Document Detail


HLA-G expression in malignant melanoma.
MedLine Citation:
PMID:  17689098     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Both, the expression of HLA-G (a non-classical HLA class I molecule) and the loss of classical HLA class I molecules enable tumor cells to evade from immunosurveillance of the host. Whereas HLA-G down-modulates the immune functions of all cells participating in the immune defence mechanisms, defects on HLA class I expression result in the resistance of tumor cells to cytotoxic T lymphocytes attacks. This contribution reviews the HLA-G expression pattern in malignant melanoma lesions, its correlation to the loss of classical HLA class I antigens, and new aspects of HLA-G regulation.
Authors:
Vera Rebmann; Stefan Wagner; Hans Grosse-Wilde
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Publication Detail:
Type:  Journal Article; Review     Date:  2007-06-28
Journal Detail:
Title:  Seminars in cancer biology     Volume:  17     ISSN:  1044-579X     ISO Abbreviation:  Semin. Cancer Biol.     Publication Date:  2007 Dec 
Date Detail:
Created Date:  2007-11-12     Completed Date:  2008-02-04     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9010218     Medline TA:  Semin Cancer Biol     Country:  England    
Other Details:
Languages:  eng     Pagination:  422-9     Citation Subset:  IM    
Affiliation:
Institut für Immunologie, Universitätsklinikum Essen, Virchowstr. 171, D-45122 Essen, Germany. immunologie@uni-essen.de
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MeSH Terms
Descriptor/Qualifier:
Cell Line, Tumor
Gene Expression Regulation, Neoplastic
HLA Antigens / chemistry,  genetics,  immunology,  metabolism*
Histocompatibility Antigens Class I / chemistry,  genetics,  immunology,  metabolism*
Humans
Immunologic Surveillance
Melanoma / genetics,  immunology*,  metabolism
Skin Neoplasms / genetics,  immunology*,  metabolism
Tumor Escape
Chemical
Reg. No./Substance:
0/HLA Antigens; 0/HLA-G antigen; 0/Histocompatibility Antigens Class I

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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