Evidence map›Paper›PMID 24968221›Full record

ArticlePloS one2014

Altered mitochondrial function and energy metabolism is associated with a radioresistant phenotype in oesophageal adenocarcinoma.

Niamh Lynam-Lennon, Stephen G Maher, Aoife Maguire, James Phelan, Cian Muldoon, John V Reynolds, Jacintha O'Sullivan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 93 citations in OpenAlex.

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  10. Mitophagy plays a "double-edged sword" role in the radiosensitivity of cancer cells.Journal of cancer research and clinical oncology · 2024
    Review
  11. Article
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  14. Energy Metabolism Is Altered in Radioresistant Rectal Cancer.International journal of molecular sciences · 2023
    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

7 authors at 3 institutions in 2 countries.

Niamh Lynam-LennonDepartment of Surgery, Trinity College Dublin, Dublin, Ireland.
Stephen G MaherDepartment of Surgery, Trinity College Dublin, Dublin, Ireland; Cancer Biology and Therapeutics Lab, School of Biological, Biomedical and Environmental Sciences, University of Hull, Hull, United Kingdom.
Aoife MaguireDepartment of Pathology, St James's Hospital, Dublin, Ireland.
James PhelanDepartment of Surgery, Trinity College Dublin, Dublin, Ireland.
Cian MuldoonDepartment of Pathology, St James's Hospital, Dublin, Ireland.
John V ReynoldsDepartment of Surgery, Trinity College Dublin, Dublin, Ireland.
Jacintha O'SullivanDepartment of Surgery, Trinity College Dublin, Dublin, Ireland.
Trinity College Dublin · IESt. James's Hospital · IEUniversity of Hull · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neoadjuvant chemoradiation therapy (CRT) is increasingly the standard of care for locally advanced oesophageal cancer. A complete pathological response to CRT is associated with a favourable outcome. Radiation therapy is important for local tumour control, however, radioresistance remains a substantial clinical problem. We hypothesise that alterations in mitochondrial function and energy metabolism are involved in the radioresistance of oesophageal adenocarcinoma (OAC). To investigate this, we used an established isogenic cell line model of radioresistant OAC. Radioresistant cells (OE33 R) demonstrated significantly increased levels of random mitochondrial mutations, which were coupled with alterations in mitochondrial function, size, morphology and gene expression, supporting a role for mitochondrial dysfunction in the radioresistance of this model. OE33 R cells also demonstrated altered bioenergetics, demonstrating significantly increased intracellular ATP levels, which was attributed to enhanced mitochondrial respiration. Radioresistant cells also demonstrated metabolic plasticity, efficiently switching between the glycolysis and oxidative phosphorylation energy metabolism pathways, which were accompanied by enhanced clonogenic survival. This data was supported in vivo, in pre-treatment OAC tumour tissue. Tumour ATP5B expression, a marker of oxidative phosphorylation, was significantly increased in patients who subsequently had a poor pathological response to neoadjuvant CRT. This suggests for the first time, a role for specific mitochondrial alterations and metabolic remodelling in the radioresistance of OAC.

Indexed as

Radiation ToleranceAdenocarcinomaAdultAgedCell Line, TumorChemoradiotherapy, AdjuvantEnergy MetabolismEsophageal NeoplasmsFemaleHumansMaleMiddle AgedMitochondriaMitochondrial SizeMutagenesisTreatment Outcome

Identifiers

PMID24968221
PMCPMC4072695
OpenAlexW1983925309

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.