Evidence map›Paper›PMID 25551557›Full record

ArticlePloS one2014

Focal chromosomal copy number aberrations identify CMTM8 and GPR177 as new candidate driver genes in osteosarcoma.

Joeri Both, Oscar Krijgsman, Johannes Bras, Gerard R Schaap, Frank Baas, Bauke Ylstra, Theo J M Hulsebos

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

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  6. The role of Evi/Wntless in exporting Wnt proteins.Development (Cambridge, England) · 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

7 authors at 2 institutions in 1 country.

Joeri BothDepartment of Genome Analysis, Academic Medical Center, Amsterdam, The Netherlands.
Oscar KrijgsmanDepartment of Pathology, VU University Medical Center, Amsterdam, the Netherlands.
Johannes BrasDepartment of Pathology, Academic Medical Center, Amsterdam, The Netherlands.
Gerard R SchaapDepartment of Orthopedic Surgery, Academic Medical Center, Amsterdam, The Netherlands.
Frank BaasDepartment of Genome Analysis, Academic Medical Center, Amsterdam, The Netherlands.
Bauke YlstraDepartment of Pathology, VU University Medical Center, Amsterdam, the Netherlands.
Theo J M HulsebosDepartment of Genome Analysis, Academic Medical Center, Amsterdam, The Netherlands.
Academic Medical Center · NLAmsterdam UMC Location VUmc · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma is an aggressive bone tumor that preferentially develops in adolescents. The tumor is characterized by an abundance of genomic aberrations, which hampers the identification of the driver genes involved in osteosarcoma tumorigenesis. Our study aims to identify these genes by the investigation of focal copy number aberrations (CNAs, <3 Mb). For this purpose, we subjected 26 primary tumors of osteosarcoma patients to high-resolution single nucleotide polymorphism array analyses and identified 139 somatic focal CNAs. Of these, 72 had at least one gene located within or overlapping the focal CNA, with a total of 94 genes. For 84 of these genes, the expression status in 31 osteosarcoma samples was determined by expression microarray analysis. This enabled us to identify the genes of which the over- or underexpression was in more than 35% of cases in accordance to their copy number status (gain or loss). These candidate genes were subsequently validated in an independent set and furthermore corroborated as driver genes by verifying their role in other tumor types. We identified CMTM8 as a new candidate tumor suppressor gene and GPR177 as a new candidate oncogene in osteosarcoma. In osteosarcoma, CMTM8 has been shown to suppress EGFR signaling. In other tumor types, CMTM8 is known to suppress the activity of the oncogenic protein c-Met and GPR177 is known as an overexpressed upstream regulator of the Wnt-pathway. Further studies are needed to determine whether these proteins also exert the latter functions in osteosarcoma tumorigenesis.

Indexed as

AdolescentAdultBone NeoplasmsCell Transformation, NeoplasticChemokinesChildChromosome AberrationsComparative Genomic HybridizationDNA Copy Number VariationsFemaleGene DosageGene Expression ProfilingGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsMaleChemokinesCMTM8 protein, humanIntracellular Signaling Peptides and ProteinsMARVEL Domain-Containing ProteinsProto-Oncogene Proteins c-metReceptors, G-Protein-CoupledTumor Suppressor ProteinsWLS protein, human

Identifiers

PMID25551557
PMCPMC4281204
OpenAlexW2048478533

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Registered trials

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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.