Document Detail


Immunoselection by T lymphocytes generates repeated MHC class I-deficient metastatic tumor variants.
MedLine Citation:
PMID:  11149409     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Alteration of MHC class I molecule expression is a widespread mechanism used by tumor cells to evade T cell responses. It has long been proposed that the origin of these MHC class I-negative or -deficient tumor variants is T cell immune selection. However, there are no experimental or clinical data to substantiate this hypothesis, and this issue is currently the subject of debate. Here we report that an H-2 class I-negative fibrosarcoma tumor clone generated MHC class I-negative spontaneous lung metastases in immunocompetent syngeneic BALB/c mice. Interestingly, the same B9 clone generated MHC class I-positive metastatic nodes, under basal conditions, in athymic nu/nu BALB/c mice. This phenomenon was observed in the metastatic nodules generated after a period of in vivo growth but not in the primary tumors growing locally in the footpad. These findings support the hypothesis that the H-2 phenotype of metastatic nodes is influenced by the T cell repertoire of the host, since in the absence of this T cell pressure (i.e., in nude mice) the metastatic nodes 'recovered' H-2 class I expression. In addition, 2 different phenotypes were found when the metastatic nodules obtained from immunocompetent mice were treated with IFN-gamma. One phenotype, present in 83% of the colonies, was characterized by resistance of the Ld molecule to IFN-gamma induction, due to a deletion involving the Ld gene. The second phenotype (17% of the colonies) was similar to the original B9 clone and was characterized by the response of K, D and L class I genes to IFN-gamma. These data provide evidence that the changes in MHC class I expression during tumor development might not be random but could be predictable.
Authors:
A Garcia-Lora; I Algarra; J J Gaforio; F Ruiz-Cabello; F Garrido
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of cancer. Journal international du cancer     Volume:  91     ISSN:  0020-7136     ISO Abbreviation:  Int. J. Cancer     Publication Date:  2001 Jan 
Date Detail:
Created Date:  2001-01-08     Completed Date:  2001-01-25     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0042124     Medline TA:  Int J Cancer     Country:  United States    
Other Details:
Languages:  eng     Pagination:  109-19     Citation Subset:  IM    
Affiliation:
Servicio de Análisis Clínicos, Hospital Universitario Virgen de las Nieves, Universidad de Granada, Spain.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Separation
Chromosome Mapping
DNA, Complementary / metabolism
Exons
Fibrosarcoma / genetics*,  immunology
Flow Cytometry
Genes, MHC Class I / genetics*
Interferon-gamma / pharmacology
Lung Neoplasms / genetics*,  immunology
Mice
Mice, Inbred BALB C
Mice, Nude
Microsatellite Repeats
Neoplasms, Experimental / genetics*,  immunology
Phenotype
Polymerase Chain Reaction
RNA / metabolism
Reverse Transcriptase Polymerase Chain Reaction
Spleen / metabolism
T-Lymphocytes / immunology*
Chemical
Reg. No./Substance:
0/DNA, Complementary; 63231-63-0/RNA; 82115-62-6/Interferon-gamma

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


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