Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005684 (bladder cancer)
 16,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glutathione S-transferases (GSTs) are a family of isoenzymes involved in cellular detoxification. Previous studies have correlated the absence of the GSTM1 protein with an increased risk of developing some cancers, especially lung or bladder cancer, in heavy smokers. In this study, we determined GSTM1 gene polymorphisms in a French western population of 437 female controls and 361 community breast cancer patients. Three distinct alleles of this gene may be identified: GST M1* A allele, GST M1* B allele, and GST M1* 0 allele (which is deleted). Null patients (GSTM1 0) are homozygous for the deletion. We determined in our two populations, patients with no, one or two GSTM1 alleles. The comparative analysis of our two populations did not demonstrate any statistically significant difference in GSTM1 allelotype distribution between the two groups (P = 0.43), although the null genotype was the more frequent in patients. The predominance of the null genotype was significant in the oldest group of patients (> or = 55) (P = 0.006), suggesting that GSTM1 null genotype may play an important role in breast cancer susceptibility in the elderly. This was not observed in the youngest age group, i.e. < 40 year old patients (P = 0.25), or in the patients aged from 40 to 55 years old (P = 0.37). Our results also point out a putative protective role of the A allele in the older female control group (P = 0.02), especially in subjects hemizygous for these alleles (P = 0.03). A prospective study will be of interest to investigate the effect of dosage of the gene.
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PMID:Allelic deletion at glutathione S-transferase M1 locus and its association with breast cancer susceptibility. 967 67

Bladder cancer is highly recurrent after therapy, which has an enormous impact on the health and financial condition of the patient. It is worth developing diagnostic tools for bladder cancer. In our previous study, we found that the bladder carcinogen BBN increased urothelial global DNA CpG methylation and decreased GSTM1 protein expression in mice. Here, the correlation of BBN-decreased GSTM1 and GSTM gene CpG methylation status was analyzed in mice bladders. BBN treatment decreased the protein and mRNA expression of GSTM1, and the CpG methylation ratio of GSTM1 gene promoter was slightly increased in mice bladders. Unlike mouse GSTM1, the human GSTM1 gene tends to be deleted in bladder cancers. Among 7 human bladder cancer cell lines, GSTM1 gene is really null in 6 cell lines except one, T24 cells. The CpG methylation level of GSTM1 was 9.9% and 5-aza-dC did not significantly increase GSTM1 protein and mRNA expression in T24 cells; however, the GSTM5 gene was CpG hypermethylated (65.4%) and 5-aza-dC also did not affect the methylation ratio and mRNA expression. However, in other cell lines without GSTM1, 5-aza-dC increased GSTM5 expression and decreased its CpG DNA methylation ratio from 84.6% to 61.5% in 5637, and from 97.4% to 75% in J82 cells. In summary, two biomarkers of bladder tumor were provided. One is the GSTM1 gene which is down-regulated in mice bladder carcinogenesis and is usually deleted in human urothelial carcinoma, while the other is the GSTM5 gene, which is inactivated by DNA CpG methylation.
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PMID:Gene Expression and DNA Methylation Status of Glutathione S-Transferase Mu1 and Mu5 in Urothelial Carcinoma. 2740 95