Expression of c-Met receptor and hepatocyte growth factor/scatter factor in synovial sarcoma and epithelioid sarcoma

被引:0
|
作者
C. Kuhnen
Edina Tolnay
Hans Ulrich Steinau
Bruno Voss
Klaus-Michael Müller
机构
[1] Institute of Pathology,
[2] University Hospital Bergmannsheil,undefined
[3] Bürkle-de-la-Camp Platz 1,undefined
[4] D-44789 Bochum,undefined
[5] Germany Tel.: (+49) 234-3026600,undefined
[6] Fax: (+49) 234-3026671,undefined
[7] Department of Plastic and Hand Surgery - Burn Centre,undefined
[8] University Hospital Bergmannsheil,undefined
[9] Bochum,undefined
[10] Germany,undefined
[11] Professional Associations’ Research Institute for Occupational Medicine,undefined
[12] Bochum,undefined
[13] Germany,undefined
来源
Virchows Archiv | 1998年 / 432卷
关键词
Key words c-Met receptor; Hepatocyte growth factor/scatter factor; Synovial sarcoma; Epithelioid sarcoma;
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学科分类号
摘要
 Overexpression of c-Met receptor/hepatocyte growth factor (scatter factor) system (c-Met/HGF/SF) as a physiologically paracrine cellular signaling system is thought to be involved in the progression of malignant tumours. In 26 synovial sarcomas and epithelioid sarcomas, c-Met and HGF/SF expression was analysed immunohistochemically. There were 10 biphasic synovial sarcomas, 7 of which showed moderate to strong c-Met expression in epithelial areas compared with the fibrous component, with corresponding expression of HGF/SF. Six of 9 monophasic fibrous synovial sarcomas showed only very faint c-Met and corresponding HGF/SF expression. In 7 epithelioid sarcomas strong expression of c-Met and HGF/SF was observed within epithelioid tumour cells. Non-radioactive in situ hybridization demonstrated the synthesis of c-Met receptor in tumor cells by detecting c-met-mRNA. This analysis shows that in synovial sarcomas and epithelioid sarcomas, tumour entities with epithelial and mesenchymal structures, c-Met and HGF/SF overexpression can be detected, indicating a role of this signaling system in these subtypes of sarcoma, and especially in the more epithelioid tumour phenotype. An autocrine interaction between overexpressed c-Met receptor and HGF/SF may be hypothesized.
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页码:337 / 342
页数:5
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