Morphological and cytogenetic studies of angiosarcoma in Stewart-Treves syndrome.
Identifieur interne : 005C41 ( PubMed/Corpus ); précédent : 005C40; suivant : 005C42Morphological and cytogenetic studies of angiosarcoma in Stewart-Treves syndrome.
Auteurs : L G Kindblom ; G. Stenman ; L. AngervallSource :
- Virchows Archiv. A, Pathological anatomy and histopathology [ 0174-7398 ] ; 1991.
English descriptors
- KwdEn :
- Adult, Chromosome Mapping, Female, Hemangiosarcoma (metabolism), Hemangiosarcoma (pathology), Humans, Immunohistochemistry, Karyotyping, Lymphedema (complications), Lymphedema (etiology), Lymphedema (pathology), Mastectomy (adverse effects), Microscopy, Electron, Postoperative Complications, Skin Neoplasms (metabolism), Skin Neoplasms (pathology), Syndrome.
- MESH :
- adverse effects : Mastectomy.
- complications : Lymphedema.
- etiology : Lymphedema.
- metabolism : Hemangiosarcoma, Skin Neoplasms.
- pathology : Hemangiosarcoma, Lymphedema, Skin Neoplasms.
- Adult, Chromosome Mapping, Female, Humans, Immunohistochemistry, Karyotyping, Microscopy, Electron, Postoperative Complications, Syndrome.
Abstract
A morphological and cytogenetic analysis of a multifocal angiosarcoma in a typical case of Stewart-Treves syndrome is reported. The morphological analysis indicated differentiation along both blood and lymph vessel endothelium lines. By light and electron microscopy there were areas with well-developed erythrocyte-containing, capillary-like vessels and poorly differentiated areas with abortive vascular formations. In these the endothelium revealed immunoreactivity to factor VIII RAg, binding of Ulex europaeus I and Psophocarpus tetragonolobus agglutinin lectins, Weibel-Palade bodies ultrastructurally and presented a continuous enclosing external lamina and immunoreactivity for laminin and collagen IV, all features of blood-vessel differentiation. There were also lymphangioma-like areas as well as poorly differentiated areas where the immunohistochemical, lectin-binding and ultrastructural features were compatible with a lymph vessel differentiation. Cytogenetic analysis of cultured tumour cells revealed chromosome counts in the diploid region. About 40% of the cells analysed had a normal diploid karyotype. The remaining cells showed a multitude of mainly nonclonal structural alterations; 17 unique marker types resulting from different translocations and deletions were observed. There were also a few cells with clonal numerical deviations showing monosomy 22, monosomy X and trisomy 2 respectively. It is of interest that the losses of chromosome 22 and the X chromosome also have been observed in Kaposi's sarcoma and that the PD-ECGF gene, a novel angiogenetic factor, has been mapped to chromosome 22.
PubMed: 1750189
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Morphological and cytogenetic studies of angiosarcoma in Stewart-Treves syndrome.</title><author><name sortKey="Kindblom, L G" sort="Kindblom, L G" uniqKey="Kindblom L" first="L G" last="Kindblom">L G Kindblom</name><affiliation><nlm:affiliation>Department of Pathology, University of Göteborg, Sweden.</nlm:affiliation></affiliation></author><author><name sortKey="Stenman, G" sort="Stenman, G" uniqKey="Stenman G" first="G" last="Stenman">G. Stenman</name></author><author><name sortKey="Angervall, L" sort="Angervall, L" uniqKey="Angervall L" first="L" last="Angervall">L. Angervall</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1991">1991</date><idno type="RBID">pubmed:1750189</idno><idno type="pmid">1750189</idno><idno type="wicri:Area/PubMed/Corpus">005C41</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">005C41</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Morphological and cytogenetic studies of angiosarcoma in Stewart-Treves syndrome.</title><author><name sortKey="Kindblom, L G" sort="Kindblom, L G" uniqKey="Kindblom L" first="L G" last="Kindblom">L G Kindblom</name><affiliation><nlm:affiliation>Department of Pathology, University of Göteborg, Sweden.</nlm:affiliation></affiliation></author><author><name sortKey="Stenman, G" sort="Stenman, G" uniqKey="Stenman G" first="G" last="Stenman">G. Stenman</name></author><author><name sortKey="Angervall, L" sort="Angervall, L" uniqKey="Angervall L" first="L" last="Angervall">L. Angervall</name></author></analytic><series><title level="j">Virchows Archiv. A, Pathological anatomy and histopathology</title><idno type="ISSN">0174-7398</idno><imprint><date when="1991" type="published">1991</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Chromosome Mapping</term><term>Female</term><term>Hemangiosarcoma (metabolism)</term><term>Hemangiosarcoma (pathology)</term><term>Humans</term><term>Immunohistochemistry</term><term>Karyotyping</term><term>Lymphedema (complications)</term><term>Lymphedema (etiology)</term><term>Lymphedema (pathology)</term><term>Mastectomy (adverse effects)</term><term>Microscopy, Electron</term><term>Postoperative Complications</term><term>Skin Neoplasms (metabolism)</term><term>Skin Neoplasms (pathology)</term><term>Syndrome</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Mastectomy</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Hemangiosarcoma</term><term>Skin Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Hemangiosarcoma</term><term>Lymphedema</term><term>Skin Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Chromosome Mapping</term><term>Female</term><term>Humans</term><term>Immunohistochemistry</term><term>Karyotyping</term><term>Microscopy, Electron</term><term>Postoperative Complications</term><term>Syndrome</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A morphological and cytogenetic analysis of a multifocal angiosarcoma in a typical case of Stewart-Treves syndrome is reported. The morphological analysis indicated differentiation along both blood and lymph vessel endothelium lines. By light and electron microscopy there were areas with well-developed erythrocyte-containing, capillary-like vessels and poorly differentiated areas with abortive vascular formations. In these the endothelium revealed immunoreactivity to factor VIII RAg, binding of Ulex europaeus I and Psophocarpus tetragonolobus agglutinin lectins, Weibel-Palade bodies ultrastructurally and presented a continuous enclosing external lamina and immunoreactivity for laminin and collagen IV, all features of blood-vessel differentiation. There were also lymphangioma-like areas as well as poorly differentiated areas where the immunohistochemical, lectin-binding and ultrastructural features were compatible with a lymph vessel differentiation. Cytogenetic analysis of cultured tumour cells revealed chromosome counts in the diploid region. About 40% of the cells analysed had a normal diploid karyotype. The remaining cells showed a multitude of mainly nonclonal structural alterations; 17 unique marker types resulting from different translocations and deletions were observed. There were also a few cells with clonal numerical deviations showing monosomy 22, monosomy X and trisomy 2 respectively. It is of interest that the losses of chromosome 22 and the X chromosome also have been observed in Kaposi's sarcoma and that the PD-ECGF gene, a novel angiogenetic factor, has been mapped to chromosome 22.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">1750189</PMID><DateCreated><Year>1992</Year><Month>01</Month><Day>23</Day></DateCreated><DateCompleted><Year>1992</Year><Month>01</Month><Day>23</Day></DateCompleted><DateRevised><Year>2017</Year><Month>08</Month><Day>03</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0174-7398</ISSN><JournalIssue CitedMedium="Print"><Volume>419</Volume><Issue>5</Issue><PubDate><Year>1991</Year></PubDate></JournalIssue><Title>Virchows Archiv. A, Pathological anatomy and histopathology</Title><ISOAbbreviation>Virchows Arch A Pathol Anat Histopathol</ISOAbbreviation></Journal><ArticleTitle>Morphological and cytogenetic studies of angiosarcoma in Stewart-Treves syndrome.</ArticleTitle><Pagination><MedlinePgn>439-45</MedlinePgn></Pagination><Abstract><AbstractText>A morphological and cytogenetic analysis of a multifocal angiosarcoma in a typical case of Stewart-Treves syndrome is reported. The morphological analysis indicated differentiation along both blood and lymph vessel endothelium lines. By light and electron microscopy there were areas with well-developed erythrocyte-containing, capillary-like vessels and poorly differentiated areas with abortive vascular formations. In these the endothelium revealed immunoreactivity to factor VIII RAg, binding of Ulex europaeus I and Psophocarpus tetragonolobus agglutinin lectins, Weibel-Palade bodies ultrastructurally and presented a continuous enclosing external lamina and immunoreactivity for laminin and collagen IV, all features of blood-vessel differentiation. There were also lymphangioma-like areas as well as poorly differentiated areas where the immunohistochemical, lectin-binding and ultrastructural features were compatible with a lymph vessel differentiation. Cytogenetic analysis of cultured tumour cells revealed chromosome counts in the diploid region. About 40% of the cells analysed had a normal diploid karyotype. The remaining cells showed a multitude of mainly nonclonal structural alterations; 17 unique marker types resulting from different translocations and deletions were observed. There were also a few cells with clonal numerical deviations showing monosomy 22, monosomy X and trisomy 2 respectively. It is of interest that the losses of chromosome 22 and the X chromosome also have been observed in Kaposi's sarcoma and that the PD-ECGF gene, a novel angiogenetic factor, has been mapped to chromosome 22.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kindblom</LastName><ForeName>L G</ForeName><Initials>LG</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Göteborg, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stenman</LastName><ForeName>G</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Angervall</LastName><ForeName>L</ForeName><Initials>L</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Virchows Arch A Pathol Anat Histopathol</MedlineTA><NlmUniqueID>8302198</NlmUniqueID><ISSNLinking>0174-7398</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Eur J Biochem. 1984 Feb 1;138(3):519-25</RefSource><PMID Version="1">6692833</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cancer Genet Cytogenet. 1986 Apr 15;21(4):309-18</RefSource><PMID Version="1">3955528</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Acta Radiol Suppl. 1972;316:1-52</RefSource><PMID Version="1">4604516</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Anat Rec. 1990 Jan;226(1):10-7</RefSource><PMID Version="1">2297076</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Virchows Arch A Pathol Anat 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MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007150" MajorTopicYN="N">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007621" MajorTopicYN="N">Karyotyping</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="N">complications</QualifierName><QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008408" MajorTopicYN="N">Mastectomy</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008854" MajorTopicYN="N">Microscopy, Electron</DescriptorName></MeshHeading><MeshHeading><DescriptorName 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