Evidence map›Paper›PMID 27308313›Full record

ReviewMolecular & cellular oncology2014

ATM activation in hypoxia - causes and consequences.

Monica M Olcina, Roger Ja Grand, Ester M Hammond

Open access · hybridAbstract readReview
In one paragraph

Review in Molecular & cellular oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

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  10. Tumor microenvironment and radioresistance.Experimental & molecular medicine · 2021
    Review
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  15. Review
  16. Modeling tumor cell adaptations to hypoxia in multicellular tumor spheroids.Journal of experimental & clinical cancer research : CR · 2017
    Review
  17. Article
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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 3 institutions in 1 country.

Monica M OlcinaCancer Research UK/MRC Oxford Institute for Radiation Oncology; Department of Oncology; University of Oxford; Oxford, UK.
Roger Ja GrandSchool of Cancer Sciences; College of Medical and Dental Sciences; University of Birmingham; Birmingham, UK.
Ester M HammondCancer Research UK/MRC Oxford Institute for Radiation Oncology; Department of Oncology; University of Oxford; Oxford, UK.
Birmingham Dental Hospital · GBCancer Research UK · GBUniversity of Oxford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The DNA damage response is a complex signaling cascade that is triggered by cellular stress. This response is essential for the maintenance of genomic integrity and is considered to act as a barrier to the early stages of tumorigenesis. The integral role of ataxia telangiectasia mutated (ATM) kinase in the response to DNA damaging agents is well characterized; however, ATM can also be activated by non-DNA damaging agents. In fact, much has been learnt recently about the mechanism of ATM activation in response to physiologic stresses such as hypoxia that do not induce DNA damage. Regions of low oxygen concentrations that occur in solid tumors are associated with a poor prognostic outcome irrespective of treatment modality. Severe levels of hypoxia induce replication stress and trigger the activation of DNA damage response pathways including ataxia telangiectasia and Rad3-related (ATR)- and ATM-mediated signaling. In this review, we discuss hypoxia-driven ATM signaling and the possible contribution of ATM activation in this context to tumorigenesis.

Indexed as

ATMChromatin,DNA damage,HypoxiaReplication

Identifiers

PMID27308313
PMCPMC4905164
OpenAlexW1989064865

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.