Familial Transitional Cell Carcinoma

Kiemeney, Lambertus A.; Schoenberg, Mark

doi:10.1016/s0022-5347(01)65644-1

Cited by 53 publications

(15 citation statements)

References 52 publications

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“…The cardinal feature by which inherited predisposition is recognized clinically is family history. Genetic predisposition to bladder cancer was evident in a comprehensive review of familial bladder cancer (Kiemeney and Schoenberg, 1996), and a significant familial component in lung cancer was indicated using segregation analysis (Sellers et al, 1994). Gene-environment interactions have been associated with numerous tobacco-related cancer risks (Shields and Harris, 2000).…”

Section: Introductionmentioning

confidence: 99%

Genetic susceptibility to tobacco-related cancer

et al. 2004

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Although cigarette smoking is the dominant risk factor for several epithelial cancers, only a small fraction of individuals with tobacco exposure develop cancer. The underlying hypothesis is that genetic factors may render certain smokers more susceptible to cancer than others. Genetic alterations in critical regulatory pathways may predispose cells to carcinogenesis. These pathways include regulation of xenobiotic metabolism; control of genomic stability, including DNA repair mechanisms, cell-cycle checkpoints, apoptosis and telomere length; and control of microenvironmental factors, such as matrix metalloproteinases, inflammation and growth factors. In addition, epigenetic events, such as promoter hypermethylation and loss of imprinting, are also involved in carcinogenesis. In this review, we will summarize recent advances in genetic susceptibility to tobacco-related cancer. Emphasizing on risk assessment, we will describe how genetic variations in the above-mentioned genetic pathways modify the tobacco-related cancer risk. In addition, we will discuss how genetic variations may assist in predicting clinical outcome, such as the natural history of cancer and treatment response. The measurements of genetic susceptibility by both genotypic and phenotypic assays are covered in the text. Finally, we present a number of current concerns that need to be addressed as the exciting field of molecular cancer epidemiology advances rapidly.

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Section: Introductionmentioning

confidence: 99%

Genetic susceptibility to tobacco-related cancer

et al. 2004

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“…Hereditary factors also contribute to the development of UUC with a 2-fold increased risk among first-degree relatives [3]. The familial cases develop due to site-specific inheritance as well as within the hereditary nonpolyposis colorectal cancer (HNPCC) syndrome [1,3-5]. Individuals with HNPCC are at increased risk for several types of cancer, with the highest life-time risks for colorectal cancer (80%), endometrial cancer (40–60%), ovarian cancer (10–15%), cancer of the small intestine and upper urothelial cancer [4], and the revised Amsterdam criteria for the diagnosis of HNPCC consider these tumor types to be associated with the syndrome [6].…”

Section: Introductionmentioning

confidence: 99%

Low frequency of defective mismatch repair in a population-based series of upper urothelial carcinoma

et al. 2005

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Background: Upper urothelial cancer (UUC), i.e. transitional cell carcinomas of the renal pelvis and the ureter, occur at an increased frequency in patients with hereditary nonpolyposis colorectal cancer (HNPCC). Defective mismatch repair (MMR) specifically characterizes HNPCC-associated tumors, but also occurs in subsets of some sporadic tumors, e.g. in gastrointestinal cancer and endometrial cancer.

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“…A study by Ilić et al found that bladder cancer risk was linked with the existence of familial bladder cancer, especially among the < 45 patients (RR = 1.45) and patients who smoked cigarettes (RR = 10.7)[60]. However, the prevalence of bladder cancer was 10% in the second-degree and third-degree relatives, and 3% in the first-degree relatives, suggesting that bladder cancer may not be a hereditary type of cancer[61]. Combined data from the Swedish, Danish, and Finnish twin registries revealed statistically significant effects of heritable factors for colorectal, breast and prostate cancer, ranging 27%-42%, but no significant association was observed in bladder cancer[62].…”

Section: Genetic Factorsmentioning

confidence: 99%

Bladder cancer epidemiology and genetic susceptibility

2013

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Bladder cancer is the most common malignancy of the urinary system. The incidence of bladder cancer of men is higher than that of women (approximately 4:1). Here, we summarize the bladder cancer-related risk factors, including environmental and genetic factors. In recent years, although the mortality rate induced by bladder cancer has been stable or decreased gradually, the public health effect may be pronounced. The well-established risk factors for bladder cancer are cigarette smoking and occupational exposure. Genetic factors also play important roles in the susceptibility to bladder cancer. A recent study demonstrated that hereditary non-polyposis colorectal cancer is associated with increased risk of bladder cancer. Since 2008, genome-wide association study (GWAS) has been used to identify the susceptibility loci for bladder cancer. Further gene-gene or gene-environment interaction studies need to be conducted to provide more information for the etiology of bladder cancer.

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Familial Transitional Cell Carcinoma

Cited by 53 publications

References 52 publications

Genetic susceptibility to tobacco-related cancer

Genetic susceptibility to tobacco-related cancer

Low frequency of defective mismatch repair in a population-based series of upper urothelial carcinoma

Bladder cancer epidemiology and genetic susceptibility

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