Evidence map›Paper›PMID 26601720›Full record

ArticleMolecular oncology2016

Genome-wide DNA methylation analyses in lung adenocarcinomas: Association with EGFR, KRAS and TP53 mutation status, gene expression and prognosis.

Maria Moksnes Bjaanæs, Thomas Fleischer, Ann Rita Halvorsen, Antoine Daunay, Florence Busato, Steinar Solberg, Lars Jørgensen, Elin Kure, Hege Edvardsen, Anne-Lise Børresen-Dale and 4 more

Abstract read
In one paragraph

Article in Molecular oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

60 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  14. Smoking, blood DNA methylation sites and lung cancer risk.Environmental pollution (Barking, Essex : 1987) · 2023
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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

14 authors.

Maria Moksnes BjaanæsDepartment of Genetics, Institute for Cancer Research, Oslo University Hospital - The Norwegian Radium Hospital, Oslo, Norway; Department of Oncology, Oslo University Hospital - The Norwegian Radium Hospital, Oslo, Norway. Electronic address: mamok@rr-research.no.
Thomas FleischerDepartment of Genetics, Institute for Cancer Research, Oslo University Hospital - The Norwegian Radium Hospital, Oslo, Norway; The K.G. Jebsen Censtre for Breast Cancer Research, Institute for Clinical Medicine, Faculty of Medicine, University of Oslo, Norway. Electronic address: thomas.fleischer@rr-research.no.
Ann Rita HalvorsenDepartment of Genetics, Institute for Cancer Research, Oslo University Hospital - The Norwegian Radium Hospital, Oslo, Norway. Electronic address: Ann.Rita.Halvorsen@rr-research.no.
Antoine DaunayLaboratory for Functional Genomics, Fondation Jean Dausset - CEPH, 75010 Paris, France. Electronic address: antoine.daunay@cephb.fr.
Florence BusatoLaboratory for Epigenetics and Environment (LEE), Centre National de Génotypage, CEA - Institut de Génomique, 91000 Evry, France. Electronic address: busato@cng.fr.
Steinar SolbergDepartment of Cardiothoracic Surgery, Oslo University Hospital-Rikshospitalet, Oslo, Norway. Electronic address: Steinar.Solberg@oslo-universitetssykehus.no.
Lars JørgensenDepartment of Cardiothoracic Surgery, Oslo University Hospital-Rikshospitalet, Oslo, Norway. Electronic address: Lars.Jorgensen@oslo-universitetssykehus.no.
Elin KureDepartment of Genetics, Institute for Cancer Research, Oslo University Hospital - The Norwegian Radium Hospital, Oslo, Norway. Electronic address: Elin.Kure@rr-research.no.
Hege EdvardsenDepartment of Genetics, Institute for Cancer Research, Oslo University Hospital - The Norwegian Radium Hospital, Oslo, Norway. Electronic address: hege.edvardsen@abbvie.com.
Anne-Lise Børresen-DaleDepartment of Genetics, Institute for Cancer Research, Oslo University Hospital - The Norwegian Radium Hospital, Oslo, Norway; Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Norway. Electronic address: a.l.borresen-dale@medisin.uio.no.
Odd Terje BrustugunDepartment of Genetics, Institute for Cancer Research, Oslo University Hospital - The Norwegian Radium Hospital, Oslo, Norway; Department of Oncology, Oslo University Hospital - The Norwegian Radium Hospital, Oslo, Norway. Electronic address: ot.brustugun@gmail.com.
Jörg TostLaboratory for Epigenetics and Environment (LEE), Centre National de Génotypage, CEA - Institut de Génomique, 91000 Evry, France. Electronic address: tost@cng.fr.
Vessela KristensenDepartment of Genetics, Institute for Cancer Research, Oslo University Hospital - The Norwegian Radium Hospital, Oslo, Norway; The K.G. Jebsen Censtre for Breast Cancer Research, Institute for Clinical Medicine, Faculty of Medicine, University of Oslo, Norway; Department of Clinical Molecular Biology and Laboratory Science (EpiGen), Division of Medicine, Akershus University Hospital, Lørenskog, Norway. Electronic address: v.n.kristensen@medisin.uio.no.
Åslaug HellandDepartment of Genetics, Institute for Cancer Research, Oslo University Hospital - The Norwegian Radium Hospital, Oslo, Norway; Department of Oncology, Oslo University Hospital - The Norwegian Radium Hospital, Oslo, Norway. Electronic address: aslaug.helland@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDNA methylation alterations are early events in tumorigenesis and important in the regulation of gene expression in cancer cells. Lung cancer patients have in general a poor prognosis, and a deeper insight into the epigenetic landscape in lung adenocarcinoma tumors and its prognostic implications is needed.

resultsWe determined whole-genome DNA methylation profiles of 164 fresh frozen lung adenocarcinoma samples and 19 samples of matched normal lung tissue using the Illumina Infinium 450K array. A large number of differentially methylated CpGs in lung adenocarcinoma tissue were identified, and specific methylation profiles were observed in tumors with mutations in the EGFR-, KRAS- or TP53 genes and according to the patients' smoking status. The methylation levels were correlated with gene expression and both positive and negative correlations were seen. Methylation profiles of the tumor samples identified subtypes of tumors with distinct prognosis, including one subtype enriched for TP53 mutant tumors. A prognostic index based on the methylation levels of 33 CpGs was established, and was significantly associated with prognosis in the univariate analysis using an independent cohort of lung adenocarcinoma patients from The Cancer Genome Atlas project. CpGs in the HOX B and HOX C gene clusters were represented in the prognostic signature.

conclusionsMethylation differences mirror biologically important features in the etiology of lung adenocarcinomas and influence prognosis.

Indexed as

DNA MethylationAdenocarcinomaAdenocarcinoma of LungAdultAgedAged, 80 and overCohort StudiesCpG IslandsErbB ReceptorsFemaleGene Expression Regulation, NeoplasticGenes, HomeoboxGenome, HumanHumansLung NeoplasmsMaleEGFR protein, humanErbB ReceptorsKRAS protein, humanMTOR protein, humanProto-Oncogene Proteins p21(ras)RNA, MessengerTOR Serine-Threonine KinasesTP53 protein, humanTumor Suppressor Protein p53450KAdenocarcinomaCpGDNA methylationEGFRKRASLUADLung cancermRNANSCLCPrognosisTP53

Identifiers

PMID26601720
PMCPMC5528958

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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.