The Role of the Urine in Vesical Neoplasm. 1. Experimental Confirmation of the Urogenous Theory of Pathogenesis

McDonald, Donald F.; Lund, Roland R.

doi:10.1016/s0022-5347(17)67826-1

Cited by 77 publications

(15 citation statements)

References 9 publications

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“…suggested a possible involvement of allelic loss of the activated X chromosome in bladder carcinogenesis and progression; however, this study was based on 6 female bladder cancer cases only 67. Concentrated urine or less frequent urination could potentially increase the exposure of the bladder urothelium to carcinogens 68, 69. A study in an adult population without voiding complaints reported no significant differences between males and females in amount of urine produced in a 24 hr time period, but females in the age groups 20–29 and 30–39 had a significant higher frequency of urination in that 24 hr period 70.…”

Section: Discussionmentioning

confidence: 99%

The effect of smoking on the male excess of bladder cancer: A meta‐analysis and geographical analyses

Hemelt

Yamamoto

Cheng

et al. 2008

Intl Journal of Cancer

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Smoking is considered the primary risk factor for bladder cancer. Although smoking prevalence and bladder cancer incidence vary around the world, bladder cancer is on average 4 times more common in males than in females. This article describes the observed male-female incidence ratio of bladder cancer for 21 world regions in 2002 and 11 geographical areas during the time period . A meta-analysis, including 34 studies, was performed to ascertain the increased risk for bladder cancer in males and females when smoking. The summary odds ratios (SORs) calculated in the meta-analysis were used to estimate the male-female incidence ratio of bladder cancer that would be expected for hypothetical smoking prevalence scenarios. These expected malefemale incidence ratios were compared with the observed ratios to evaluate the role of smoking on the male excess of bladder cancer. The male-female incidence ratio of bladder cancer was higher than expected worldwide and over time, based on a smoking prevalence of 75% in males, 10% in females and an increased risk (SOR) of bladder cancer associated with smoking of 4.23 for males and 1.35 for females, respectively. This implied that, at least in the Western world, smoking can only partially explain the difference in bladder cancer incidence. Consequently, other factors are responsible for the difference in bladder cancer incidence. ' 2008 Wiley-Liss, Inc.Key words: cigarette smoking; bladder cancer; meta-analysis; incidenceThe incidence of bladder cancer varies worldwide with the highest rates occurring in more developed countries. 1 Bladder cancer is more common in males than in females, with a world age standardized incidence rate of 10.1 per 100,000 persons-years for males and 2.5 per 100,000 persons-years for females. 1 Although almost all studies on bladder cancer mention a male-excess of bladder cancer, it has not been described in detail whether this male excess has been changing over time and if it differs between geographical areas. Smoking is considered the most important risk factor for bladder cancer 2 and the prevalence of smoking has been varying over time, between sexes and geographical regions. 3 In Western Europe and North America, smoking prevalence has been declining since 1960. 3 In the United Kingdom, the percentage of smokers decreased in the period from 1960 to 1998 from 61 to 28 in males and from 42 to 26 in females. 4 The Sub-Saharan area has a low smoking prevalence while many countries in Latin America and South-East Asia have a smoking prevalence in males above 50%. [3][4][5] It is therefore plausible that when smoking prevalence differs between males and females that at least a part of the difference in bladder cancer incidence between males and females can be explained by smoking. We will firstly describe the male-female incidence ratio of bladder cancer over time and for different geographical areas. Secondly, a meta-analysis on smoking and bladder cancer will be performed aimed at assessing whether males and females have the same increased risk for...

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Section: Discussionmentioning

confidence: 99%

The effect of smoking on the male excess of bladder cancer: A meta‐analysis and geographical analyses

Hemelt

Yamamoto

Cheng

et al. 2008

Intl Journal of Cancer

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“…Mice, rats, guinea pigs, hamsters, and rabbits are also sensitive; however, it is the dog that most closely parallels man's response to these chemicals (3,5). From the studies of McDonald and Lund (6) and Scott and Boyd (7), it became apparent that an agent contained in the urine of dogs exposed to arylamines was responsible for tumor induction. Based on these data and others, various models for bladder tumor formation have been developed.…”

Section: Introductionmentioning

confidence: 99%

Arylamine-DNA adducts in vitro and in vivo: their role in bacterial mutagenesis and urinary bladder carcinogenesis

Beland¹,

Beranek²,

Dooley³

et al. 1983

Environ Health Perspect

176

126

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Hepatic N-oxidation, followed by N-glucuronidation, has been proposed as a route of metabolic activation for arylamine bladder carcinogens. It is postulated that the N-glucuronides are transported to the bladder lumen where they are hydrolyzed under slightly acidic conditions to release directacting carcinogenic and mutagenic N-hydroxyarylamines. In this study, 4-aminobiphenyl (ABP), 1-naphthylamine (1-NA), 2-naphthylamine (2-NA), 2-acetylaminofluorene (AAF), 4-nitrobiphenyl (NBP), benzidine (BZ), and N-acetylbenzidine (ABZ) were administered to male beagle dogs (60 mmole/kg), and the bladder epithelium DNA adducts were quantified at various times after treatment. At 24-48 hr after administration, the order of binding to bladder epithelium DNA was: ABP >> AAF > NBP 2-NA-BZ ABZ>> 1-NA. The level of DNA modification by ABP remained constant for 7 days, whereas 2-NA and AAF residues decreased by 35% and 80%, respectively. The extent and relative persistence of total DNA binding correlated with the compounds' ability to induce bladder tumors in dogs. ABP, AAF, NBP, 2-NA and ABZ administration resulted in DNA binding sufficient for adduct analysis. Enzymatic hydrolysis of the DNA and examination of the adducts by high pressure liquid chromatography indicated that arylamine substitution at C8 of deoxyguanosine was the dominant product. Additional adducts were detected in animals treated with ABP, NBP, and 2-NA. Furthermore, the profiles of adducts obtained in vivo were remarkably similar to the profiles obtained when the N-hydroxy arylamine metabolites of these carcinogens were reacted with DNA in vitro at pH 5.0. To evaluate the mutagenic potential of these arylamine-DNA adducts, Salmonella typhimurium strains TA 1535 and TA 1538 were incubated with N-hydroxy-2-NA, N-hydroxy-2-aminofluorene (AF), N-hydroxy-ABP, and N-hydroxy-ABZ and the resulting DNA adducts and reversions were quantified. Arylamine-C8-deoxyguanosine substitution was correlated with frameshift reversions induced by these agents, with the lesions showing a relative order of mutagenic efficiency of ABZ>AF-2-NA>ABP. These data suggest that mutagenic N-hydroxyarylamines may be ultimate carcinogens for the bladder epithelium. Furthermore, if one assumes that a mutagenic lesion is important for tumor initiation, then C8-deoxyguanosine substitution by these compounds may be significant for urinary bladder carcinogenesis.

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“…McDonald and Lund [5] showed experimentally that mucosa of the dome is not intrinsically less susceptible to malignant changes than the mucosa of the lower hemisphere, and that continued contact with urine is the main determining factor in the etiology of carcinomas. In experiments with dogs, in which the dome half of the bladder was surgically trans formed into a pouch isolated of contact with urine, the carcinogen (600 mg daily of /Tnaphthylamine administered orally) did not produce tumors in this part in 9 out of 10 dogs over a period of 2 years.…”

Section: Discussionmentioning

confidence: 99%

“…As suming that contact with urine is an important factor in the etiology of cancer [4][5][6][10][11][12][13] those parts of mucosa of the bladder (lower hemi sphere), which are normally longer in contact with urine, should show a significantly higher rate of carcinomas per unit surface area than those in Parkash Kiusswi r n r the upper hemisphere (vault or the dome). If, however, other endogenous biological factors are of primary importance, a uniform distribution (same rate of carcinomas per unit surface area of the mucosa all over the blad der) must be expected.…”

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confidence: 99%

The Role of Urine in the Etiology of Cancer of the Urinary Bladder

Parkash

Kiesswetter²

1976

Urol Int

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It is shown that the site-frequency distribution of carcinomas relative to the upper and lower hemispheres of the urinary bladder is inhomogeneous. It is pointed out that the contact with urine is the important etiological factor and that other factors, if any, play only a secondary role. It is suggested that prolonged (forced) retention of urine should be avoided. Investigation of urinary carcinogens is needed.

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The Role of the Urine in Vesical Neoplasm. 1. Experimental Confirmation of the Urogenous Theory of Pathogenesis

Cited by 77 publications

References 9 publications

The effect of smoking on the male excess of bladder cancer: A meta‐analysis and geographical analyses

The effect of smoking on the male excess of bladder cancer: A meta‐analysis and geographical analyses

Arylamine-DNA adducts in vitro and in vivo: their role in bacterial mutagenesis and urinary bladder carcinogenesis

The Role of Urine in the Etiology of Cancer of the Urinary Bladder

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