Occupational history and genetic N-acetyltransferase polymorphism in urothelial cancer patients of Leverkusen, Germany

被引:47
作者
Golka, K
Prior, V
Blaszkewicz, M
Cascorbi, I
Schops, W
Kierfeld, G
Roots, I
Blot, HM
机构
[1] UNIV DORTMUND,INST ARBEITSPHYSIOL,D-44139 DORTMUND,GERMANY
[2] KLINIKUM LEVERKUSEN,UROL KLIN,DEPT UROL,LEVERKUSEN,GERMANY
[3] HUMBOLDT UNIV BERLIN,INST KLIN PHARMAKOL,BERLIN,GERMANY
关键词
acetylation phenotype; aromatic amines; bladder cancer;
D O I
10.5271/sjweh.150
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
Objectives The study was designed to realize possible shifts in the ratio of slow to fast acetylators within a group of 196 urothelial cancer patients in an area with earlier benzidine production. Methods The subjects were interviewed for occupational and nonoccupational risk factors, The patients were phenotyped for N-acetyltransferase 2 (NAT2) by Grant's caffeine test. A subgroup of 54 patients was additionally genotyped for NAT2. Results The antimode in the NAT2 phenotyping with the caffeine test (AFMU:1X ratio) was 1.0, as evidenced by additional genotyping of the subgroup of 54 patients. The prevalence of slow acetylators in the entire group of bladder cancer patients was 55%, in accordance with published figures for European populations. In a subgroup of 40 patients with occupational histories as workers in chemical or rubber industries 65% were slow acetylators. In a further subgroup of 28 cases having specifically worked at chemical production sites of the local chemical industry, 68% were slow acetylators. Conclusions in contrast to earlier studies, this study shows no increased prevalence of slow acetylators among urothelial cancer patients in comparison with the normal population. However, in subgroups of cases with a likelihood of past occupational contacts with aromatic amines, there was a trend towards a higher representation of slow acetylators. This finding is in accordance with observations of others that the percentage of slow acetylators in urothelial cancer patients is generally decreasing, possibly because the production of benzidine and benzidine-based dyes ceased in the early 1970s.
引用
收藏
页码:332 / 338
页数:7
相关论文
共 39 条
[1]  
[Anonymous], KLASS BER SYST ALPH
[2]   GENETIC RISK AND CARCINOGEN EXPOSURE - A COMMON INHERITED DEFECT OF THE CARCINOGEN-METABOLISM GENE GLUTATHIONE-S-TRANSFERASE M1 (GSTM1) THAT INCREASES SUSCEPTIBILITY TO BLADDER-CANCER [J].
BELL, DA ;
TAYLOR, JA ;
PAULSON, DF ;
ROBERTSON, CN ;
MOHLER, JL ;
LUCIER, GW .
JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1993, 85 (14) :1159-1164
[3]   GENETIC MONITORING OF HUMAN POLYMORPHIC CANCER SUSCEPTIBILITY GENES BY POLYMERASE CHAIN-REACTION - APPLICATION TO GLUTATHIONE TRANSFERASE MU [J].
BELL, DA ;
THOMPSON, CL ;
TAYLOR, J ;
MILLER, CR ;
PERERA, F ;
HSIEH, LL ;
LUCIER, GW .
ENVIRONMENTAL HEALTH PERSPECTIVES, 1992, 98 :113-117
[4]  
BOLT HM, 1993, Z ARBEITSWISS, V47, P50
[5]   DETERMINATION OF CYP1A2 AND NAT2 PHENOTYPES IN HUMAN-POPULATIONS BY ANALYSIS OF CAFFEINE URINARY METABOLITES [J].
BUTLER, MA ;
LANG, NP ;
YOUNG, JF ;
CAPORASO, NE ;
VINEIS, P ;
HAYES, RB ;
TEITEL, CH ;
MASSENGILL, JP ;
LAWSEN, MF ;
KADLUBAR, FF .
PHARMACOGENETICS, 1992, 2 (03) :116-127
[6]   RELEVANCE OF METABOLIC POLYMORPHISMS TO HUMAN CARCINOGENESIS - EVALUATION OF EPIDEMIOLOGIC EVIDENCE [J].
CAPORASO, N ;
LANDI, MT ;
VINEIS, P .
PHARMACOGENETICS, 1991, 1 (01) :4-19
[7]  
CARTWRIGHT RA, 1982, LANCET, V2, P842
[8]  
CASCORBI I, 1995, AM J HUM GENET, V57, P581
[9]  
Cascorbi I., 1994, Naunyn-Schmiedeberg's Archives of Pharmacology, V349, pR132
[10]   THE ASSOCIATION OF THE SLOW ACETYLATOR PHENOTYPE WITH BLADDER-CANCER [J].
EVANS, DAP ;
EZE, LC ;
WHIBLEY, EJ .
JOURNAL OF MEDICAL GENETICS, 1983, 20 (05) :330-333