Evidence map›Paper›PMID 30606699›Full record

ArticleEBioMedicine2019

Characterization of heterogeneous redox responses in hepatocellular carcinoma patients using network analysis.

Rui Benfeitas, Gholamreza Bidkhori, Bani Mukhopadhyay, Martina Klevstig, Muhammad Arif, Cheng Zhang, Sunjae Lee, Resat Cinar, Jens Nielsen, Mathias Uhlen and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 46 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

13 authors at 5 institutions in 3 countries.

Rui BenfeitasScience for Life Laboratory, KTH - Royal Institute of Technology, SE-171 21 Stockholm, Sweden. Electronic address: rui.benfeitas@scilifelab.se.
Gholamreza BidkhoriScience for Life Laboratory, KTH - Royal Institute of Technology, SE-171 21 Stockholm, Sweden. Electronic address: gholamreza.bidkhori@scilifelab.se.
Bani MukhopadhyayLaboratory of Physiologic Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA. Electronic address: mukhopadhyayb@mail.nih.gov.
Martina KlevstigDepartment of Molecular and Clinical Medicine, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden. Electronic address: martina.klevstig@wlab.gu.se.
Muhammad ArifScience for Life Laboratory, KTH - Royal Institute of Technology, SE-171 21 Stockholm, Sweden. Electronic address: muhammad.arif@scilifelab.se.
Cheng ZhangScience for Life Laboratory, KTH - Royal Institute of Technology, SE-171 21 Stockholm, Sweden. Electronic address: cheng.zhang@scilifelab.se.
Sunjae LeeScience for Life Laboratory, KTH - Royal Institute of Technology, SE-171 21 Stockholm, Sweden. Electronic address: sunjae.lee@scilifelab.se.
Resat CinarLaboratory of Physiologic Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA. Electronic address: resat.cinar@nih.gov.
Jens NielsenDepartment of Biology and Biological Engineering, Chalmers University of Technology, Gothenburg, Sweden. Electronic address: nielsenj@chalmers.se.
Mathias UhlenScience for Life Laboratory, KTH - Royal Institute of Technology, SE-171 21 Stockholm, Sweden. Electronic address: mathias.uhlen@scilifelab.se.
Jan BorenDepartment of Molecular and Clinical Medicine, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden. Electronic address: jan.boren@wlab.gu.se.
George KunosLaboratory of Physiologic Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA. Electronic address: george.kunos@nih.gov.
Adil MardinogluScience for Life Laboratory, KTH - Royal Institute of Technology, SE-171 21 Stockholm, Sweden; Department of Biology and Biological Engineering, Chalmers University of Technology, Gothenburg, Sweden; Centre for Host-Microbiome Interactions, Dental Institute, King's College London, London, UK. Electronic address: adilm@scilifelab.se.
Science for Life Laboratory · SENational Institutes of Health · USSahlgrenska University Hospital · SEChalmers University of Technology · SEKing's College London · GB

Funding

Endocannabinoids And Energy HomeostasisZIAAA000350 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI KUNOS, GEORGE · 2009 to 2025
$28.4M
6 · The paper itself

Abstract

backgroundRedox metabolism is often considered a potential target for cancer treatment, but a systematic examination of redox responses in hepatocellular carcinoma (HCC) is missing.

methodsHere, we employed systems biology and biological network analyses to reveal key roles of genes associated with redox metabolism in HCC by integrating multi-omics data.

findingsWe found that several redox genes, including 25 novel potential prognostic genes, are significantly co-expressed with liver-specific genes and genes associated with immunity and inflammation. Based on an integrative analysis, we found that HCC tumors display antagonistic behaviors in redox responses. The two HCC groups are associated with altered fatty acid, amino acid, drug and hormone metabolism, differentiation, proliferation, and NADPH-independent vs -dependent antioxidant defenses. Redox behavior varies with known tumor subtypes and progression, affecting patient survival. These antagonistic responses are also displayed at the protein and metabolite level and were validated in several independent cohorts. We finally showed the differential redox behavior using mice transcriptomics in HCC and noncancerous tissues and associated with hypoxic features of the two redox gene groups.

interpretationOur integrative approaches highlighted mechanistic differences among tumors and allowed the identification of a survival signature and several potential therapeutic targets for the treatment of HCC.

Indexed as

Models, BiologicalOxidation-ReductionAlgorithmsBiomarkers, TumorCarcinoma, HepatocellularComputational BiologyDisease ProgressionGene Expression ProfilingGene Regulatory NetworksHumansLiver NeoplasmsMetabolic Networks and PathwaysMolecular Sequence AnnotationPrognosisReproducibility of ResultsSignal TransductionBiomarkers, TumorCancerHepatocellular carcinomaLiver cancerPrecision medicineRedox metabolismSystems biologyTranscriptomics

Identifiers

PMID30606699
PMCPMC6412169
OpenAlexW2907873857

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.