Evidence map›Paper›PMID 20008140›Full record

ArticleThe American journal of pathology2010

MYC high level gene amplification is a distinctive feature of angiosarcomas after irradiation or chronic lymphedema.

Johanna Manner, Bernhard Radlwimmer, Peter Hohenberger, Katharina Mössinger, Stefan Küffer, Christian Sauer, Djeda Belharazem, Andreas Zettl, Jean-Michel Coindre, Christian Hallermann and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 2 pooled it
4.4field-weighted citation impact, top 5% 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

106 citing papers in PubMed, 2 syntheses or guidelines pooled it, 317 citations in OpenAlex.

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  10. TRPS1 expression in breast angiosarcoma.Virchows Archiv : an international journal of pathology · 2025
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46 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

19 authors at 7 institutions in 3 countries.

Johanna MannerInstitute of Pathology, Division of Surgical Oncology and Thoracic Surgery, University Medical Centre Mannheim, University of Heidelberg, D-68135 Mannheim, Germany.
Bernhard Radlwimmer
Peter Hohenberger
Katharina Mössinger
Stefan Küffer
Christian Sauer
Djeda Belharazem
Andreas Zettl
Jean-Michel Coindre
Christian Hallermann
Jörg Thomas Hartmann
Detlef Katenkamp
Kathrin Katenkamp
Patrick Schöffski
Raf Sciot
Agnieszka Wozniak
Peter Lichter
Alexander Marx
Philipp Ströbel
Heidelberg University · DEKU Leuven · BEFriedrich Schiller University Jena · DEGerman Cancer Research Center · DEFachklinik Hornheide · DEInserm · FRUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiosarcomas (AS) are rare vascular malignancies that arise either de novo as primary tumors or secondary to irradiation or chronic lymphedema. The cytogenetics of angiosarcomas are poorly characterized. We applied array-comparative genomic hybridization as a screening method to identify recurrent alterations in 22 cases. Recurrent genetic alterations were identified only in secondary but not in primary AS. The most frequent recurrent alterations were high level amplifications on chromosome 8q24.21 (50%), followed by 10p12.33 (33%) and 5q35.3 (11%). Fluorescence in situ hybridization analysis in 28 primary and 33 secondary angiosarcomas (31 tumors secondary to irradiation, 2 tumors secondary to chronic lymphedema) confirmed high level amplification of MYC on chromosome 8q24.21 as a recurrent genetic alteration found exclusively in 55% of AS secondary to irradiation or chronic lymphedema, but not in primary AS. Amplification of MYC did not predispose to high grade morphology or increased cell turnover. In conclusion, despite their identical morphology, secondary AS are genetically different from primary AS and are characterized by a high frequency of high level amplifications of MYC. This finding may have implications both for the diagnosis and treatment of these tumors.

Indexed as

AdultAgedAged, 80 and overChromosome DeletionChronic DiseaseDNA Copy Number VariationsFemaleGene AmplificationGenetic LociHemangiosarcomaHomozygoteHumansIn Situ Hybridization, FluorescenceLymphedemaMaleMiddle AgedProto-Oncogene Proteins c-myc

Identifiers

PMID20008140
PMCPMC2797867
OpenAlexW2144691565

What OpenQuestion holds

Textmetadata
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.