Role of N-acetyltransferase phenotypes in bladder carcinogenesis: a pharmacogenetic epidemiological approach to bladder cancer.
A large excess of patients with bladder cancer who have previously been exposed to N-substituted aryl compounds as a result of the production of dyestuff intermediates have the slow phenotype of the enzyme N-acetyltransferase. Among bladder-cancer patients in general, those presenting with T3 or T4 disease or carcinoma-in-situ also show an excess of the slower subtypes. Either N-substituted aryl compounds more frequently produce tumours with this invasive potential if linked with slow acetylation or slow acetylators are more susceptible to tumour production when exposed to some N-substituted aryl compounds. It is suggested that acetylator status could be used to identify susceptible individuals in potentially hazardous occupations.
D000107:Acetylation; D000123:Acetyltransferases / Q000009:adverse effects*; D001191:Arylamine N-Acetyltransferase / Q000009:adverse effects* / Q000235:genetics; D002278:Carcinoma in Situ / Q000139:chemically induced* / Q000235:genetics / Q000473:pathology; D004396:Coloring Agents / Q000009:adverse effects; D005260:Female; D006801:Humans; D008297:Male; D009784:Occupational Diseases / Q000139:chemically induced*; D010641:Phenotype; D011110:Polymorphism, Genetic; D013045:Species Specificity; D013997:Time Factors; D001749:Urinary Bladder Neoplasms / Q000139:chemically induced* / Q000235:genetics / Q000473:pathology
D004396:Coloring Agents; D000123:Acetyltransferases; D001191:Arylamine N-Acetyltransferase