Key Roles for MYC, KIT and RET signaling in secondary angiosarcomas
Identifieur interne : 006809 ( Ncbi/Curation ); précédent : 006808; suivant : 006810Key Roles for MYC, KIT and RET signaling in secondary angiosarcomas
Auteurs : E. Styring [Suède] ; J. Seinen [Pays-Bas] ; M. Dominguez-Valentin [Suède] ; H A Domanski [Suède] ; M. Jönsson [Suède] ; F V Von Steyern [Suède] ; H J Hoekstra [Pays-Bas] ; A J H. Suurmeijer [Pays-Bas] ; M. Nilbert [Suède, Danemark]Source :
- British Journal of Cancer [ 0007-0920 ] ; 2014.
Abstract
Angiosarcomas 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.
Whole-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.
In total, 103 genes were significantly deregulated between primary and secondary angiosarcomas. Secondary angiosarcomas showed upregulation of
Upregulation of
Url:
DOI: 10.1038/bjc.2014.359
PubMed: 24983371
PubMed Central: 4102954
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Key Roles for <italic>MYC</italic>
, <italic>KIT</italic>
and <italic>RET</italic>
signaling in secondary angiosarcomas</title>
<author><name sortKey="Styring, E" sort="Styring, E" uniqKey="Styring E" first="E" last="Styring">E. Styring</name>
<affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Orthopedics, Section III, Clinical Sciences, Lund University</institution>
, 22185 Lund,<country>Sweden</country>
</nlm:aff>
<country xml:lang="fr">Suède</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Department of Oncology, Section V, Clinical Sciences, Lund University</institution>
, 22185 Lund,<country>Sweden</country>
</nlm:aff>
<country xml:lang="fr">Suède</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Seinen, J" sort="Seinen, J" uniqKey="Seinen J" first="J" last="Seinen">J. Seinen</name>
<affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Division of Surgical Oncology, Department of Surgery, University Medical Center Groningen, University of Groningen</institution>
, Hanzeplein 1, PO Box 30.001, 9700 Groningen,<country>The Netherlands</country>
</nlm:aff>
<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Dominguez Valentin, M" sort="Dominguez Valentin, M" uniqKey="Dominguez Valentin M" first="M" last="Dominguez-Valentin">M. Dominguez-Valentin</name>
<affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Department of Oncology, Section V, Clinical Sciences, Lund University</institution>
, 22185 Lund,<country>Sweden</country>
</nlm:aff>
<country xml:lang="fr">Suède</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Domanski, H A" sort="Domanski, H A" uniqKey="Domanski H" first="H A" last="Domanski">H A Domanski</name>
<affiliation wicri:level="1"><nlm:aff id="aff4"><institution>Department of Pathology, Section V, Clinical Sciences, Lund University</institution>
, 22185 Lund,<country>Sweden</country>
</nlm:aff>
<country xml:lang="fr">Suède</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Jonsson, M" sort="Jonsson, M" uniqKey="Jonsson M" first="M" last="Jönsson">M. Jönsson</name>
<affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Department of Oncology, Section V, Clinical Sciences, Lund University</institution>
, 22185 Lund,<country>Sweden</country>
</nlm:aff>
<country xml:lang="fr">Suède</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Von Steyern, F V" sort="Von Steyern, F V" uniqKey="Von Steyern F" first="F V" last="Von Steyern">F V Von Steyern</name>
<affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Orthopedics, Section III, Clinical Sciences, Lund University</institution>
, 22185 Lund,<country>Sweden</country>
</nlm:aff>
<country xml:lang="fr">Suède</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Hoekstra, H J" sort="Hoekstra, H J" uniqKey="Hoekstra H" first="H J" last="Hoekstra">H J Hoekstra</name>
<affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Division of Surgical Oncology, Department of Surgery, University Medical Center Groningen, University of Groningen</institution>
, Hanzeplein 1, PO Box 30.001, 9700 Groningen,<country>The Netherlands</country>
</nlm:aff>
<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Suurmeijer, A J H" sort="Suurmeijer, A J H" uniqKey="Suurmeijer A" first="A J H" last="Suurmeijer">A J H. Suurmeijer</name>
<affiliation wicri:level="1"><nlm:aff id="aff5"><institution>Department of Pathology, University Medical Center Groningen, University of Groningen</institution>
, Hanzeplein 1, PO Box 30.001, 9700 Groningen,<country>The Netherlands</country>
</nlm:aff>
<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Nilbert, M" sort="Nilbert, M" uniqKey="Nilbert M" first="M" last="Nilbert">M. Nilbert</name>
<affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Department of Oncology, Section V, Clinical Sciences, Lund University</institution>
, 22185 Lund,<country>Sweden</country>
</nlm:aff>
<country xml:lang="fr">Suède</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="aff6"><institution>Clinical Research Centre, Hvidovre Hospital, Copenhagen University</institution>
, 2650 Hvidovre,<country>Denmark</country>
</nlm:aff>
<country xml:lang="fr">Danemark</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
</affiliation>
</author>
</analytic>
<series><title level="j">British Journal of Cancer</title>
<idno type="ISSN">0007-0920</idno>
<idno type="eISSN">1532-1827</idno>
<imprint><date when="2014">2014</date>
</imprint>
</series>
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<front><div type="abstract" xml:lang="en"><sec><title>Background:</title>
<p>Angiosarcomas 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.</p>
</sec>
<sec><title>Methods:</title>
<p>Whole-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.</p>
</sec>
<sec><title>Results:</title>
<p>In total, 103 genes were significantly deregulated between primary and secondary angiosarcomas. Secondary angiosarcomas showed upregulation of <italic>MYC, KIT</italic>
and <italic>RET</italic>
and downregulation of <italic>CDKN2C</italic>
. 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.</p>
</sec>
<sec><title>Conclusions:</title>
<p>Upregulation of <italic>MYC</italic>
, <italic>KIT</italic>
and <italic>RET</italic>
and downregulation of <italic>CDKN2C</italic>
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.</p>
</sec>
</div>
</front>
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