Evidence map›Paper›PMID 28649990›Full record

ArticleNature communications2017

A pan-cancer genome-wide analysis reveals tumour dependencies by induction of nonsense-mediated decay.

Zhiyuan Hu, Christopher Yau, Ahmed Ashour Ahmed

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

45 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Nonsense-mediated mRNA decay: friend or foe in cancer biology?Cell communication and signaling : CCS · 2026
    Review
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  4. Article
  5. Review
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  16. Cell cycle (Georgetown, Tex.) · 2023
    Article
  17. Article
  18. Article
  19. 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

3 authors at 2 institutions in 1 country.

Zhiyuan HuWeatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DU, UK.ORCID 0000-0002-1688-6032
Christopher YauWellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX3 7BN, UK.
Ahmed Ashour AhmedWeatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DU, UK.
Centre for Human Genetics · GBUniversity of Oxford · GB

Funding

Medical Research Council G0902418Medical Research Council MR/L001411/1Wellcome Trust
6 · The paper itself

Abstract

Nonsense-mediated decay (NMD) eliminates transcripts with premature termination codons. Although NMD-induced loss-of-function has been shown to contribute to the genesis of particular cancers, its global functional consequence in tumours has not been characterized. Here we develop an algorithm to predict NMD and apply it on somatic mutations reported in The Cancer Genome Atlas. We identify more than 73 K mutations that are predicted to elicit NMD (NMD-elicit). NMD-elicit mutations in tumour suppressor genes (TSGs) are associated with significant reduction in gene expression. We discover cancer-specific NMD-elicit signatures in TSGs and cancer-associated genes. Our analysis reveals a previously unrecognized dependence of hypermutated tumours on hypofunction of genes that are involved in chromatin remodelling and translation. Half of hypermutated stomach adenocarcinomas are associated with NMD-elicit mutations of the translation initiators LARP4B and EIF5B. Our results unravel strong therapeutic opportunities by targeting tumour dependencies on NMD-elicit mutations.

Indexed as

Nonsense Mediated mRNA DecayAlgorithmsAutoantigensCohort StudiesGenomeHumansMutationNeoplasmsRibonucleoproteinsRNA, MessengerSS-B AntigenAutoantigensRibonucleoproteinsRNA, MessengerSS-B Antigen

Identifiers

PMID28649990
PMCPMC5490262
OpenAlexW2668553901

What OpenQuestion holds

Textmetadata
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.