Evidence map›Paper›PMID 25378332›Full record

ArticleNucleic acids research2014

Aberrant transcriptional regulations in cancers: genome, transcriptome and epigenome analysis of lung adenocarcinoma cell lines.

Ayako Suzuki, Hideki Makinoshima, Hiroyuki Wakaguri, Hiroyasu Esumi, Sumio Sugano, Takashi Kohno, Katsuya Tsuchihara, Yutaka Suzuki

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

63 citing papers in PubMed, 120 citations in OpenAlex.

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3 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 1 country.

Ayako SuzukiDepartment of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan.
Hideki MakinoshimaDivision of TR, The Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Chiba, Japan.
Hiroyuki WakaguriDepartment of Computational Biology, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan.
Hiroyasu EsumiDivision of TR, The Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Chiba, Japan.
Sumio SuganoDepartment of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan.
Takashi KohnoDivision of Genome Biology, National Cancer Center Research Institute, Tokyo, Japan Division of TR, The Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Tokyo, Japan.
Katsuya TsuchiharaDivision of TR, The Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Chiba, Japan.
Yutaka SuzukiDepartment of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan Department of Computational Biology, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan ysuzuki@hgc.jp.
The University of Tokyo · JPChiba Cancer Center · JPJapan Clinical Cancer Research Organization · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Here we conducted an integrative multi-omics analysis to understand how cancers harbor various types of aberrations at the genomic, epigenomic and transcriptional levels. In order to elucidate biological relevance of the aberrations and their mutual relations, we performed whole-genome sequencing, RNA-Seq, bisulfite sequencing and ChIP-Seq of 26 lung adenocarcinoma cell lines. The collected multi-omics data allowed us to associate an average of 536 coding mutations and 13,573 mutations in promoter or enhancer regions with aberrant transcriptional regulations. We detected the 385 splice site mutations and 552 chromosomal rearrangements, representative cases of which were validated to cause aberrant transcripts. Averages of 61, 217, 3687 and 3112 mutations are located in the regulatory regions which showed differential DNA methylation, H3K4me3, H3K4me1 and H3K27ac marks, respectively. We detected distinct patterns of aberrations in transcriptional regulations depending on genes. We found that the irregular histone marks were characteristic to EGFR and CDKN1A, while a large genomic deletion and hyper-DNA methylation were most frequent for CDKN2A. We also used the multi-omics data to classify the cell lines regarding their hallmarks of carcinogenesis. Our datasets should provide a valuable foundation for biological interpretations of interlaced genomic and epigenomic aberrations.

Indexed as

Epigenesis, GeneticGene Expression Regulation, NeoplasticTranscriptomeAdenocarcinomaAdenocarcinoma of LungCell Line, TumorChromatin ImmunoprecipitationDNA MethylationGene Expression ProfilingGenome, HumanGenomicsHistonesHumansLung NeoplasmsMutationRNA Polymerase IIHistonesRNA Polymerase II

Identifiers

PMID25378332
PMCPMC4267666
OpenAlexW2083084802

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.