Evidence map›Paper›PMID 31059574›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2019

Genome-Wide CRISPR Screening Identifies the Tumor Suppressor Candidate OVCA2 As a Determinant of Tolerance to Acetaldehyde.

Amin Sobh, Alex Loguinov, Alessia Stornetta, Silvia Balbo, Abderrahmane Tagmount, Luoping Zhang, Chris D Vulpe

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

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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 4 institutions in 1 country.

Amin SobhDepartment of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, Florida.
Alex LoguinovDepartment of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, Florida.
Alessia StornettaMasonic Cancer Center, University of Minnesota, Minneapolis, Minnesota.
Silvia BalboMasonic Cancer Center, University of Minnesota, Minneapolis, Minnesota.
Abderrahmane TagmountDepartment of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, Florida.
Luoping ZhangDivision of Environmental Health Sciences, School of Public Health, University of California, Berkeley, California.
Chris D VulpeDepartment of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, Florida.
University of Florida · USUniversity of California, Berkeley · USUniversity of Minnesota · USUniversity of Minnesota Medical Center · US

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Jeffrey S. Miller · 1998 to 2026
$100.4M
Training CoreP42ES004705 · NIEHS · UNIVERSITY OF CALIFORNIA BERKELEY · PI MCHALE, CLIONA · 1987 to 2025
$74.6M
NCI NIH HHS P30 CA077598NIEHS NIH HHS P42 ES004705
6 · The paper itself

Abstract

Acetaldehyde, a metabolite of ethanol, is a cellular toxicant and a human carcinogen. A genome-wide CRISPR-based loss-of-function screen in erythroleukemic K562 cells revealed candidate genetic contributors affecting acetaldehyde cytotoxicity. Secondary screening exposing cells to a lower acetaldehyde dose simultaneously validated multiple candidate genes whose loss results in increased sensitivity to acetaldehyde. Disruption of genes encoding components of various DNA repair pathways increased cellular sensitivity to acetaldehyde. Unexpectedly, the tumor suppressor gene OVCA2, whose function is unknown, was identified in our screen as a determinant of acetaldehyde tolerance. Disruption of the OVCA2 gene resulted in increased acetaldehyde sensitivity and higher accumulation of the acetaldehyde-derived DNA adduct N2-ethylidene-dG. Together these results are consistent with a role for OVCA2 in adduct removal and/or DNA repair.

Indexed as

CRISPR-Cas SystemsAcetaldehydeCell SurvivalCell Transformation, NeoplasticDNA AdductsDose-Response Relationship, DrugGene Expression Regulation, NeoplasticGenome-Wide Association StudyHEK293 CellsHumansK562 CellsNeoplasmsProteinsRisk AssessmentTumor Suppressor ProteinsAcetaldehydeDNA AdductsOVCA2 protein, humanProteinsTumor Suppressor ProteinsacetaldehydeCRISPR screeningDNA repairethanolOVCA2

Identifiers

PMID31059574
PMCPMC6484886
OpenAlexW2911577807

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.