Role of <i>N</i>-Acetyltransferase Phenotype in Human Susceptibility To Bladder Carcinogenic Arylamines

Wolf, Hans; Lower, Gerald M.; Bryan, George T.

doi:10.3109/00365598009179555

Cited by 36 publications

(14 citation statements)

References 6 publications

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“…Many adverse drug and chemical reactions have been associated with acetylator status (Lunde et al, 1983;Drayer & Reidenberg, 1977;Wolf et al, 1980;Cartwright et al, 1982). It can therefore be of some importance in clinical and occupational settings to know the acetylator phenotype of individuals, and a number of screening methods using test drugs (such as isoniazid, sulphamethazine and dapsone) have been developed for this purpose (Evans, 1969;Schroder, 1972;Eidus & Hodgkin, 1973;Weber & Brenner, 1974;Carr et al, 1978;du Souich et al, 1979).…”

Section: Introductionmentioning

confidence: 99%

A simple test for acetylator phenotype using caffeine.

Grant¹,

Tang²,

Kalow³

1984

Brit J Clinical Pharma

186

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A method is presented for the use of caffeine, in the forms commonly ingested by a large proportion of the world's population, to test for the clinically important acetylation polymorphism. Each of 146 subjects provided a spot sample of urine between 2 and 6 h after coffee, tea or cola soft drink consumption, and the molar ratio of 5‐acetylamino‐6‐ formylamino −3‐methyluracil (AFMU) to 1‐methylxanthine (1X) was determined by a simple h.p.l.c. assay. The ratio afforded segregation of three apparent modes of acetylation capacity in this population, in concordance with a standard sulphamethazine phenotyping procedure and with other methods using controlled caffeine intake and urine collections. The day‐to‐day consistency of the method was established in eight selected subjects.

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Section: Introductionmentioning

confidence: 99%

A simple test for acetylator phenotype using caffeine.

Grant¹,

Tang²,

Kalow³

1984

Brit J Clinical Pharma

186

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“…In 1979, Lower et al [5] and Lower and Bryan [4] reported that slow acetylator phenotype had an increased bladder cancer risk in Sweden and Denmark, but it was not statistically signifi cant. However, certain published articles indicated no association between bladder cancer carcinogenesis and slow acetylator phenotype [4,5,[14][15][16][17][18][19][20][21] . On the other hand, Hanssen et al [23] and Roots et al [22] implied an elevated risk in slow acetylator phenotype.…”

Section: Discussionmentioning

confidence: 99%

Interaction Effect in Bladder Cancer between N-Acetyltransferase 2 Genotype and Alcohol Drinking

Chung²,

Huang³

et al. 2005

Urol Int

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Cigarette smoking, aromatic amines and ionizing radiation are known carcinogens of bladder cancer. NAT2 genotype might play a role in bladder cancer carcinogenesis. This hospital-based, case-control study was conducted in Kaohsiung, Taiwan, which neighbors the high incidence region of bladder cancer in the black-foot disease area. A total of 103 cases with diagnosed bladder cancer were collected. For each case, 1 control was selected from the same hospital. A structured questionnaire was applied for all cases and controls. DNA was extracted from peripheral blood cell. The ASO-PCR/RFLP technique was used to determine the NAT2 genotype. For bladder cancer, the significantly excessive risks were observed in regular drinkers (OR = 2.74, 95% CI = 1.28–5.87) and residents of the black-foot disease endemic area (OR = 7.53, 95% CI = 2.16–26.33), and interaction of regular drinking and slow type of NAT2 (OR = 18.04, 95% CI = 2.28–142.80). We suggested that NAT2 genotype might play a role of effect modifier in bladder cancer carcinogenesis.

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“…Phenotype gives the investigator a simpler classification system (rapid vs slow) than is easily achieved with a system of 15 or more alleles combined in many possible ways. The ability of NA T2 phenotype to predict risk has been shown in colon cancer and in bladder cancer (6,8,10,(39)(40)(41)(42)(43). Failure to identify an association with other diseases may be due to a lack of understanding of the mechanism of the disease and its link to NAT2.…”

Section: Discussionmentioning

confidence: 99%

Acetylation as an Indicator of Risk

Lang¹

1997

Environmental Health Perspectives

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Aromatic amine acetylation has been recognized for many years as an important metabolic polymorphism in humans because of its relationship to disease. This system serves as a model in risk assessment because of its role in drug and carcinogen activation and detoxification and because of the ease with which it is measured. However, possible interactions of NAT1-NAT2 phenotypes or genotypes illustrate the complexity of xenobiotic metabolism pathways. Moreover, the use of such information for risk assessment is further complicated by the association of the rapid phenotype with increased risk in colon cancer and the slow phenotype with increased risk in urinary bladder cancer. Before this biomarker can be effectively utilized as a significant predictor of individual risk, it will be necessary to identify specific sources of aromatic amine exposure and to characterize further the substrate specificity of NAT1 and NAT2 in relation to the multiplicity of enzyme variants occurring in human populations. Environ Health Perspect 105(Suppl 4): 763-766 (1997)

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Role of N-Acetyltransferase Phenotype in Human Susceptibility To Bladder Carcinogenic Arylamines

Cited by 36 publications

References 6 publications

A simple test for acetylator phenotype using caffeine.

A simple test for acetylator phenotype using caffeine.

Interaction Effect in Bladder Cancer between N-Acetyltransferase 2 Genotype and Alcohol Drinking

Acetylation as an Indicator of Risk

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