Evidence map›Paper›PMID 34764293›Full record

ArticleNature communications2021

Discovery of putative tumor suppressors from CRISPR screens reveals rewired lipid metabolism in acute myeloid leukemia cells.

W Frank Lenoir, Micaela Morgado, Peter C DeWeirdt, Megan McLaughlin, Audrey L Griffith, Annabel K Sangree, Marissa N Feeley, Nazanin Esmaeili Anvar, Eiru Kim, Lori L Bertolet and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  9. Optimal methods for analyzing targeted pairwise knockout screens.bioRxiv : the preprint server for biology · 2024
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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

14 authors at 2 institutions in 1 country.

W Frank LenoirThe University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences; The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID http://orcid.org/0000-0002-7413-1885
Micaela MorgadoDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Peter C DeWeirdtGenetic Perturbation Platform, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Megan McLaughlinThe University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences; The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID http://orcid.org/0000-0002-9971-0111
Audrey L GriffithGenetic Perturbation Platform, Broad Institute of MIT and Harvard, Cambridge, MA, USA.ORCID http://orcid.org/0000-0001-5552-2939
Annabel K SangreeGenetic Perturbation Platform, Broad Institute of MIT and Harvard, Cambridge, MA, USA.ORCID http://orcid.org/0000-0002-0298-1856
Marissa N FeeleyGenetic Perturbation Platform, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Nazanin Esmaeili AnvarThe University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences; The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Eiru KimDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Lori L BertoletDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Medina ColicThe University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences; The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID http://orcid.org/0000-0003-1442-1589
Merve DedeThe University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences; The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
John G DoenchGenetic Perturbation Platform, Broad Institute of MIT and Harvard, Cambridge, MA, USA.ORCID http://orcid.org/0000-0002-3707-9889
Traver HartDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. traver@hart-lab.org.ORCID http://orcid.org/0000-0002-1880-3341
The University of Texas MD Anderson Cancer Center · USBroad Institute · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
High-content microscopy platform for multiplex perturbation/multiplex readout studiesR35GM130119 · NIGMS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Traver Hart · 2018 to 2026
$3.9M
NCI NIH HHS P30 CA016672NIGMS NIH HHS R35 GM130119
6 · The paper itself

Abstract

CRISPR knockout fitness screens in cancer cell lines reveal many genes whose loss of function causes cell death or loss of fitness or, more rarely, the opposite phenotype of faster proliferation. Here we demonstrate a systematic approach to identify these proliferation suppressors, which are highly enriched for tumor suppressor genes, and define a network of 145 such genes in 22 modules. One module contains several elements of the glycerolipid biosynthesis pathway and operates exclusively in a subset of acute myeloid leukemia cell lines. The proliferation suppressor activity of genes involved in the synthesis of saturated fatty acids, coupled with a more severe loss of fitness phenotype for genes in the desaturation pathway, suggests that these cells operate at the limit of their carrying capacity for saturated fatty acids, which we confirm biochemically. Overexpression of this module is associated with a survival advantage in juvenile leukemias, suggesting a clinically relevant subtype.

Indexed as

Bacterial ProteinsClustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Associated ProteinsCyclin-Dependent Kinase Inhibitor p21EndodeoxyribonucleasesHumansLeukemia, Myeloid, AcuteLipid MetabolismTumor Suppressor p53-Binding Protein 1Tumor Suppressor Protein p53Bacterial ProteinsCas12a proteinCRISPR-Associated ProteinsCyclin-Dependent Kinase Inhibitor p21EndodeoxyribonucleasesTP53 protein, humanTumor Suppressor p53-Binding Protein 1Tumor Suppressor Protein p53

Identifiers

PMID34764293
PMCPMC8586352
OpenAlexW3214474849

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.