MYC high level gene amplification is a distinctive feature of angiosarcomas after irradiation or chronic lymphedema.
Identifieur interne : 002C43 ( PubMed/Corpus ); précédent : 002C42; suivant : 002C44MYC high level gene amplification is a distinctive feature of angiosarcomas after irradiation or chronic lymphedema.
Auteurs : Johanna Manner ; 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 StröbelSource :
- The American journal of pathology [ 1525-2191 ] ; 2010.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Chromosome Deletion, Chronic Disease, DNA Copy Number Variations (genetics), Female, Gene Amplification (genetics), Genetic Loci (genetics), Hemangiosarcoma (etiology), Hemangiosarcoma (genetics), Homozygote, Humans, In Situ Hybridization, Fluorescence, Lymphedema (complications), Lymphedema (genetics), Male, Middle Aged, Proto-Oncogene Proteins c-myc (genetics), Radiotherapy (adverse effects).
- MESH :
- chemical , genetics : Proto-Oncogene Proteins c-myc.
- adverse effects : Radiotherapy.
- complications : Lymphedema.
- etiology : Hemangiosarcoma.
- genetics : DNA Copy Number Variations, Gene Amplification, Genetic Loci, Hemangiosarcoma, Lymphedema.
- Adult, Aged, Aged, 80 and over, Chromosome Deletion, Chronic Disease, Female, Homozygote, Humans, In Situ Hybridization, Fluorescence, Male, Middle Aged.
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.
DOI: 10.2353/ajpath.2010.090637
PubMed: 20008140
Links to Exploration step
pubmed:20008140Le document en format XML
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last="Manner">Johanna Manner</name><affiliation><nlm:affiliation>Institute of Pathology, Division of Surgical Oncology and Thoracic Surgery, University Medical Centre Mannheim, University of Heidelberg, D-68135 Mannheim, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Radlwimmer, Bernhard" sort="Radlwimmer, Bernhard" uniqKey="Radlwimmer B" first="Bernhard" last="Radlwimmer">Bernhard Radlwimmer</name></author><author><name sortKey="Hohenberger, Peter" sort="Hohenberger, Peter" uniqKey="Hohenberger P" first="Peter" last="Hohenberger">Peter Hohenberger</name></author><author><name sortKey="Mossinger, Katharina" sort="Mossinger, Katharina" uniqKey="Mossinger K" first="Katharina" last="Mössinger">Katharina Mössinger</name></author><author><name sortKey="Kuffer, Stefan" sort="Kuffer, Stefan" uniqKey="Kuffer S" first="Stefan" last="Küffer">Stefan Küffer</name></author><author><name sortKey="Sauer, Christian" sort="Sauer, Christian" uniqKey="Sauer C" first="Christian" last="Sauer">Christian Sauer</name></author><author><name sortKey="Belharazem, Djeda" sort="Belharazem, Djeda" uniqKey="Belharazem D" first="Djeda" last="Belharazem">Djeda Belharazem</name></author><author><name sortKey="Zettl, Andreas" sort="Zettl, Andreas" uniqKey="Zettl A" first="Andreas" last="Zettl">Andreas Zettl</name></author><author><name sortKey="Coindre, Jean Michel" sort="Coindre, Jean Michel" uniqKey="Coindre J" first="Jean-Michel" last="Coindre">Jean-Michel Coindre</name></author><author><name sortKey="Hallermann, Christian" sort="Hallermann, Christian" uniqKey="Hallermann C" first="Christian" last="Hallermann">Christian Hallermann</name></author><author><name sortKey="Hartmann, Jorg Thomas" sort="Hartmann, Jorg Thomas" uniqKey="Hartmann J" first="Jörg Thomas" last="Hartmann">Jörg Thomas Hartmann</name></author><author><name sortKey="Katenkamp, Detlef" sort="Katenkamp, Detlef" uniqKey="Katenkamp D" first="Detlef" last="Katenkamp">Detlef 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last="Ströbel">Philipp Ströbel</name></author></analytic><series><title level="j">The American journal of pathology</title><idno type="eISSN">1525-2191</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Chromosome Deletion</term><term>Chronic Disease</term><term>DNA Copy Number Variations (genetics)</term><term>Female</term><term>Gene Amplification (genetics)</term><term>Genetic Loci (genetics)</term><term>Hemangiosarcoma (etiology)</term><term>Hemangiosarcoma (genetics)</term><term>Homozygote</term><term>Humans</term><term>In Situ Hybridization, Fluorescence</term><term>Lymphedema (complications)</term><term>Lymphedema (genetics)</term><term>Male</term><term>Middle Aged</term><term>Proto-Oncogene Proteins c-myc (genetics)</term><term>Radiotherapy (adverse effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Proto-Oncogene Proteins c-myc</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Radiotherapy</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Hemangiosarcoma</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>DNA Copy Number Variations</term><term>Gene Amplification</term><term>Genetic Loci</term><term>Hemangiosarcoma</term><term>Lymphedema</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Chromosome Deletion</term><term>Chronic Disease</term><term>Female</term><term>Homozygote</term><term>Humans</term><term>In Situ Hybridization, Fluorescence</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20008140</PMID><DateCreated><Year>2009</Year><Month>12</Month><Day>30</Day></DateCreated><DateCompleted><Year>2010</Year><Month>03</Month><Day>15</Day></DateCompleted><DateRevised><Year>2014</Year><Month>12</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1525-2191</ISSN><JournalIssue CitedMedium="Internet"><Volume>176</Volume><Issue>1</Issue><PubDate><Year>2010</Year><Month>Jan</Month></PubDate></JournalIssue><Title>The American journal of pathology</Title><ISOAbbreviation>Am. J. Pathol.</ISOAbbreviation></Journal><ArticleTitle>MYC high level gene amplification is a distinctive feature of angiosarcomas after irradiation or chronic lymphedema.</ArticleTitle><Pagination><MedlinePgn>34-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.2353/ajpath.2010.090637</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Manner</LastName><ForeName>Johanna</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Institute of Pathology, Division of Surgical Oncology and Thoracic Surgery, University Medical Centre Mannheim, University of Heidelberg, D-68135 Mannheim, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Radlwimmer</LastName><ForeName>Bernhard</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Hohenberger</LastName><ForeName>Peter</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Mössinger</LastName><ForeName>Katharina</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Küffer</LastName><ForeName>Stefan</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Sauer</LastName><ForeName>Christian</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Belharazem</LastName><ForeName>Djeda</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Zettl</LastName><ForeName>Andreas</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Coindre</LastName><ForeName>Jean-Michel</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Hallermann</LastName><ForeName>Christian</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Hartmann</LastName><ForeName>Jörg Thomas</ForeName><Initials>JT</Initials></Author><Author ValidYN="Y"><LastName>Katenkamp</LastName><ForeName>Detlef</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Katenkamp</LastName><ForeName>Kathrin</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Schöffski</LastName><ForeName>Patrick</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Sciot</LastName><ForeName>Raf</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Wozniak</LastName><ForeName>Agnieszka</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Lichter</LastName><ForeName>Peter</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Marx</LastName><ForeName>Alexander</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Ströbel</LastName><ForeName>Philipp</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2009</Year><Month>12</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Pathol</MedlineTA><NlmUniqueID>0370502</NlmUniqueID><ISSNLinking>0002-9440</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016271">Proto-Oncogene Proteins c-myc</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Cancer. 1999 Dec 1;86(11):2406-12</RefSource><PMID Version="1">10590384</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Surg Pathol. 1998 Jun;22(6):683-97</RefSource><PMID Version="1">9630175</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Genet. 2000 Jun;25(2):153-9</RefSource><PMID Version="1">10835628</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Appl Immunohistochem Mol Morphol. 2001 Mar;9(1):24-8</RefSource><PMID Version="1">11277410</PMID></CommentsCorrections><CommentsCorrections 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IdType="pubmed">20008140</ArticleId><ArticleId IdType="pii">S0002-9440(10)60322-7</ArticleId><ArticleId IdType="doi">10.2353/ajpath.2010.090637</ArticleId><ArticleId IdType="pmc">PMC2797867</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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