Source:http://linkedlifedata.com/resource/pubmed/id/17183065
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2007-4-26
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pubmed:abstractText |
The FAS-FASL system plays crucial role in counterattack of cancer cell against immune system. This study examined the effects of FAS (-1377G/A and -670A/G) and FASL (-844T/C and 7896G/C) polymorphisms on breast cancer risk and apoptosis of T lymphocytes. The effect on breast cancer risk was determined by case-control analysis of 840 patients and 840 controls. The effects on T-lymphocyte apoptosis were determined by activation-induced cell death (AICD) of T cells ex vivo and by analyzing apoptotic tumor-infiltrating lymphocytes (TILs) in breast cancer tissue. We found moderately increased risk associated with FAS -1377AG [odds ratio (OR), 1.29; 95% confidence interval (CI), 1.05-1.59] and -1377AA (OR, 1.36; 95% CI, 1.01-1.82) genotypes compared with the -1377GG genotype and decreased risk associated with FASL -844CT (OR, 0.76; 95% CI, 0.62-0.94) and -844TT (OR, 0.66; 95% CI, 0.43-1.00) genotypes compared with the -844CC genotype. T lymphocytes with the FASL -844CC genotype had heightened FASL expression that is associated with increased AICD of the T cells stimulated by MCF-7 cells or phytohemagglutinin compared with the FASL -844TT genotype (10.38 +/- 4.09% and 24.29 +/- 1.50% versus 6.03 +/- 0.41% and 17.96 +/- 3.66%; P < 0.05 and 0.001). Breast cancer patients with the FASL -844CC genotype had higher apoptotic TILs in their cancer tissues than those with the FASL -844TT genotype (33.7 +/- 1.2% versus 19.1 +/- 2.0%; P = 0.007). These findings indicate that functional polymorphisms in FAS and FASL contribute to increased apoptosis of tumor infiltration lymphocytes and risk of breast cancer.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0143-3334
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pubmed:author |
pubmed-author:CoxK BKB,
pubmed-author:GuoYongliY,
pubmed-author:HanXiaohongX,
pubmed-author:LaneD MDM,
pubmed-author:LinDongxinD,
pubmed-author:ShiYuankaiY,
pubmed-author:SunTongT,
pubmed-author:XueLiyanL,
pubmed-author:ZhangBailinB,
pubmed-author:ZhangBaoningB,
pubmed-author:ZhangXuemeiX,
pubmed-author:ZhaoDanD,
pubmed-author:ZhouYifengY
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pubmed:issnType |
Print
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pubmed:volume |
28
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1067-73
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pubmed:meshHeading |
pubmed-meshheading:17183065-Adult,
pubmed-meshheading:17183065-Antigens, CD95,
pubmed-meshheading:17183065-Apoptosis,
pubmed-meshheading:17183065-Breast Neoplasms,
pubmed-meshheading:17183065-Case-Control Studies,
pubmed-meshheading:17183065-Fas Ligand Protein,
pubmed-meshheading:17183065-Female,
pubmed-meshheading:17183065-Humans,
pubmed-meshheading:17183065-Lymphocytes, Tumor-Infiltrating,
pubmed-meshheading:17183065-Male,
pubmed-meshheading:17183065-Middle Aged,
pubmed-meshheading:17183065-Polymorphism, Genetic,
pubmed-meshheading:17183065-Polymorphism, Single Nucleotide,
pubmed-meshheading:17183065-Risk,
pubmed-meshheading:17183065-Tumor Cells, Cultured
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pubmed:year |
2007
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pubmed:articleTitle |
Functional polymorphisms in FAS and FASL contribute to increased apoptosis of tumor infiltration lymphocytes and risk of breast cancer.
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pubmed:affiliation |
Center of Breast Diseases and Department of Abdominal Surgery, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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