Detection of GST1 gene deletion by the polymerase chain reaction and its possible correlation with stomach cancer in Japanese

Harada, Shoji; Misawa, Shogo; Nakamura, Takako; Tanaka, Naomi; Ueno, Ei; Nozoe, Mutsumi

doi:10.1007/bf00210745

Cited by 82 publications

(46 citation statements)

References 12 publications

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“…This is consistent with results previously reported for smaller groups by Harada et al (1992), Zhong et al (1993) or Paradiso et al (1994) comparing null and non-null genotypes.…”

Section: Discussionsupporting

confidence: 94%

“…Zhong et al (1993) compared 225 controls and 197 breast cancer patients; Harada et al (1992) studied 84 controls and 65 patients. Ambrosone et al (1995) restricted their study to postmenopausal women: they compared 212 Caucasian patients and 282 community controls and discovered a trend towards an increased breast cancer risk among GSTM1 null post-menopausal women under 58 years of age [odds ratio (OR) = 2.44].…”

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confidence: 99%

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

et al. 1998

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SummaryThe 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].

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“…This is consistent with results previously reported for smaller groups by Harada et al (1992), Zhong et al (1993) or Paradiso et al (1994) comparing null and non-null genotypes.…”

Section: Discussionsupporting

confidence: 94%

mentioning

confidence: 99%

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

et al. 1998

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“…Several studies have reported an independent, increased risk of gastric cancer for the GSTM1 null [7] , GSTT1 null [6] , CYP2E1 c1/c2 or c2/c2 [50] , *2-allele containing ALDH2 genotypes [9] , and shorter (s) allele-containing L-myc [10] genotypes. However, other studies have not found any association between gastric cancer and these genotypes [51][52][53] .…”

Section: Discussion Discussion Discussion Discussion Discussionmentioning

confidence: 99%

“…Genetic polymorphisms of xenobiotic-metabolizing enzymes can also affect susceptibility to cancer. Several studies have reported that the genetic polymorphisms of metabolic enzymes, such as cytochrome p450 2E1 (CYP2E1) [5] , glutathione S-transferase mu 1 (GSTM1) [6] , glutathione Stransferase theta 1 (GSTT1) [7] , aldehyde dehydrogenase 2 (ALDH2) [8] , and L-myc proto-oncogene [9] , and mutations of p53 [10] and Ki-ras [11] genes are associated with the development of gastric cancer.…”

Section: Introduction Introduction Introduction Introduction Introducmentioning

confidence: 99%

Effects of dietary intake and genetic factors on hypermethylation of thehMLH1gene promoter in gastric cancer

Nan¹

2005

WJG

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Abstract Abstract AbstractAIM: Hypermethylation of the promoter of the hMLH1 gene, which plays an important role in mismatch repair during DNA replication, occurs in more than 30% of human gastric cancer tissues. The purpose of this study was to investigate the effects of environmental factors, genetic polymorphisms of major metabolic enzymes, and microsatellite instability on hypermethylation of the promoter of the hMLH1 gene in gastric cancer. METHODS:Data were obtained from a hospital-based, case-control study of gastric cancer. One hundred and ten gastric cancer patients and 220 age-and sex-matched control patients completed a structured questionnaire regarding their exposure to environmental risk factors. Hypermethylation of the hMLH1 gene promoter, polymorphisms of the GSTM1, GSTT1, CYP1A1, CYP2E1, ALDH2 and L-myc genes, microsatellite instability and mutations of p53 and Ki-ras genes were investigated. RESULTS:Both smoking and alcohol consumption were associated with a higher risk of gastric cancer with hypermethylation of the hMLH1 gene promoter. High intake of vegetables and low intake of potato were associated with increased likelihood of gastric cancer with hypermethylation of the hMLH1 gene promoter. Genetic polymorphisms of the GSTM1, GSTT1, CYP1A1, CYP2E1, ALDH2, and L-myc genes were not significantly associated with the risk of gastric cancer either with or without hypermethylation in the promoter of the hMLH1 gene. Hypermethylation of the hMLH1 promoter was significantly associated with microsatellite instability (MSI): 10 of the 14 (71.4%) MSI-positive tumors showed hypermethylation, whereas 28 of 94 (29.8%) the MSI-negative tumors were hypermethylated at the hMLH1 promoter region. Hypermethylation of the hMLH1 gene promoter was significantly inversely correlated with mutation of the p53 gene. CONCLUSION:These results suggest that cigarette smoking and alcohol consumption may influence the development of hMLH1-positive gastric cancer. Most dietary factors and polymorphisms of GSTM1, GSTT1, CYP1A1, CYP2E1, ALDH2, and L-myc genes are not independent risk factors for gastric cancer with hypermethylation of the hMLH1 promoter. These data also suggest that there could be two or more different molecular pathways in the development of gastric cancer, perhaps involving tumor suppression mechanisms or DNA mismatch repair.

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“…For example, a considerable number of investigations indicate that individuals with a homozygous deletion of the GSTM1 gene (GSTM1 null genotype) are susceptible to lung and urinary bladder cancers [1,3,5]. However, the link between the GSTM1 polymorphism and gastric carcinoma is controversial [6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Genotypes of glutathione S-transferase M1 and N-acetyltransferase 2 in Japanese patients with gastric cancer

Oda

Kobayashi

Ooi³

et al. 1999

Gastric Cancer

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Detection of GST1 gene deletion by the polymerase chain reaction and its possible correlation with stomach cancer in Japanese

Cited by 82 publications

References 12 publications

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

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

Effects of dietary intake and genetic factors on hypermethylation of thehMLH1gene promoter in gastric cancer

Genotypes of glutathione S-transferase M1 and N-acetyltransferase 2 in Japanese patients with gastric cancer

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