Catechol-O-Methyltransferase (COMT) gene polymorphism and breast cancer risk in young women

被引:46
作者
Bergman-Jungeström, M [1 ]
Wingren, S [1 ]
机构
[1] Linkoping Univ Hosp, Fac Hlth Sci, Div Oncol, Dept Biomed & Surg, S-58185 Linkoping, Sweden
关键词
Catechol-O-Methyltransferase; COMT; genetic polymorphism; breast cancer; early onset; catechol oestrogens;
D O I
10.1054/bjoc.2001.2009
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Oestrogen exposure has long been considered to be a main risk factor of breast cancer. More recently, interest has also focused on the possible carcinogenic influence from oestrogen metabolites, such as catechol oestrogens. O-methylation, catalysed by Catechol-O-Methyltransferase (COMT), is one pathway by which the potentially carcinogenic catechol oestrogens can be inactivated. The gene coding for COMT protein contains a single-nucleotide polymorphism (SNP), resulting in an amino acid shift Val --> Met, which has been shown to determine high- and low-activity configuration of the enzyme. We hypothesized that the low-activity allele, COMTMet, may be implicated in early onset breast cancer. In the present case-control study, including 126 young breast cancer patients (less than or equal to 36 years) and 117 healthy female blood donors, we analysed the association between COMTMet genotype and risk of breast cancer. No significant difference in the frequency of low-/high-activity alleles was found between cases and controls, indicating that the polymorphism, as a single factor, may not contribute to breast carcinogenesis in young women. (C) 2001 Cancer Research Campaign.
引用
收藏
页码:859 / 862
页数:4
相关论文
共 30 条
[21]   CATECHOL-O-METHYLTRANSFERASE - THERMOLABILE ENZYME IN ERYTHROCYTES OF SUBJECTS HOMOZYGOUS FOR ALLELE FOR LOW ACTIVITY [J].
SCANLON, PD ;
RAYMOND, FA ;
WEINSHILBOUM, RM .
SCIENCE, 1979, 203 (4375) :63-65
[22]  
SPRUDLE AB, 2000, JNCI-J NATL CANCER I, V92, P1674
[23]  
TAIOLI E, 1995, CANCER RES, V55, P3757
[24]  
Thompson PA, 1998, CANCER RES, V58, P2107
[25]   Pooled analysis of prospective cohort studies on height, weight, and breast cancer risk [J].
van den Brandt, PA ;
Spiegelman, D ;
Yaun, SS ;
Adami, HO ;
Beeson, L ;
Folsom, AR ;
Fraser, G ;
Goldbohm, RA ;
Graham, S ;
Kushi, L ;
Marshall, JR ;
Miller, AB ;
Rohan, T ;
Smith-Warner, SA ;
Speizer, FE ;
Willett, WC ;
Wolk, A ;
Hunter, DJ .
AMERICAN JOURNAL OF EPIDEMIOLOGY, 2000, 152 (06) :514-527
[26]   Low penetrance genes associated with increased risk for breast cancer [J].
Weber, BL ;
Nathanson, KL .
EUROPEAN JOURNAL OF CANCER, 2000, 36 (10) :1193-1199
[27]  
WEISZ J, 1994, POLYCYCL AROMAT COMP, V6, P241, DOI 10.1080/10406639408031190
[28]   Molecular mechanisms of estrogen carcinogenesis [J].
Yager, JD ;
Liehr, JG .
ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY, 1996, 36 :203-232
[29]   RELATIONSHIP BETWEEN THE GSTM1 GENETIC-POLYMORPHISM AND SUSCEPTIBILITY TO BLADDER, BREAST AND COLON-CANCER [J].
ZHONG, S ;
WYLLIE, AH ;
BARNES, D ;
WOLF, CR ;
SPURR, NK .
CARCINOGENESIS, 1993, 14 (09) :1821-1824
[30]   Functional role of estrogen metabolism in target cells: review and perspectives [J].
Zhu, BT ;
Conney, AH .
CARCINOGENESIS, 1998, 19 (01) :1-27