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Alterations of HLA class I and class II antigen expressions in borderline, invasive and metastatic ovarian cancers
In an effort to understand whether HLA class I and II plays any role in the process of tumorigenesis and metastasis, we have immunohistochemically examined expression of HLA class I and II antigen by using the monoclonal antibodies (mAb) L368 (for beta2m of HLA class I), HC-10 (for HLA-B, C heavy ch...
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Published in: | Experimental & molecular medicine 2002-03, Vol.34 (1), p.18-26 |
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Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | In an effort to understand whether HLA class I and II plays any role in the process of tumorigenesis and metastasis, we have immunohistochemically examined expression of HLA class I and II antigen by using the monoclonal antibodies (mAb) L368 (for beta2m of HLA class I), HC-10 (for HLA-B, C heavy chains), and LGII-612.14 (for HLA class II heavy chain) in 5 borderline serous malignancy (BSM), 20 serous adenocarcinomas (SA), 15 borderline mucinous malignancy (BMM), and 10 mucinous adenocarcinomas (MA) of human ovary tumor case tissues. In BSM, the distribution and intensity of HLA expressions failed to reach statistical significance. In SA, HLA class I beta2-microglobulin (beta2m), HLA-B, C heavy chains and HLA class II heavy chain antigen expressions were down-regulated. Although expressions of HLA-B, C heavy chains and class II heavy chain were down-regulated in metastatic SA, there were no differences in HLA expression levels between primary and metastatic lesions. In BMM, class II heavy chain expressions were down-regulated. In MA, beta2m, HLA-B, C heavy chains and class II heavy chain expressions were also down-regulated. Thus, we could distinguish the reduction or absence of HLA molecule expression was related to malignant potential. Loss of HLA class I and II molecules in invasive ovarian cancers raises the possibility that this could be a factor for tumor cells to retain invasiveness. |
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ISSN: | 1226-3613 2092-6413 2092-6413 |
DOI: | 10.1038/emm.2002.3 |