Evidence map›Paper›PMID 36641763›Full record

ArticleThe Journal of pathology2023

CRISPR-induced exon skipping of β-catenin reveals tumorigenic mutants driving distinct subtypes of liver cancer.

Haiwei Mou, Onur Eskiocak, Kadir A Özler, Megan Gorman, Junjiayu Yue, Ying Jin, Zhikai Wang, Ya Gao, Tobias Janowitz, Hannah V Meyer and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of pathology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

6 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
  3. Liver cancer wars: plant-derived polyphenols strike back.Medical oncology (Northwood, London, England) · 2024
    Review
  4. Review
  5. Review
  6. Article
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

15 authors at 4 institutions in 2 countries.

Haiwei MouCold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
Onur EskiocakCold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
Kadir A ÖzlerCold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
Megan GormanCold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.ORCID 0000-0002-8984-8248
Junjiayu YueCold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
Ying JinCold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
Zhikai WangCold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
Ya GaoCold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
Tobias JanowitzCold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
Hannah V MeyerCold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
Tianxiong YuProgram in Bioinformatics and Integrative Biology, University of Massachusetts Medical School, Worcester, MA, USA.
John E WilkinsonDepartment of Comparative Medicine, University of Washington, Seattle, WA, USA.
Alper KucukuralBioinformatics Core, University of Massachusetts Medical School, Worcester, MA, USA.
Deniz M Ozata *Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.ORCID 0000-0001-5215-8684
Semir Beyaz *Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
Cold Spring Harbor Laboratory · USUniversity of Massachusetts Chan Medical School · USStockholm University · SEUniversity of Washington · US

Funding

Single-Cell Biology Shared ResourceP30CA045508 · NCI · COLD SPRING HARBOR LABORATORY · PI John Edward Moses · 1987 to 2026
$118.9M
University of Massachusetts Center for Clinical Science and Translational SupplementUL1TR001453 · NCATS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LUZURIAGA, KATHERINE F · 2015 to 2024
$39.0M
NCATS NIH HHS TR001453-01NCATS NIH HHS UL1 TR001453NCI NIH HHS 5P30CA045508NCI NIH HHS P30 CA045508NIH HHS P30CA045508-33
6 · The paper itself

Abstract

CRISPR/Cas9-driven cancer modeling studies are based on the disruption of tumor suppressor genes by small insertions or deletions (indels) that lead to frame-shift mutations. In addition, CRISPR/Cas9 is widely used to define the significance of cancer oncogenes and genetic dependencies in loss-of-function studies. However, how CRISPR/Cas9 influences gain-of-function oncogenic mutations is elusive. Here, we demonstrate that single guide RNA targeting exon 3 of Ctnnb1 (encoding β-catenin) results in exon skipping and generates gain-of-function isoforms in vivo. CRISPR/Cas9-mediated exon skipping of Ctnnb1 induces liver tumor formation in synergy with YAP

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAnimalsbeta CateninCarcinogenesisExonsMicebeta CateninCTNNB1 protein, mouseCRISPR/Cas9exon skippinghepatoblastomahepatocellular carcinomaliver cancerβ-catenin

Identifiers

PMID36641763
PMCPMC10273193
OpenAlexW4316260368

What OpenQuestion holds

Textmetadata
LicenceTDM
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.