Evidence map›Paper›PMID 29976574›Full record

ArticleCancer research2018

Replication Stress Drives Constitutive Activation of the DNA Damage Response and Radioresistance in Glioblastoma Stem-like Cells.

Ross D Carruthers, Shafiq U Ahmed, Shaliny Ramachandran, Karen Strathdee, Kathreena M Kurian, Ann Hedley, Natividad Gomez-Roman, Gabriela Kalna, Mathew Neilson, Lesley Gilmour and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 185 citations in OpenAlex.

  1. Review
  2. NAT10-dependent NCell reports · 2026
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  19. Poly-ADP-ribosylation dynamics, signaling, and analysis.Environmental and molecular mutagenesis · 2024
    Review
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44 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 2 countries.

Ross D Carruthers *Institute of Cancer Sciences, Wolfson Wohl Cancer Research Centre, University of Glasgow, Glasgow, United Kingdom. ross.carruthers@glasgow.ac.uk.
Shafiq U Ahmed *School of Pharmacy and Pharmaceutical Sciences, Faculty of Health Sciences and Wellbeing, University of Sunderland, Sunderland, United Kingdom.
Shaliny RamachandranCancer Research UK/MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, Oxford, United Kingdom.
Karen StrathdeeInstitute of Cancer Sciences, Wolfson Wohl Cancer Research Centre, University of Glasgow, Glasgow, United Kingdom.
Kathreena M KurianDepartment of Neuropathology, Brain Tumour Research Group, Frenchay Hospital, North Bristol NHS Trust Bristol, Bristol, United Kingdom.
Ann HedleyCancer Research UK Beatson Institute, Glasgow, United Kingdom.
Natividad Gomez-RomanInstitute of Cancer Sciences, Wolfson Wohl Cancer Research Centre, University of Glasgow, Glasgow, United Kingdom.
Gabriela KalnaCancer Research UK Beatson Institute, Glasgow, United Kingdom.
Mathew NeilsonCancer Research UK Beatson Institute, Glasgow, United Kingdom.
Lesley GilmourInstitute of Cancer Sciences, Wolfson Wohl Cancer Research Centre, University of Glasgow, Glasgow, United Kingdom.
Katrina H StevensonInstitute of Cancer Sciences, Wolfson Wohl Cancer Research Centre, University of Glasgow, Glasgow, United Kingdom.
Ester M HammondCancer Research UK/MRC Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, Oxford, United Kingdom.
Anthony J ChalmersInstitute of Cancer Sciences, Wolfson Wohl Cancer Research Centre, University of Glasgow, Glasgow, United Kingdom.
Cancer Research UK Scotland Institute · GBUniversity of Sunderland · GB

Funding

Cancer Research UK 19276Cancer Research UK 23920Cancer Research UK C5255/A23755Medical Research Council G0802755
6 · The paper itself

Abstract

Glioblastoma (GBM) is a lethal primary brain tumor characterized by treatment resistance and inevitable tumor recurrence, both of which are driven by a subpopulation of GBM cancer stem-like cells (GSC) with tumorigenic and self-renewal properties. Despite having broad implications for understanding GSC phenotype, the determinants of upregulated DNA-damage response (DDR) and subsequent radiation resistance in GSC are unknown and represent a significant barrier to developing effective GBM treatments. In this study, we show that constitutive DDR activation and radiation resistance are driven by high levels of DNA replication stress (RS). CD133

Indexed as

CarcinogenesisNeoplastic Stem CellsAC133 AntigenAtaxia Telangiectasia Mutated ProteinsCell Line, TumorDNA Breaks, Double-StrandedDNA DamageDNA ReplicationGlioblastomaHumansNeoplasm Recurrence, LocalPhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsRadiation ToleranceAC133 AntigenAtaxia Telangiectasia Mutated ProteinsATR protein, humanolaparibPhthalazinesPiperazinesPoly(ADP-ribose) Polymerase Inhibitors

Identifiers

PMID29976574
PMCPMC6128404
OpenAlexW2838310729

What OpenQuestion holds

Textmetadata
LicenceTDM
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.