Evidence map›Paper›PMID 24170126›Full record

ArticleCancer research2013

YEATS4 is a novel oncogene amplified in non-small cell lung cancer that regulates the p53 pathway.

Larissa A Pikor, William W Lockwood, Kelsie L Thu, Emily A Vucic, Raj Chari, Adi F Gazdar, Stephen Lam, Wan L Lam

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

38 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  9. Article
  10. GAS41 promotes H2A.Z deposition through recognition of the N terminus of histone H3 by the YEATS domain.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Review
  12. Article
  13. Histone Readers and Their Roles in Cancer.Cancer treatment and research · 2023
    Article
  14. Article
  15. Review
  16. Review
  17. Article
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  19. Integrative Profiling of T790M-Negative EGFR-Mutated NSCLC Reveals Pervasive Lineage Transition and Therapeutic Opportunities.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
  20. 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

8 authors at 2 institutions in 1 country.

Larissa A PikorAuthors' Affiliations: Integrative Oncology, BC Cancer Research Center, Vancouver, BC, Canada; National Institutes of Health, Bethesda, Maryland; Department of Genetics, Harvard Medical School, Boston, Massachusetts; and Hamon Center of Therapeutics, University of Texas South Western, Dallas, Texas.
William W Lockwood
Kelsie L Thu
Emily A Vucic
Raj Chari
Adi F Gazdar
Stephen Lam
Wan L Lam
Harvard University · USNational Institutes of Health · US

Funding

CIHR 94867CIHR MOP 86731Intramural NIH HHS Z99 HG999999NCI NIH HHS U01CA0864021
6 · The paper itself

Abstract

Genetic analyses of lung cancer have helped found new treatments in this disease. We conducted an integrative analysis of gene expression and copy number in 261 non-small cell lung cancers (NSCLC) relative to matched normal tissues to define novel candidate oncogenes, identifying 12q13-15 and more specifically the YEATS4 gene as amplified and overexpressed in ~20% of the NSCLC cases examined. Overexpression of YEATS4 abrogated senescence in human bronchial epithelial cells. Conversely, RNAi-mediated attenuation of YEATS4 in human lung cancer cells reduced their proliferation and tumor growth, impairing colony formation and inducing cellular senescence. These effects were associated with increased levels of p21WAF1 and p53 and cleavage of PARP, implicating YEATS4 as a negative regulator of the p21-p53 pathway. We also found that YEATS4 expression affected cellular responses to cisplastin, with increased levels associated with resistance and decreased levels with sensitivity. Taken together, our findings reveal YEATS4 as a candidate oncogene amplified in NSCLC, and a novel mechanism contributing to NSCLC pathogenesis.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCell Growth ProcessesCyclin-Dependent Kinase Inhibitor p21Gene AmplificationGene Expression ProfilingHeterograftsHumansLung NeoplasmsMiceMice, Inbred NODMice, SCIDNucleic Acid HybridizationTranscription FactorsTransfectionTumor Suppressor Protein p53CDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21TP53 protein, humanTranscription FactorsTumor Suppressor Protein p53YEATS4 protein, human

Identifiers

PMID24170126
PMCPMC3959870
OpenAlexW2143923333

What OpenQuestion holds

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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.