Evidence map›Paper›PMID 24983371›Full record

ArticleBritish journal of cancer2014

Key roles for MYC, KIT and RET signaling in secondary angiosarcomas.

E Styring, J Seinen, M Dominguez-Valentin, H A Domanski, M Jönsson, F V von Steyern, H J Hoekstra, A J H Suurmeijer, M Nilbert

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 29 citations in OpenAlex.

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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

9 authors at 4 institutions in 3 countries.

E Styring1] Department of Orthopedics, Section III, Clinical Sciences, Lund University, 22185 Lund, Sweden [2] Department of Oncology, Section V, Clinical Sciences, Lund University, 22185 Lund, Sweden.
J SeinenDivision of Surgical Oncology, Department of Surgery, University Medical Center Groningen, University of Groningen, Hanzeplein 1, PO Box 30.001, 9700 Groningen, The Netherlands.
M Dominguez-ValentinDepartment of Oncology, Section V, Clinical Sciences, Lund University, 22185 Lund, Sweden.
H A DomanskiDepartment of Pathology, Section V, Clinical Sciences, Lund University, 22185 Lund, Sweden.
M JönssonDepartment of Oncology, Section V, Clinical Sciences, Lund University, 22185 Lund, Sweden.
F V von SteyernDepartment of Orthopedics, Section III, Clinical Sciences, Lund University, 22185 Lund, Sweden.
H J HoekstraDivision of Surgical Oncology, Department of Surgery, University Medical Center Groningen, University of Groningen, Hanzeplein 1, PO Box 30.001, 9700 Groningen, The Netherlands.
A J H SuurmeijerDepartment of Pathology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, PO Box 30.001, 9700 Groningen, The Netherlands.
M Nilbert1] Department of Oncology, Section V, Clinical Sciences, Lund University, 22185 Lund, Sweden [2] Clinical Research Centre, Hvidovre Hospital, Copenhagen University, 2650 Hvidovre, Denmark.
Lund University · SEUniversity of Groningen · NLHvidovre Hospital · DKUniversity Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAngiosarcomas may develop as primary tumours of unknown cause or as secondary tumours, most commonly following radiotherapy to the involved field. The different causative agents may be linked to alternate tumorigenesis, which led us to investigate the genetic profiles of morphologically indistinguishable primary and secondary angiosarcomas.

methodsWhole-genome (18k) c-DNA-mediated annealing, selection, extension and ligation analysis was used to genetically profile 26 primary and 29 secondary angiosarcomas. Key findings were thereafter validated using RT-qPCR, immunohistochemistry and validation of the gene signature to an external data set.

resultsIn total, 103 genes were significantly deregulated between primary and secondary angiosarcomas. Secondary angiosarcomas showed upregulation of MYC, KIT and RET and downregulation of CDKN2C. Functional annotation analysis identified multiple target genes in the receptor protein tyrosine kinase pathway. The results were validated using RT-qPCR and immunohistochemistry. Further, the gene signature was applied to an external data set and, herein, distinguished primary from secondary angiosarcomas.

conclusionsUpregulation of MYC, KIT and RET and downregulation of CDKN2C characterise secondary angiosarcoma, which implies possibilities for diagnostic application and a mechanistic basis for therapeutic evaluation of RET-kinase-inhibitors in these highly aggressive tumours.

Indexed as

Genes, mycAdolescentAdultAgedAged, 80 and overChildChild, PreschoolFemaleGene AmplificationGenome, HumanHemangiosarcomaHumansImmunohistochemistryMaleMiddle AgedNeoplasms, Second PrimaryProto-Oncogene Proteins c-kitProto-Oncogene Proteins c-retRET protein, human

Identifiers

PMID24983371
PMCPMC4102954
OpenAlexW2009083177

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.