Morphological and cytogenetic studies of angiosarcoma in Stewart-Treves syndrome.
Identifieur interne : 002706 ( Ncbi/Curation ); précédent : 002705; suivant : 002707Morphological and cytogenetic studies of angiosarcoma in Stewart-Treves syndrome.
Auteurs : L G Kindblom [Suède] ; G. Stenman ; L. AngervallSource :
- Virchows Archiv. A, Pathological anatomy and histopathology [ 0174-7398 ] ; 1991.
Descripteurs français
- KwdFr :
- Adulte, Cartographie chromosomique, Caryotypage, Complications postopératoires, Femelle, Humains, Hémangiosarcome (anatomopathologie), Hémangiosarcome (métabolisme), Immunohistochimie, Lymphoedème (), Lymphoedème (anatomopathologie), Lymphoedème (étiologie), Mastectomie (effets indésirables), Microscopie électronique, Syndrome, Tumeurs cutanées (anatomopathologie), Tumeurs cutanées (métabolisme).
- MESH :
- anatomopathologie : Hémangiosarcome, Lymphoedème, Tumeurs cutanées.
- effets indésirables : Mastectomie.
- métabolisme : Hémangiosarcome, Tumeurs cutanées.
- étiologie : Lymphoedème.
- Adulte, Cartographie chromosomique, Caryotypage, Complications postopératoires, Femelle, Humains, Immunohistochimie, Lymphoedème, Microscopie électronique, Syndrome.
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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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="KwdFr" xml:lang="fr"><term>Adulte</term><term>Cartographie chromosomique</term><term>Caryotypage</term><term>Complications postopératoires</term><term>Femelle</term><term>Humains</term><term>Hémangiosarcome (anatomopathologie)</term><term>Hémangiosarcome (métabolisme)</term><term>Immunohistochimie</term><term>Lymphoedème ()</term><term>Lymphoedème (anatomopathologie)</term><term>Lymphoedème (étiologie)</term><term>Mastectomie (effets indésirables)</term><term>Microscopie électronique</term><term>Syndrome</term><term>Tumeurs cutanées (anatomopathologie)</term><term>Tumeurs cutanées (métabolisme)</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Mastectomy</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Hémangiosarcome</term><term>Lymphoedème</term><term>Tumeurs cutanées</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Mastectomie</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="métabolisme" xml:lang="fr"><term>Hémangiosarcome</term><term>Tumeurs cutanées</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Hemangiosarcoma</term><term>Lymphedema</term><term>Skin Neoplasms</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Lymphoedème</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><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Cartographie chromosomique</term><term>Caryotypage</term><term>Complications postopératoires</term><term>Femelle</term><term>Humains</term><term>Immunohistochimie</term><term>Lymphoedème</term><term>Microscopie électronique</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></record>Pour manipuler ce document sous Unix (Dilib)
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