Evidence map›Paper›PMID 28167502›Full record

ArticleGenes & development2017

A genetic interaction analysis identifies cancer drivers that modify EGFR dependency.

Sida Liao, Teresa Davoli, Yumei Leng, Mamie Z Li, Qikai Xu, Stephen J Elledge

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing 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

49 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. CBX5 loss drives EGFR inhibitor resistance and results in therapeutically actionable vulnerabilities in lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Genetic analysis of cancer drivers reveals cohesin and CTCF as suppressors of PD-L1.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  20. Review
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

6 authors at 2 institutions in 1 country.

Sida LiaoDivision of Genetics, Department of Medicine, Brigham and Women's Hospital, Department of Genetics, Program in Virology, Howard Hughes Medical Institute, Harvard University Medical School, Boston, Massachusetts 02115, USA.
Teresa DavoliDivision of Genetics, Department of Medicine, Brigham and Women's Hospital, Department of Genetics, Program in Virology, Howard Hughes Medical Institute, Harvard University Medical School, Boston, Massachusetts 02115, USA.
Yumei LengDivision of Genetics, Department of Medicine, Brigham and Women's Hospital, Department of Genetics, Program in Virology, Howard Hughes Medical Institute, Harvard University Medical School, Boston, Massachusetts 02115, USA.
Mamie Z LiDivision of Genetics, Department of Medicine, Brigham and Women's Hospital, Department of Genetics, Program in Virology, Howard Hughes Medical Institute, Harvard University Medical School, Boston, Massachusetts 02115, USA.
Qikai XuDivision of Genetics, Department of Medicine, Brigham and Women's Hospital, Department of Genetics, Program in Virology, Howard Hughes Medical Institute, Harvard University Medical School, Boston, Massachusetts 02115, USA.
Stephen J ElledgeDivision of Genetics, Department of Medicine, Brigham and Women's Hospital, Department of Genetics, Program in Virology, Howard Hughes Medical Institute, Harvard University Medical School, Boston, Massachusetts 02115, USA.
Harvard University · USHoward Hughes Medical Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A large number of cancer drivers have been identified through tumor sequencing efforts, but how they interact and the degree to which they can substitute for each other have not been systematically explored. To comprehensively investigate how cancer drivers genetically interact, we searched for modifiers of epidermal growth factor receptor (EGFR) dependency by performing CRISPR, shRNA, and expression screens in a non-small cell lung cancer (NSCLC) model. We elucidated a broad spectrum of tumor suppressor genes (TSGs) and oncogenes (OGs) that can genetically modify proliferation and survival of cancer cells when EGFR signaling is altered. These include genes already known to mediate EGFR inhibitor resistance as well as many TSGs not previously connected to EGFR and whose biological functions in tumorigenesis are not well understood. We show that mutation of

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinomaAdenocarcinoma of LungAntineoplastic AgentsCell Line, TumorDNA-Binding ProteinsDrug Resistance, NeoplasmEnzyme ActivationErbB ReceptorsGefitinibHEK293 CellsHumansLung NeoplasmsNuclear ProteinsOncogene Protein v-aktQuinazolinesAntineoplastic AgentsDNA-Binding ProteinsErbB ReceptorsGefitinibNuclear ProteinsOncogene Protein v-aktPBRM1 protein, humanQuinazolinesRepressor ProteinsTranscription Factorscancer driversEGFRgenetic interaction

Identifiers

PMID28167502
PMCPMC5322732
OpenAlexW2586070849

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.