Allelotype influence at glutathione S-transferase M1 locus on breast cancer susceptibility

被引:44
作者
Charrier, J
Maugard, CM
Le Mevel, B
Bignon, YJ
机构
[1] CRLCC Nantes Atlantique, Ctr Rene Gauducheau, Unite Oncol Genet Mol, F-44805 Nantes 01, France
[2] INSERM, Lab Oncol Mol, CRI 9502, F-63011 Clermont Ferrand, France
[3] INSERM, Lab Oncol Mol, EA 2145, F-63011 Clermont Ferrand 1, France
关键词
cancer susceptibility; breast cancer; glutathione S-transferase; allelic polymorphism;
D O I
10.1038/sj.bjc.6690055
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The influence of polymorphisms of the glutathione S-transferase gene GSTM1 in breast cancer susceptibility has been assessed in this study. Previous studies correlated the absence of the GSTM1 protein with an increased risk of developing some cancers, especially lung or bladder cancers, in heavy smokers. In this study, we determined GSTM1 polymorphisms in a population of 437 female controls from the west of France and 361 community breast cancer patients. Three distinct alleles of this gene exist: GSTM1*A, GSTM1*B and GSTM1*0 (deleted allele). Null subjects (GSTM1 null) are homozygous for this deletion. The comparative analysis of GSTM1 allelotypes in our two populations did not demonstrate a statistically significant difference in distribution (P = 0.22), although the null genotype was more frequent in cancer patients. However, breast cancer risk was increased in null subjects ≥ 50 years of age compared with non-null subjects [odds ratio = 1.99 (1.19-3.32), P = 0.009], but not in null subjects < 50 years of age compared with non-null subjects (P = 0.86). Our results suggest that the GSTM1 null genotype may play a role in post-menopausal breast cancer development. They also point to a putative protective role of the A allele in the older female control group, especially in hemizygous subjects [odds ratio = 0.42 (0.23-0.77), P = 0.03].
引用
收藏
页码:346 / 353
页数:8
相关论文
共 38 条
  • [1] AMBROSONE CB, 1995, CANCER RES, V55, P3483
  • [2] [Anonymous], 1989, MOL CLONING LAB MANU
  • [3] CLAUS EB, 1994, MONOGR NCI, V16, P49
  • [4] GST1 GENE DELETION DETERMINED BY POLYMERASE CHAIN-REACTION
    COMSTOCK, KE
    SANDERSON, BJS
    CLAFLIN, G
    HENNER, WD
    [J]. NUCLEIC ACIDS RESEARCH, 1990, 18 (12) : 3670 - 3670
  • [5] THE CAUSES OF CANCER - QUANTITATIVE ESTIMATES OF AVOIDABLE RISKS OF CANCER IN THE UNITED-STATES TODAY
    DOLL, R
    PETO, R
    [J]. JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1981, 66 (06): : 1191 - +
  • [6] SUSCEPTIBILITY TO ULCERATIVE-COLITIS AND CROHNS-DISEASE - INTERACTIONS BETWEEN GLUTATHIONE-S-TRANSFERASE GSTM1 AND GSTT1 GENOTYPES
    DUNCAN, H
    SWAN, C
    GREEN, J
    JONES, P
    BRANNIGAN, K
    ALLDERSEA, J
    FRYER, AA
    STRANGE, RC
    [J]. CLINICA CHIMICA ACTA, 1995, 240 (01) : 53 - 61
  • [7] EASTON D, 1993, CANCER SURV, V18, P95
  • [8] Breast cancer genes - What are the real risks?
    Easton, D
    [J]. NATURE GENETICS, 1997, 16 (03) : 210 - 211
  • [9] BREAST-CANCER RISK AND HISTORY OF SELECTED MEDICAL CONDITIONS LINKED WITH FEMALE HORMONES
    FRANCESCHI, S
    LAVECCHIA, C
    NEGRI, E
    PARAZZINI, F
    BOYLE, P
    [J]. EUROPEAN JOURNAL OF CANCER, 1990, 26 (07) : 781 - 785
  • [10] USE OF SITE-DIRECTED MUTAGENESIS OF ALLELE-SPECIFIC PCR PRIMERS TO IDENTIFY THE GSTM1-A, GSTM1-B, GSTM1-A,B AND GSTM1 NULL POLYMORPHISMS AT THE GLUTATHIONE-S-TRANSFERASE, GSTM1 LOCUS
    FRYER, AA
    ZHAO, L
    ALLDERSEA, J
    PEARSON, WR
    STRANGE, RC
    [J]. BIOCHEMICAL JOURNAL, 1993, 295 : 313 - 315