Polymorphisms in the FAS and FASL genes and risk of lung cancer in a Korean population

被引:34
作者
Park, Sun Ha
Choi, Jin Eun
Kim, Eun Jin
Jang, Jin Sung
Lee, Won Kee
Cha, Sung Ick
Kim, Chang Ho
Kam, Sin
Kim, Dong Sun
Park, Rang-Woon
Kim, Young-Chul
Han, Sung Beom
Jung, Tae Hoon
Park, Jae Yong
机构
[1] Kyungpook Natl Univ, Sch Med, Canc Res Inst, Taegu 700422, South Korea
[2] Kyungpook Natl Univ, Sch Med, Dept Biochem, Taegu 700422, South Korea
[3] Kyungpook Natl Univ, Sch Med, Dept Internal Med, Taegu 700412, South Korea
[4] Kyungpook Natl Univ, Sch Med, Dept Prevent Med, Taegu 700422, South Korea
[5] Kyungpook Natl Univ, Sch Med, Dept Anat, Taegu 700422, South Korea
[6] Chonnam Natl Univ, Sch Med, Dept Internal Med, Gwanguj 501746, South Korea
[7] Keimyung Univ, Sch Med, Dept Internal Med, Taegu 700712, South Korea
关键词
FAS; FASL; polymorphism; lung cancer susceptibitity;
D O I
10.1016/j.lungcan.2006.09.002
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background: The FAS and FASL system play an important role in regulating extrinsic apoptotic pathway and inappropriate regulation of this signaling pathway contributes to lung tumorigenesis. Polymorphisms in the promoter region of the FAS (-1377G>A and -670A>G) and FASL (-844C>T) have been shown to alter the transcriptional activities of these genes. In order to evaluate the contribution of these polymorphisms to the risk of lung cancer, we carried out a case-control study in a Korean population. Methods: The FAS and FASL genotypes were determined in 582 lung cancer patients and 582 healthy control subjects who were frequency-matched for age and gender. Results: The FAS and FASL genotypes and the FAS haplotypes exhibited no apparent relationship with the risk of lung cancer. In addition, there was no significant interaction between the FAS and FASL polymorphisms in the development of lung cancer. Conclusion: These results suggest that the FAS-1377G>A and -670A>G and FASL-844C>T polymorphisms do not significantly affect the susceptibility to lung cancer in Koreans. (C) 2006 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:303 / 308
页数:6
相关论文
共 40 条
[1]   Apoptosis control by death and decoy receptors [J].
Ashkenazi, A ;
Dixit, VM .
CURRENT OPINION IN CELL BIOLOGY, 1999, 11 (02) :255-260
[2]   Biochemical pathways of caspase activation during apoptosis [J].
Budihardjo, I ;
Oliver, H ;
Lutter, M ;
Luo, X ;
Wang, XD .
ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, 1999, 15 :269-290
[3]   A decade of caspases [J].
Degterev, A ;
Boyce, M ;
Yuan, JY .
ONCOGENE, 2003, 22 (53) :8543-8567
[4]  
Gratas C, 1998, CANCER RES, V58, P2057
[5]   FAS LIGAND-INDUCED APOPTOSIS AS A MECHANISM OF IMMUNE PRIVILEGE [J].
GRIFFITH, TS ;
BRUNNER, T ;
FLETCHER, SM ;
GREEN, DR ;
FERGUSON, TA .
SCIENCE, 1995, 270 (5239) :1189-1192
[6]   Apoptosome dysfunction in human cancer [J].
Hajra, KM ;
Liu, JR .
APOPTOSIS, 2004, 9 (06) :691-704
[7]   Identification and characterisation of polymorphisms in the promoter region of the human Apo-1/Fas (CD95) gene [J].
Huang, QR ;
Morris, D ;
Manolios, N .
MOLECULAR IMMUNOLOGY, 1997, 34 (8-9) :577-582
[8]   THE POLYPEPTIDE ENCODED BY THE CDNA FOR HUMAN CELL-SURFACE ANTIGEN FAS CAN MEDIATE APOPTOSIS [J].
ITOH, N ;
YONEHARA, S ;
ISHII, A ;
YONEHARA, M ;
MIZUSHIMA, S ;
SAMESHIMA, M ;
HASE, A ;
SETO, Y ;
NAGATA, S .
CELL, 1991, 66 (02) :233-243
[9]   Re:: Polymorphisms of death pathway genes FAS and FASL in esophageal squamous-cell carcinoma [J].
Krippl, P ;
Langsenlehner, U ;
Renner, W ;
Köppel, H ;
Samonigg, H .
JOURNAL OF THE NATIONAL CANCER INSTITUTE, 2004, 96 (19) :1478-1479
[10]   Genetic polymorphisms of FAS and FASL (CD95/CD95L) genes in cervical carcinogenesis:: An analysis of haplotype and gene-gene interaction [J].
Lai, HC ;
Lin, WY ;
Lin, YW ;
Chang, CC ;
Yu, MH ;
Chen, CC ;
Chu, TY .
GYNECOLOGIC ONCOLOGY, 2005, 99 (01) :113-118