Evidence map›Paper›PMID 35740268›Full record

ArticleBiomedicines2022

Oxidative Stress and Deregulated DNA Damage Response Network in Lung Cancer Patients.

Dimitra T Stefanou, Marousa Kouvela, Dimitris Stellas, Konstantinos Voutetakis, Olga Papadodima, Konstantinos Syrigos, Vassilis L Souliotis

Open access · goldAbstract read
In one paragraph

Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

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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 2 institutions in 1 country.

Dimitra T StefanouFirst Department of Medicine, Laiko General Hospital, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece.
Marousa KouvelaOncology Unit, Third Department of Medicine, Sotiria General Hospital, School of Medicine, University of Athens, 11527 Athens, Greece.ORCID 0000-0003-3002-9851
Dimitris StellasInstitute of Chemical Biology, National Hellenic Research Foundation, 11635 Athens, Greece.ORCID 0000-0002-7787-3921
Konstantinos VoutetakisInstitute of Chemical Biology, National Hellenic Research Foundation, 11635 Athens, Greece.ORCID 0000-0001-7163-7381
Olga PapadodimaInstitute of Chemical Biology, National Hellenic Research Foundation, 11635 Athens, Greece.ORCID 0000-0003-3896-4270
Konstantinos SyrigosOncology Unit, Third Department of Medicine, Sotiria General Hospital, School of Medicine, University of Athens, 11527 Athens, Greece.
Vassilis L SouliotisInstitute of Chemical Biology, National Hellenic Research Foundation, 11635 Athens, Greece.ORCID 0000-0002-2945-1329
National Hellenic Research Foundation · GRNational and Kapodistrian University of Athens · GR

Funding

Hellenic Society of Medical Oncology (HeSMO) 8177/10-02-2021
6 · The paper itself

Abstract

The deregulated DNA damage response (DDR) network is associated with the onset and progression of cancer. Herein, we searched for DDR defects in peripheral blood mononuclear cells (PBMCs) from lung cancer patients, and we evaluated factors leading to the augmented formation of DNA damage and/or its delayed/decreased removal. In PBMCs from 20 lung cancer patients at diagnosis and 20 healthy controls (HC), we analyzed oxidative stress and DDR-related parameters, including critical DNA repair mechanisms and apoptosis rates. Cancer patients showed higher levels of endogenous DNA damage than HC (p < 0.001), indicating accumulation of DNA damage in the absence of known exogenous genotoxic insults. Higher levels of oxidative stress and apurinic/apyrimidinic sites were observed in patients rather than HC (all p < 0.001), suggesting that increased endogenous DNA damage may emerge, at least in part, from these intracellular factors. Lower nucleotide excision repair and double-strand break repair capacities were found in patients rather than HC (all p < 0.001), suggesting that the accumulation of DNA damage can also be mediated by defective DNA repair mechanisms. Interestingly, reduced apoptosis rates were obtained in cancer patients compared with HC (p < 0.001). Consequently, the expression of critical DDR-associated genes was found deregulated in cancer patients. Together, oxidative stress and DDR-related aberrations contribute to the accumulation of endogenous DNA damage in PBMCs from lung cancer patients and can potentially be exploited as novel therapeutic targets and non-invasive biomarkers.

Indexed as

apoptosis ratesDNA damage responsedouble-strand breaks repairendogenous DNA damagelung cancernucleotide excision repairoxidative stress

Identifiers

PMID35740268
PMCPMC9219789
OpenAlexW4281557267

What Socratic holds

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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 Socratic graph.