Evidence map›Paper›PMID 35548777›Full record

ArticleOncoscience2022

A CRISPR-p53 interactome with potential implications for clinical CRISPR/Cas9 use.

Long Jiang, Fredrik Wermeling

Abstract read
In one paragraph

Article in Oncoscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Long JiangDepartment of Medicine Solna, Center for Molecular Medicine, Karolinska University Hospital and Karolinska Institutet, Stockholm, Sweden.
Fredrik WermelingDepartment of Medicine Solna, Center for Molecular Medicine, Karolinska University Hospital and Karolinska Institutet, Stockholm, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CRISPR/Cas9-based tools are anticipated to transform the gene therapy field by facilitating the correction of disease-causing mutations. However, CRISPR/Cas9 generates DNA damage, which triggers a DNA damage response centered around the tumor-suppressor p53. In this research perspective, we discuss implications of this and describe a CRISPR-p53 interactome with cancer-related genes that, if mutated, can give cells a selective advantage following exposure to CRISPR/Cas9. We propose that the genes in the CRISPR-p53 interactome should be monitored in the clinical setting and describe that transient p53 inhibition could be used to limit the enrichment of cells with such mutations.

Indexed as

cancerCRISPRDNA damage responsegene therapyp53

Identifiers

PMID35548777
PMCPMC9084925

What OpenQuestion holds

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LicenceCC BY
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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.