Comparative genomic hybridization in epithelioid sarcoma

Summary Background  Epithelioid sarcoma is a rare mesenchymal neoplasm of unknown histogenesis. Data on genome‐wide surveys for chromosomal aberrations in epithelioid sarcoma are limited. Objectives  To investigate genetic aberrations in epithelioid sarcoma. Methods  We analysed seven cases of epith...

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Published inBritish journal of dermatology (1951) Vol. 151; no. 5; pp. 1054 - 1059
Main Authors Lee, M-W., Jee, K-J., Han, S-S., Gong, G-Y., Choi, J-H., Moon, K-C., Koh, J-K.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Science Ltd 01.11.2004
Blackwell
Oxford University Press
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Summary:Summary Background  Epithelioid sarcoma is a rare mesenchymal neoplasm of unknown histogenesis. Data on genome‐wide surveys for chromosomal aberrations in epithelioid sarcoma are limited. Objectives  To investigate genetic aberrations in epithelioid sarcoma. Methods  We analysed seven cases of epithelioid sarcoma (classic type, three cases and proximal type, four cases) by comparative genomic hybridization (CGH), and correlated findings with the results of additional immunohistochemical study. Results and conclusions  CGH analysis showed DNA copy number changes at one to five different genomic sites in six of seven cases (86%). The majority of the changes were gains. The most frequent gain was at 22q (six cases). Other recurrent changes include gains of 12q24‐qter (four cases), 17 (four cases), and 5q32‐qter (three cases). High‐level homology was seen in chromosomal aberration in both types. In addition, expression of interleukin‐2 receptorβ, located in 22q, was revealed by immunohistochemical method in six cases with gain of 22q, suggesting it may play a role in epithelioid sarcoma tumorigenesis.
Bibliography:istex:5DA68F7EA8CDE15F8BEC4D165E0B6AE347059CDC
ark:/67375/WNG-1QLMR98X-G
ArticleID:BJD6246
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0007-0963
1365-2133
DOI:10.1111/j.1365-2133.2004.06246.x