInstitute of Human Genetics, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany.ORCID 0000-0001-6099-7066
Leila TaherDivision of Bioinformatics, Department of Biology, Friedrich-Alexander Universität Erlangen-Nürnberg (FAU), 91054 Erlangen, Germany.ORCID 0000-0002-2013-5426
Christian PilarskyDepartment of Surgery, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany.ORCID 0000-0002-7968-3283
Robert GrützmannDepartment of Surgery, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91054 Erlangen, Germany.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In 90% of pancreatic ductal adenocarcinoma cases, genetic alteration of the proto-oncogene Kras has occurred, leading to uncontrolled proliferation of cancerous cells. Targeting Kras has proven to be difficult and the battle against pancreatic cancer is ongoing. A promising approach to combat cancer was the discovery of the clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR-associated (Cas) system, which can be used to genetically modify cells. To assess the potential of a CRISPR/CRISPR-associated protein 9 (Cas9) method to eliminate Kras mutations in cells, we aimed to knock-out the c.35G>A (p.G12D) Kras mutation. Therefore, three cell lines with a heterozygous Kras mutation (the human cell lines SUIT-2 and Panc-1 and the cell line TB32047 from a KPC mouse model) were used. After transfection, puromycin selection and single-cell cloning, proteins from two negative controls and five to seven clones were isolated to verify the knock-out and to analyze changes in key signal transduction proteins. Western blots showed a specific knock-out in the Kras

Indexed as

CRISPR-Cas SystemsGene Knockout TechniquesMutationAllelesAmino Acid SubstitutionCell Line, TumorGene EditingGene Expression ProfilingGene TargetingHumansPancreatic NeoplasmsProto-Oncogene MasProto-Oncogene Proteins p21(ras)Signal TransductionKRAS protein, humanMAS1 protein, humanProto-Oncogene MasProto-Oncogene Proteins p21(ras)CRISPR/Cas9 systemG12DKrasPanc-1Suit-2TB32047

Identifiers

PMID31739488
PMCPMC6888344
OpenAlexW2985747972

What OpenQuestion holds

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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.