Re‐evaluation of the latent period of bladder cancer in dyestuff‐plant workers in Japan

Miyakawa, Michiko; Tachibana, Masaaki; Miyakawa, Ayako; Yoshida, Katsumi; Shimada, Naoki; Murai, Masaru; Kondo, Takefumi

doi:10.1046/j.1442-2042.2001.00342.x

Cited by 30 publications

(21 citation statements)

References 7 publications

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“…[41][42][43][44] Second, exposure to benzidine and other arylamines has been associated with increased risks of bladder cancer in both Asian and Caucasian workers. 17,[45][46][47][48][49][50] Third, as shown in the metaanalysis presented in Table III of Asian populations not exposed to arylamines in the workplace, studies have shown that slow acetylation is a risk factor for bladder cancer comparable to the risk found in Caucasian populations, and the magnitude of the relative risk is the same. 3 Fourth, even though racial differences in the allele distribution among different ethnic groups have been reported, almost all of the alleles found in Caucasian groups have been described in Asian populations.…”

Section: Discussionmentioning

confidence: 93%

NAT2 slow acetylation and bladder cancer in workers exposed to benzidine

Carreón

Ruder

Schulte

et al. 2005

Intl Journal of Cancer

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This study expands a previous study of NAT2 polymorphisms and bladder cancer in male subjects occupationally exposed only to benzidine. The combined analysis of 68 cases and 107 controls from a cohort of production workers in China exposed to benzidine included 30 new cases and 67 controls not previously studied. NAT2 enzymatic activity phenotype was characterized by measuring urinary caffeine metabolite ratios. PCR-based methods identified genotypes for NAT2, NAT1 and GSTM1. NAT2 phenotype and genotype data were consistent. A protective association was observed for the slow NAT2 genotype (bladder cancer OR = 0.3; 95% CI = 0.1 = 1.0) after adjustment for cumulative benzidine exposure and lifetime smoking. Individuals carrying NAT1wt/*10 and NAT1*10/*10 showed higher relative risks of bladder cancer (OR = 2.8, 95% CI = 0.8-10.1 and OR = 2.2, 95% CI = 0.6-8.3, respectively). No association was found between GSTM1 null and bladder cancer. A metaanalysis risk estimate of case-control studies of NAT2 acetylation and bladder cancer in Asian populations without occupational arylamine exposures showed an increased risk for slow acetylators. The lower limit of the confidence interval (OR = 1.4; 95% CI = 1.0-2.0) approximated the upper confidence interval for the estimate obtained in our analysis. These results support the earlier finding of a protective association between slow acetylation and bladder cancer in benzidine-exposed workers, in contrast to its established link as a risk factor for bladder cancer in people exposed to 2-naphthylamine and 4-aminobiphenyl. Study findings suggest the existence of key differences in the metabolism of mono- and diarylamines.

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Section: Discussionmentioning

confidence: 93%

NAT2 slow acetylation and bladder cancer in workers exposed to benzidine

Carreón

Ruder

Schulte

et al. 2005

Intl Journal of Cancer

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“…A prospective study to demonstrate this effect would be both expensive and time consuming because of the long lag between exposure to carcinogens and the development of bladder cancer. 79 So-called 'secondary prevention' treats people with well-defined premalignant conditions to prevent the development of clinical cancer. As such premalignant disease states have not been generally recognized in bladder cancer, this approach has not been used in this disease.…”

Section: Implications For the Detection And Prevention Of Bladder Cancermentioning

confidence: 99%

The origins of bladder cancer

Crawford

2008

Laboratory Investigation

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Bladder cancer, arising from the transitional cells of the mucosal urothelium, may present as a noninvasive, papillary tumor protruding from the mucosal surface, or as a solid, nonpapillary tumor that invades the bladder wall and has a high propensity for metastasis. The nonpapillary tumors originate from in situ dysplasia. The most common environmental risk for bladder cancer is active smoking; occupational exposure to arsenic or other carcinogens is also a risk factor. A possible familial component to bladder cancer has been described. Conventional models of carcinogenesis suppose the existence of successive mutation events within a specific cell clone, enabling its eventual escape from regulation of cell division and maintenance of genomic integrity. Important new information has emerged from whole-organ mapping of the mucosal genome in bladders resected for invasive cancer (Majewski et al, Lab Invest; published online 5 May 2008). Mapping of genetic hits across the entire mucosa demonstrates genetic alterations in six chromosomal regions, not only in mucosal regions of evident dysplasia, but also in morphologically normal mucosa. These clonally expanded regions cover vast expanses of the bladder surface, as a 'first wave' of pre-neoplasia. Target genes in these regions are termed 'forerunner genes' (FR genes), based on the concept that these genes enable the initial clonal expansion of in situ urothelial neoplasia. Extensive further analysis of human populations with urothelial cancer implicates genetic polymorphisms in one of these genes, P2RY5, as being present in a familial cluster of cancers of multiple organs, and as imparting risk for development of bladder cancer in active smokers. P2RY5 is a gene encoded within intron 17 of RB1, a prototypic tumor suppressor gene whose expression is lost at a later stage of bladder carcinogenesis. Alterations of the FR gene status provide a novel opportunity to screen individuals at risk for the earliest stage of bladder pre-neoplasia and represent attractive targets for therapeutic and chemopreventive interventions. These findings support the hypothesis that bladder carcinogenesis is initiated by clonal expansion of genetically altered but histologically normal cells that cover broad expanses of the mucosa. Effort must now be given to identifying the biological function of these novel FR genes. KEYWORDS: bladder cancer; forerunner genes; P2RY5; RB1; whole-organ mapping; genomic mapping EPIDEMIOLOGY OF BLADDER CANCER Bladder cancer is the fourth most incident cancer in males and ninth most incident in females. In the United States, over 67 000 new cases are diagnosed per year, 1 and over 350 000 cases diagnosed worldwide. 2 In the United States, the annual age-adjusted incidence rate for men is approximately 32 per 100 000. 3 Men have a higher risk of bladder cancer than women, by a rate ratio of at least 3:1. Approximately 66% of bladder cancers are diagnosed among individuals age 65 years or older.Bladder cancer arises primarily from the transitional cells of the b...

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“…During the first two time periods (1946–1965, 1966–1985), SIRs were elevated for men with the highest exposures. The latent period between date of hire and bladder cancer diagnosis (or death) were similar (19.5 and 24.1 years) and within the 15‐ to 40‐year range considered reasonable [Miyakawa et al, 2001]. Mean employment durations during the earlier two periods were also similar at 14.8 and 14.5 years, respectively.…”

Section: Discussionmentioning

confidence: 87%