Glutathione S-transferase μ polymorphism and gastric cancer in the Portuguese population

被引:14
作者
Martins, G
Alves, M
Dias, J
Santos, R
Neves, BC
Mafra, M
Martins, AP
Ramos, S
Ramos, M
Mexia, J
Quina, M
Rueff, J
Monteiro, C
机构
[1] Fac Ciencias Med, UNL Dept Genet, P-1300 Lisbon, Portugal
[2] Hosp Pulido Valente, Serv Gastroenterol, P-1700 Lisbon, Portugal
[3] Fac Ciencias Med, UNL Clin Univ Med 3, P-1700 Lisbon, Portugal
[4] Hosp S Jose, Serv Anat Patol, P-1100 Lisbon, Portugal
[5] Hosp Santa Cruz, Serv Anat Patol, P-2775 Carnaxide, Linda A Velha, Portugal
[6] Hosp Pulido Valente, Serv Anat Patol, P-1700 Lisbon, Portugal
[7] Univ Nova Lisboa, Fac Ciencias & Tecnol, Dept Matemat, P-2825 Monte De Caparica, Portugal
关键词
glutathione S-transferase; GSTM1; polymorphism; gastric cancer; cancer susceptibility; Portuguese population; cancer epidemiology; null allele;
D O I
10.1080/135475098231084
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The glutathione S-transferases appear to form part of a protective mechanism against the development of cancer where environmental chemical carcinogens are involved. In humans one member of the mu class gene family (GSTM1) has been shown to be polymorphic and is only expressed in similar to 50% of individuals. Previous studies have shown a possible link between the null phenotype and susceptibility to cancer but have been equivocal regarding stomach cancer. To evaluate any association in Portuguese gastric cancer individuals with GSTM1 variability, we performed GSTIM1 polymorphism by PCR amplification in 148 gastric cancer patients and in 84 healthy control individuals. We found no statistical differences between the gastric cancer and control populations (wild type phenotype: 52%, 48%; null phenotype: 48%, 52%, respectively). A subset analysis into site of tumour also revealed no significant differences between the groups, although we found a slight increase of the wild type phenotype in the samples of the antrum compared with the control population (57% vs 48%, respectively; chi(2)=1.18; p less than or equal to 0.28) and a slight increase of the null phenotype in the signet ring cells/mucocellular group (chi(2)=1.05; p less than or equal to 0.3). However, in both cases it did not reach statistical significance. A subset analysis of the histological groups following the WHO criteria revealed a statistically significant difference (chi(2)=3.704; p less than or equal to 0.05) between the moderately differentiated gastric adenocarcinoma and the presence of the wild type phenotype. These results do not support the hypothesis that the GSTM1 null phenotype predisposes to gastric cancer in the Portuguese population and the moderately differentiated gastric adenocarcinoma seems to be associated with the presence of the GSTM1 wild type phenotype.
引用
收藏
页码:441 / 447
页数:7
相关论文
共 30 条
[1]   COMBINED EFFECT OF CYP1A1 INDUCIBILITY AND GSTM1 POLYMORPHISM ON HISTOLOGICAL TYPE OF LUNG-CANCER [J].
ANTTILA, S ;
HIRVONEN, A ;
HUSGAFVELPURSIAINEN, K ;
KARJALAINEN, A ;
NURMINEN, T ;
VAINIO, H .
CARCINOGENESIS, 1994, 15 (06) :1133-1135
[2]   THE ROLE OF GLUTATHIONE-DEPENDENT ENZYMES IN DRUG-RESISTANCE [J].
BLACK, SM ;
WOLF, CR .
PHARMACOLOGY & THERAPEUTICS, 1991, 51 (01) :139-154
[3]   GENETIC-HETEROGENEITY OF THE HUMAN GLUTATHIONE TRANSFERASES - A COMPLEX OF GENE FAMILIES [J].
BOARD, P ;
COGGAN, M ;
JOHNSTON, P ;
ROSS, V ;
SUZUKI, T ;
WEBB, G .
PHARMACOLOGY & THERAPEUTICS, 1990, 48 (03) :357-369
[4]  
BOARD PG, 1981, AM J HUM GENET, V33, P36
[5]  
BRUCE WR, 1987, CANCER RES, V47, P4237
[6]   GST1 GENE DELETION DETERMINED BY POLYMERASE CHAIN-REACTION [J].
COMSTOCK, KE ;
SANDERSON, BJS ;
CLAFLIN, G ;
HENNER, WD .
NUCLEIC ACIDS RESEARCH, 1990, 18 (12) :3670-3670
[7]   Glutathione S-transferase GSTT1 genotypes and susceptibility to cancer: Studies of interactions with GSTM1 in lung, oral, gastric and colorectal cancers [J].
Deakin, M ;
Elder, J ;
Hendrickse, C ;
Peckham, D ;
Baldwin, D ;
Pantin, C ;
Wild, N ;
Leopard, P ;
Bell, DA ;
Jones, P ;
Duncan, H ;
Brannigan, K ;
Alldersea, J ;
Fryer, AA ;
Strange, RC .
CARCINOGENESIS, 1996, 17 (04) :881-884
[8]  
DEAKIN M, 1994, AM J GASTRONETEROL S, V89, pS1
[9]  
EDWARDS MC, 1994, PCR METH APPL, V3, pS65
[10]  
HARADA S, 1992, HUM GENET, V90, P62