Evidence map›Paper›PMID 28683746›Full record

ArticleMolecular cancer2017

Multi-omics of 34 colorectal cancer cell lines - a resource for biomedical studies.

Kaja C G Berg, Peter W Eide, Ina A Eilertsen, Bjarne Johannessen, Jarle Bruun, Stine A Danielsen, Merete Bjørnslett, Leonardo A Meza-Zepeda, Mette Eknæs, Guro E Lind and 4 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 265 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
265citing papers in PubMed, 2 pooled it
17.2field-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

265 citing papers in PubMed, 2 syntheses or guidelines pooled it, 386 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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205 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

14 authors at 4 institutions in 1 country.

Kaja C G BergDepartment of Molecular Oncology, Institute for Cancer Research & K.G.Jebsen Colorectal Cancer Research Centre, Oslo University Hospital, P.O.Box 4953 Nydalen, -0424, Oslo, NO, Norway.
Peter W EideDepartment of Molecular Oncology, Institute for Cancer Research & K.G.Jebsen Colorectal Cancer Research Centre, Oslo University Hospital, P.O.Box 4953 Nydalen, -0424, Oslo, NO, Norway.
Ina A EilertsenDepartment of Molecular Oncology, Institute for Cancer Research & K.G.Jebsen Colorectal Cancer Research Centre, Oslo University Hospital, P.O.Box 4953 Nydalen, -0424, Oslo, NO, Norway.
Bjarne JohannessenDepartment of Molecular Oncology, Institute for Cancer Research & K.G.Jebsen Colorectal Cancer Research Centre, Oslo University Hospital, P.O.Box 4953 Nydalen, -0424, Oslo, NO, Norway.
Jarle BruunDepartment of Molecular Oncology, Institute for Cancer Research & K.G.Jebsen Colorectal Cancer Research Centre, Oslo University Hospital, P.O.Box 4953 Nydalen, -0424, Oslo, NO, Norway.
Stine A DanielsenDepartment of Molecular Oncology, Institute for Cancer Research & K.G.Jebsen Colorectal Cancer Research Centre, Oslo University Hospital, P.O.Box 4953 Nydalen, -0424, Oslo, NO, Norway.
Merete BjørnslettDepartment of Molecular Oncology, Institute for Cancer Research & K.G.Jebsen Colorectal Cancer Research Centre, Oslo University Hospital, P.O.Box 4953 Nydalen, -0424, Oslo, NO, Norway.
Leonardo A Meza-ZepedaNorwegian Cancer Genomic Consortium, Oslo University Hospital, Oslo, Norway.
Mette EknæsDepartment of Molecular Oncology, Institute for Cancer Research & K.G.Jebsen Colorectal Cancer Research Centre, Oslo University Hospital, P.O.Box 4953 Nydalen, -0424, Oslo, NO, Norway.
Guro E LindDepartment of Molecular Oncology, Institute for Cancer Research & K.G.Jebsen Colorectal Cancer Research Centre, Oslo University Hospital, P.O.Box 4953 Nydalen, -0424, Oslo, NO, Norway.
Ola MyklebostNorwegian Cancer Genomic Consortium, Oslo University Hospital, Oslo, Norway.
Rolf I SkotheimDepartment of Molecular Oncology, Institute for Cancer Research & K.G.Jebsen Colorectal Cancer Research Centre, Oslo University Hospital, P.O.Box 4953 Nydalen, -0424, Oslo, NO, Norway.
Anita SveenDepartment of Molecular Oncology, Institute for Cancer Research & K.G.Jebsen Colorectal Cancer Research Centre, Oslo University Hospital, P.O.Box 4953 Nydalen, -0424, Oslo, NO, Norway.
Ragnhild A LotheDepartment of Molecular Oncology, Institute for Cancer Research & K.G.Jebsen Colorectal Cancer Research Centre, Oslo University Hospital, P.O.Box 4953 Nydalen, -0424, Oslo, NO, Norway. rlothe@rr-research.no.
Oslo University Hospital · NOUniversity of Oslo · NOOslo Cancer Cluster · NOUniversity of Bergen · NO

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
NCI NIH HHS P30 CA016672
6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) cell lines are widely used pre-clinical model systems. Comprehensive insights into their molecular characteristics may improve model selection for biomedical studies.

methodsWe have performed DNA, RNA and protein profiling of 34 cell lines, including (i) targeted deep sequencing (n = 612 genes) to detect single nucleotide variants and insertions/deletions; (ii) high resolution DNA copy number profiling; (iii) gene expression profiling at exon resolution; (iv) small RNA expression profiling by deep sequencing; and (v) protein expression analysis (n = 297 proteins) by reverse phase protein microarrays.

resultsThe cell lines were stratified according to the key molecular subtypes of CRC and data were integrated at two or more levels by computational analyses. We confirm that the frequencies and patterns of DNA aberrations are associated with genomic instability phenotypes and that the cell lines recapitulate the genomic profiles of primary carcinomas. Intrinsic expression subgroups are distinct from genomic subtypes, but consistent at the gene-, microRNA- and protein-level and dominated by two distinct clusters; colon-like cell lines characterized by expression of gastro-intestinal differentiation markers and undifferentiated cell lines showing upregulation of epithelial-mesenchymal transition and TGFβ signatures. This sample split was concordant with the gene expression-based consensus molecular subtypes of primary tumors. Approximately ¼ of the genes had consistent regulation at the DNA copy number and gene expression level, while expression of gene-protein pairs in general was strongly correlated. Consistent high-level DNA copy number amplification and outlier gene- and protein- expression was found for several oncogenes in individual cell lines, including MYC and ERBB2.

conclusionsThis study expands the view of CRC cell lines as accurate molecular models of primary carcinomas, and we present integrated multi-level molecular data of 34 widely used cell lines in easily accessible formats, providing a resource for preclinical studies in CRC.

Indexed as

Biomedical ResearchGenomicsProteomicsBase SequenceCell DifferentiationCell Line, TumorColonColorectal NeoplasmsDNA Copy Number VariationsGene AmplificationGene Expression Regulation, NeoplasticGenes, NeoplasmGenomic InstabilityHumansINDEL MutationMicroRNAsMicroRNAsRNA, MessengerColorectal cancer cell linesConsensus molecular subtypesCopy number aberrationsGene expressionGenomicsMethylationMicrosatellite instabilitymiRNAMutationsProtein expression

Identifiers

PMID28683746
PMCPMC5498998
OpenAlexW2729239885

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.