Evidence map›Paper›PMID 33759347›Full record

ArticleMolecular oncology2021

Detection of phenotype-specific therapeutic vulnerabilities in breast cells using a CRISPR loss-of-function screen.

Anna Barkovskaya, Craig M Goodwin, Kotryna Seip, Bylgja Hilmarsdottir, Solveig Pettersen, Clint Stalnecker, Olav Engebraaten, Eirikur Briem, Channing J Der, Siver A Moestue and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. 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

13 authors at 4 institutions in 3 countries.

Anna BarkovskayaDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, Oslo, Norway.ORCID 0000-0001-9465-9444
Craig M GoodwinLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, NC, USA.
Kotryna SeipDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, Oslo, Norway.
Bylgja HilmarsdottirDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, Oslo, Norway.
Solveig PettersenDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, Oslo, Norway.
Clint StalneckerLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, NC, USA.
Olav EngebraatenDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, Oslo, Norway.
Eirikur BriemBiomedical Center, School of Health Sciences, University of Iceland, Reykjavik, Iceland.
Channing J DerLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, NC, USA.
Siver A MoestueDepartment of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway.ORCID 0000-0002-1940-5695
Thorarinn GudjonssonBiomedical Center, School of Health Sciences, University of Iceland, Reykjavik, Iceland.
Gunhild M MaelandsmoDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, Oslo, Norway.ORCID 0000-0002-4797-1600
Lina PrasmickaiteDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, Oslo, Norway.ORCID 0000-0002-8358-7964
Oslo University Hospital · NOReykjavík University · ISUniversity of North Carolina at Chapel Hill · USNorwegian University of Science and Technology · NO

Funding

Integrated Training in Cancer Model SystemsT32CA009156 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 1985 to 2020
$19.7M
Targeting undruggable RAS for cancer treatmentR35CA232113 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 2018 to 2024
$6.3M
Targeting CDK4/6 for pancreatic cancer treatmentF32CA221005 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI GOODWIN, CRAIG · 2017 to 2018
$116k
NCI NIH HHS F32 CA221005NCI NIH HHS R35 CA232113NCI NIH HHS T32 CA009156
6 · The paper itself

Abstract

Cellular phenotype plasticity between the epithelial and mesenchymal states has been linked to metastasis and heterogeneous responses to cancer therapy, and remains a challenge for the treatment of triple-negative breast cancer (TNBC). Here, we used isogenic human breast epithelial cell lines, D492 and D492M, representing the epithelial and mesenchymal phenotypes, respectively. We employed a CRISPR-Cas9 loss-of-function screen targeting a 2240-gene 'druggable genome' to identify phenotype-specific vulnerabilities. Cells with the epithelial phenotype were more vulnerable to the loss of genes related to EGFR-RAS-MAPK signaling, while the mesenchymal-like cells had increased sensitivity to knockout of G

Indexed as

CRISPR-Cas SystemsLoss of Function MutationPhenotypeAntineoplastic AgentsCell ProliferationDrug Screening Assays, AntitumorEpithelial-Mesenchymal TransitionEverolimusFemaleFluorouracilHumansSignal TransductionTriple Negative Breast NeoplasmsAntineoplastic AgentsEverolimusFluorouracilactionable targetsCRISPR knockout screenepithelial-mesenchymal transitionphenotype plasticitytherapeutic vulnerabilitiestriple-negative breast cancer

Identifiers

PMID33759347
PMCPMC8333781
OpenAlexW3138716029

What OpenQuestion holds

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Registered trials

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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.