Evidence map›Paper›PMID 21364760›Full record

ArticlePloS one2011

Integrated analysis of gene expression, CpG island methylation, and gene copy number in breast cancer cells by deep sequencing.

Zhifu Sun, Yan W Asmann, Krishna R Kalari, Brian Bot, Jeanette E Eckel-Passow, Tiffany R Baker, Jennifer M Carr, Irina Khrebtukova, Shujun Luo, Lu Zhang and 3 more

Open access · goldAbstract readValidation Study
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
9.3field-weighted citation impact, top 1% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.

  1. Aberrant promoter methylation of HIN-1 gene may contribute to the pathogenesis of breast cancer: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Pooled it
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  7. 5'isomiR-183-5p|+2 elicits tumor suppressor activity in a negative feedback loop with E2F1.Journal of experimental & clinical cancer research : CR · 2022
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  15. Epigenetic upregulation of FKBP5 by aging and stress contributes to NF-κB-driven inflammation and cardiovascular risk.Proceedings of the National Academy of Sciences of the United States of America · 2019
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23 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

13 authors at 6 institutions in 1 country.

Zhifu SunDivision of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic College of Medicine, Rochester, Minnesota, United States of America.
Yan W Asmann
Krishna R Kalari
Brian Bot
Jeanette E Eckel-Passow
Tiffany R Baker
Jennifer M Carr
Irina Khrebtukova
Shujun Luo
Lu Zhang
Gary P Schroth
Edith A Perez
E Aubrey Thompson
Illumina (United States) · USMayo Clinic · USCancer Clinic · USMayo Clinic in Florida · USSylvester Comprehensive Cancer Center · USWinnMed · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We used deep sequencing technology to profile the transcriptome, gene copy number, and CpG island methylation status simultaneously in eight commonly used breast cell lines to develop a model for how these genomic features are integrated in estrogen receptor positive (ER+) and negative breast cancer. Total mRNA sequence, gene copy number, and genomic CpG island methylation were carried out using the Illumina Genome Analyzer. Sequences were mapped to the human genome to obtain digitized gene expression data, DNA copy number in reference to the non-tumor cell line (MCF10A), and methylation status of 21,570 CpG islands to identify differentially expressed genes that were correlated with methylation or copy number changes. These were evaluated in a dataset from 129 primary breast tumors. Gene expression in cell lines was dominated by ER-associated genes. ER+ and ER- cell lines formed two distinct, stable clusters, and 1,873 genes were differentially expressed in the two groups. Part of chromosome 8 was deleted in all ER- cells and part of chromosome 17 amplified in all ER+ cells. These loci encoded 30 genes that were overexpressed in ER+ cells; 9 of these genes were overexpressed in ER+ tumors. We identified 149 differentially expressed genes that exhibited differential methylation of one or more CpG islands within 5 kb of the 5' end of the gene and for which mRNA abundance was inversely correlated with CpG island methylation status. In primary tumors we identified 84 genes that appear to be robust components of the methylation signature that we identified in ER+ cell lines. Our analyses reveal a global pattern of differential CpG island methylation that contributes to the transcriptome landscape of ER+ and ER- breast cancer cells and tumors. The role of gene amplification/deletion appears to more modest, although several potentially significant genes appear to be regulated by copy number aberrations.

Indexed as

CpG IslandsDNA MethylationGene DosageHigh-Throughput Nucleotide SequencingBreast NeoplasmsCarcinomaCell Line, TumorCells, CulturedCluster AnalysisFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansSequence Analysis, DNASystems Integration

Identifiers

PMID21364760
PMCPMC3045451
OpenAlexW2006559366

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.