{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1363951795415438592.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1158/0008-5472.can-04-1567"}},{"identifier":{"@type":"URI","@value":"https://aacrjournals.org/cancerres/article-pdf/64/22/8249/2521240/zch02204008249.pdf"}},{"identifier":{"@type":"NAID","@value":"30018590576"}}],"dc:title":[{"@value":"Tumor-Associated Endothelial Cells with Cytogenetic Abnormalities"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>Abstract</jats:title>\n                  <jats:p>Tumor angiogenesis is necessary for solid tumor progression and metastasis. Tumor blood vessels have been shown to differ from normal counterparts, for example, by changes in morphology. An important concept in tumor angiogenesis is that tumor endothelial cells are assumed to be genetically normal, although these endothelial cells are structurally and functionally abnormal. However, we hypothesized that given the phenotypic differences between tumor and normal blood vessels, there may be genotypic alterations as well. Mouse endothelial cells were isolated from two different human tumor xenografts, melanoma and liposarcoma, and from two normal endothelial cell counterparts, skin and adipose. Tumor-associated endothelial cells expressed typical endothelial cell markers, such as CD31. They had relatively large, heterogeneous nuclei. Unexpectedly, tumor endothelial cells were cytogenetically abnormal. Fluorescence in situ hybridization (FISH) analysis showed that freshly isolated uncultured tumor endothelial cells were aneuploid and had abnormal multiple centrosomes. The degree of aneuploidy was exacerbated by passage in culture. Multicolor FISH indicated that the structural chromosomal aberrations in tumor endothelial cells were heterogeneous, indicating that the cytogenetic alterations were not clonal. There was no evidence of human tumor-derived chromosomal material in the mouse tumor endothelial cells. In marked contrast, freshly isolated normal skin and adipose endothelial cells were diploid, had normal centrosomes, and remained cytogenetically stable in culture even up to 20 passages. FISH analysis of tumor sections also showed endothelial cell aneuploidy. We conclude that tumor endothelial cells can acquire cytogenetic abnormalities while in the tumor microenvironment.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1383951795415438597","@type":"Researcher","foaf:name":[{"@value":"Kyoko Hida"}],"jpcoar:affiliationName":[{"@value":"1Vascular Biology Program,"},{"@value":"2Department of Surgery,"}]},{"@id":"https://cir.nii.ac.jp/crid/1383951795415438595","@type":"Researcher","foaf:name":[{"@value":"Yasuhiro Hida"}],"jpcoar:affiliationName":[{"@value":"1Vascular Biology Program,"},{"@value":"2Department of Surgery,"}]},{"@id":"https://cir.nii.ac.jp/crid/1383951795415438598","@type":"Researcher","foaf:name":[{"@value":"Dhara N. Amin"}],"jpcoar:affiliationName":[{"@value":"1Vascular Biology Program,"},{"@value":"2Department of Surgery,"}]},{"@id":"https://cir.nii.ac.jp/crid/1383951795415438594","@type":"Researcher","foaf:name":[{"@value":"Alan F. Flint"}],"jpcoar:affiliationName":[{"@value":"4Division of Genetics, Children’s Hospital and Harvard Medical School; and"}]},{"@id":"https://cir.nii.ac.jp/crid/1383951795415438596","@type":"Researcher","foaf:name":[{"@value":"Dipak Panigrahy"}],"jpcoar:affiliationName":[{"@value":"1Vascular Biology Program,"},{"@value":"2Department of Surgery,"}]},{"@id":"https://cir.nii.ac.jp/crid/1383951795415438592","@type":"Researcher","foaf:name":[{"@value":"Cynthia C. Morton"}],"jpcoar:affiliationName":[{"@value":"5Dana-Farber/Harvard Cancer Center Cytogenetics Core, Departments of Obstetrics, Gynecology and Reproductive Biology, and Pathology, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts"}]},{"@id":"https://cir.nii.ac.jp/crid/1383951795415438593","@type":"Researcher","foaf:name":[{"@value":"Michael Klagsbrun"}],"jpcoar:affiliationName":[{"@value":"1Vascular Biology Program,"},{"@value":"2Department of Surgery,"},{"@value":"3Department of Pathology, and"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00085472"},{"@type":"EISSN","@value":"15387445"},{"@type":"PISSN","@value":"http://id.crossref.org/issn/00085472"}],"prism:publicationName":[{"@value":"Cancer Research"}],"dc:publisher":[{"@value":"American Association for Cancer Research (AACR)"}],"prism:publicationDate":"2004-11-15","prism:volume":"64","prism:number":"22","prism:startingPage":"8249","prism:endingPage":"8255"},"reviewed":"false","url":[{"@id":"https://aacrjournals.org/cancerres/article-pdf/64/22/8249/2521240/zch02204008249.pdf"}],"createdAt":"2005-09-20","modifiedAt":"2022-06-16","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050025031479115904","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Suprabasin as a novel tumor endothelial cell marker"}]},{"@id":"https://cir.nii.ac.jp/crid/1050025031481155072","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Tumor-Derived Microvesicles Induce Proangiogenic Phenotype in Endothelial Cells via Endocytosis"}]},{"@id":"https://cir.nii.ac.jp/crid/1050306506453910912","@type":"Article","resourceType":"学術雑誌論文(journal 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