Evidence map›Paper›PMID 30332653›Full record

ArticleCell reports2018

The p38α Stress Kinase Suppresses Aneuploidy Tolerance by Inhibiting Hif-1α.

Susana Simões-Sousa, Samantha Littler, Sarah L Thompson, Paul Minshall, Helen Whalley, Bjorn Bakker, Klaudyna Belkot, Daniela Moralli, Daniel Bronder, Anthony Tighe and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. AScience signaling · 2026
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  5. Use of Radiomics in Characterizing Tumor Hypoxia.International journal of molecular sciences · 2025
    Review
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  10. The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024
    Review
  11. Permission to pass: on the role of p53 as a gatekeeper for aneuploidy.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023
    Review
  12. Article
  13. Whole-Genome Doubling as a source of cancer: how, when, where, and why?Frontiers in cell and developmental biology · 2023
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

18 authors at 6 institutions in 2 countries.

Susana Simões-SousaDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Cancer Research Centre, Wilmslow Road, Manchester M20 4QL, UK.
Samantha LittlerDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Cancer Research Centre, Wilmslow Road, Manchester M20 4QL, UK.
Sarah L ThompsonDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Cancer Research Centre, Wilmslow Road, Manchester M20 4QL, UK.
Paul MinshallDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Cancer Research Centre, Wilmslow Road, Manchester M20 4QL, UK.
Helen WhalleyDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Cancer Research Centre, Wilmslow Road, Manchester M20 4QL, UK.
Bjorn BakkerEuropean Research Institute for the Biology of Ageing (ERIBA), University of Groningen, University Medical Center Groningen, 9713 AV Groningen, the Netherlands.
Klaudyna BelkotDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Cancer Research Centre, Wilmslow Road, Manchester M20 4QL, UK.
Daniela MoralliWellcome Centre Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, UK.
Daniel BronderDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Cancer Research Centre, Wilmslow Road, Manchester M20 4QL, UK.
Anthony TigheDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Cancer Research Centre, Wilmslow Road, Manchester M20 4QL, UK.
Diana C J SpieringsEuropean Research Institute for the Biology of Ageing (ERIBA), University of Groningen, University Medical Center Groningen, 9713 AV Groningen, the Netherlands.
Nourdine BahDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Cancer Research Centre, Wilmslow Road, Manchester M20 4QL, UK.
Joshua GrahamDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Cancer Research Centre, Wilmslow Road, Manchester M20 4QL, UK.
Louisa NelsonDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Cancer Research Centre, Wilmslow Road, Manchester M20 4QL, UK.
Catherine M GreenWellcome Centre Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, UK.
Floris FoijerEuropean Research Institute for the Biology of Ageing (ERIBA), University of Groningen, University Medical Center Groningen, 9713 AV Groningen, the Netherlands.
Paul A TownsendDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Cancer Research Centre, Wilmslow Road, Manchester M20 4QL, UK.
Stephen S TaylorDivision of Cancer Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Cancer Research Centre, Wilmslow Road, Manchester M20 4QL, UK. Electronic address: stephen.taylor@manchester.ac.uk.
Cancer Research UK Manchester CentreUniversity of Manchester · GBUniversity of Groningen · NLCentre for Human Genetics · GBUniversity Medical Center Groningen · NLUniversity of Oxford · GB

Funding

Cancer Research UK 11913Cancer Research UK 19842Medical Research Council MR/L006839/1Wellcome Trust 203141
6 · The paper itself

Abstract

Deviating from the normal karyotype dramatically changes gene dosage, in turn decreasing the robustness of biological networks. Consequently, aneuploidy is poorly tolerated by normal somatic cells and acts as a barrier to transformation. Paradoxically, however, karyotype heterogeneity drives tumor evolution and the emergence of therapeutic drug resistance. To better understand how cancer cells tolerate aneuploidy, we focused on the p38 stress response kinase. We show here that p38-deficient cells upregulate glycolysis and avoid post-mitotic apoptosis, leading to the emergence of aneuploid subclones. We also show that p38 deficiency upregulates the hypoxia-inducible transcription factor Hif-1α and that inhibiting Hif-1α restores apoptosis in p38-deficent cells. Because hypoxia and aneuploidy are both barriers to tumor progression, the ability of Hif-1α to promote cell survival following chromosome missegregation raises the possibility that aneuploidy tolerance coevolves with adaptation to hypoxia.

Indexed as

AneuploidyApoptosisHypoxiaChromosomes, HumanColonic NeoplasmsCRISPR-Cas SystemsGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitMitogen-Activated Protein Kinase 14Signal TransductionTumor Cells, CulturedHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMitogen-Activated Protein Kinase 14aneuploidychromosome instabilitymitosis

Identifiers

PMID30332653
PMCPMC6205844
OpenAlexW2896800728

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.