Document Detail

A role for the Fas/FasL system in modulating genetic susceptibility to T-cell lymphoblastic lymphomas.
MedLine Citation:
PMID:  17545588     Owner:  NLM     Status:  MEDLINE    
The Fas/FasL system mediates induced apoptosis of immature thymocytes and peripheral T lymphocytes, but little is known about its implication in genetic susceptibility to T-cell malignancies. In this article, we report that the expression of FasL increases early in all mice after gamma-radiation treatments, maintaining such high levels for a long time in mice that resisted tumor induction. However, its expression is practically absent in T-cell lymphoblastic lymphomas. Interestingly, there exist significant differences in the level of expression between two mice strains exhibiting extremely distinct susceptibilities that can be attributed to promoter functional polymorphisms. In addition, several functional nucleotide changes in the coding sequences of both Fas and FasL genes significantly affect their biological activity. These results lead us to propose that germ-line functional polymorphisms affecting either the levels of expression or the biological activity of both Fas and FasL genes could be contributing to the genetic risk to develop T-cell lymphoblastic lymphomas and support the use of radiotherapy as an adequate procedure to choose in the treatment of T-cell malignancies.
María Villa-Morales; Javier Santos; Eduardo Pérez-Gómez; Miguel Quintanilla; José Fernández-Piqueras
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cancer research     Volume:  67     ISSN:  0008-5472     ISO Abbreviation:  Cancer Res.     Publication Date:  2007 Jun 
Date Detail:
Created Date:  2007-06-04     Completed Date:  2007-07-26     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5107-16     Citation Subset:  IM    
Laboratorio de Genética Molecular Humana, Departamento de Biología, Universidad Autónoma de Madrid, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Madrid, Spain.
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MeSH Terms
Antigens, CD95 / biosynthesis,  genetics*
Base Sequence
Cloning, Molecular
DNA, Complementary / genetics
Fas Ligand Protein / biosynthesis,  genetics*
Genetic Predisposition to Disease
Mice, Inbred C57BL
Molecular Sequence Data
Polymorphism, Genetic
Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics*,  metabolism
Promoter Regions, Genetic
Reverse Transcriptase Polymerase Chain Reaction
Transcription, Genetic
Reg. No./Substance:
0/Antigens, CD95; 0/DNA, Complementary; 0/Fas Ligand Protein

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