Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Japanese urothelial (bladder, renal pelvis and ureter) cancer patients (n = 83) and community controls (n = 101) were compared for rates of polymorphism in exon 7 of the cytochrome P4501A1 (CYP1A1) gene or homozygous deletion of the glutathione S-transferase class mu (GSTM1) gene. A CYP1A1 polymorphism was detected in a HinCII polymorphism assay utilizing a primer with a single base pair mismatch. The frequency distribution of the CYP1A1 genotypes in urothelial cancer patients showed no significant difference from that in healthy controls. The increased frequency of homozygous deletions of GSTM1 gene loci in patients with urothelial cancer was statistically significant compared with the controls, 51 of 83 (61%) and 43 of 101 (43%) (odds ratio = .2.15, 95% confidence interval = 1.18-3.86). These results lead us to conclude that homozygous deletion of the GSTM1 gene may be associated with susceptibility to urothelial cancer.
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PMID:Cytochrome P4501A1 gene polymorphism and homozygous deletion of the glutathione S-transferase M1 gene in urothelial cancer patients. 769 28

Primary cultured human urothelial cells derived from ureter specimens of urological patients were used to evaluate induction of DNA-damage by OTA in the alkaline single-cell gel electrophoresis (comet) assay. With the cultured cells from each donor a separate comet assay was performed and tail length of the damaged DNA was measured. A broad spectrum of effects was detected between the individual cell cultures with effects reaching from tail lengths on control level up to strongly enhanced tail lengths.All donors of urothelial tissue were additionally genotyped for several xenobiotic metabolising enzymes (cytochrome P450 1A2, glutathione S-transferases T1, M1, and P1, N-acetyltransferase 2) in lymphocyte DNA. The genotype was then correlated with the genotoxic effects obtained in the comet assay.No correlation was found with CYP1A2, GSTT1, and GSTM1 genotypes whereas for GSTP1 stronger genotoxic effects were found in cells from donors with hetero-and homozygously mutated (w/m, m/m) genotypes compared to homozygous wildtypes. The strongest hint for a correlation was found for NAT2, as cells from donors with homozygous mutated alleles (m/m), known as slow acetylators, displayed a higher susceptibility to OTA in the comet assay than cells from donors with the heterozygously mutated or wildtype alleles (rapid acetylators).
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PMID:Is there an influence of enzyme polymorphisms on ochratoxin A genotoxicity? 2360 57