Evidence map›Paper›PMID 23158748›Full record

ArticleGenome medicine2012

Comprehensive analysis of the genome transcriptome and proteome landscapes of three tumor cell lines.

Pelin Akan, Andrey Alexeyenko, Paul Igor Costea, Lilia Hedberg, Beata Werne Solnestam, Sverker Lundin, Jimmie Hällman, Emma Lundberg, Mathias Uhlén, Joakim Lundeberg

Open access · goldAbstract read
In one paragraph

Article in Genome medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

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  12. Computational Analysis Concerning the Impact of DNA Accessibility on CRISPR-Cas9 Cleavage Efficiency.Molecular therapy : the journal of the American Society of Gene Therapy · 2020
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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

10 authors at 2 institutions in 1 country.

Pelin AkanKTH - Royal Institute of Technology, Science for Life Laboratory, School of Biotechnology, SE-171 65 Solna, Sweden.
Andrey AlexeyenkoKTH - Royal Institute of Technology, Science for Life Laboratory, School of Biotechnology, SE-171 65 Solna, Sweden.
Paul Igor CosteaKTH - Royal Institute of Technology, Science for Life Laboratory, School of Biotechnology, SE-171 65 Solna, Sweden.
Lilia HedbergKTH - Royal Institute of Technology, Science for Life Laboratory, School of Biotechnology, SE-171 65 Solna, Sweden.
Beata Werne SolnestamKTH - Royal Institute of Technology, Science for Life Laboratory, School of Biotechnology, SE-171 65 Solna, Sweden.
Sverker LundinKTH - Royal Institute of Technology, Science for Life Laboratory, School of Biotechnology, SE-171 65 Solna, Sweden.
Jimmie HällmanKTH - Royal Institute of Technology, Science for Life Laboratory, School of Biotechnology, SE-171 65 Solna, Sweden.
Emma LundbergKTH - Royal Institute of Technology, Science for Life Laboratory, School of Biotechnology, SE-171 65 Solna, Sweden.
Mathias UhlénKTH - Royal Institute of Technology, Science for Life Laboratory, School of Biotechnology, SE-171 65 Solna, Sweden.
Joakim LundebergKTH - Royal Institute of Technology, Science for Life Laboratory, School of Biotechnology, SE-171 65 Solna, Sweden.
Science for Life Laboratory · SEKTH Royal Institute of Technology · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We here present a comparative genome, transcriptome and functional network analysis of three human cancer cell lines (A431, U251MG and U2OS), and investigate their relation to protein expression. Gene copy numbers significantly influenced corresponding transcript levels; their effect on protein levels was less pronounced. We focused on genes with altered mRNA and/or protein levels to identify those active in tumor maintenance. We provide comprehensive information for the three genomes and demonstrate the advantage of integrative analysis for identifying tumor-related genes amidst numerous background mutations by relating genomic variation to expression/protein abundance data and use gene networks to reveal implicated pathways.

Identifiers

PMID23158748
PMCPMC3580420
OpenAlexW2021887146

What Socratic 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 Socratic graph.