Family history of urogenital cancers in patients with bladder, renal cell and prostate cancers

Randi, Giorgia; Pelucchi, Claudio; Negri, Eva; Talamini, Renato; Galeone, Carlotta; Franceschi, Silvia; Vecchia, Carlo La

doi:10.1002/ijc.23037

Cited by 30 publications

(38 citation statements)

References 43 publications

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“…Increased risk of renal cancer has been associated with a family history of kidney cancer in most previous case -control (Mellemgaard et al, 1994;Schlehofer et al, 1996;Gago-Dominguez et al, 2001;Negri et al, 2006;Clague et al, 2009) and cohort studies (Goldgar et al, 1994;Czene and Hemminki, 2002;Gudbjartsson et al, 2002;Clague et al, 2009), although results for some are null or not statistically significant (McLaughlin et al, 1984;Kreiger et al, 1993;Hung et al, 2007;Randi et al, 2007). The reported excess risks generally ranged from two-to five-fold for both study designs.…”

Section: Discussionmentioning

confidence: 96%

“…Smoking, obesity, and hypertension are primary risk factors that may explain half of all RCC diagnoses in the United States (Benichou et al, 1998;Chow and Devesa, 2008). RCC risk has been examined in relation to familial history of cancer in a number of epidemiological studies (McLaughlin et al, 1984;Kreiger et al, 1993;Goldgar et al, 1994;Mellemgaard et al, 1994;Schlehofer et al, 1996;Gago-Dominguez et al, 2001;Hemminki, 2002, 2003;Gudbjartsson et al, 2002;Negri et al, 2006;Hung et al, 2007;Randi et al, 2007;Clague et al, 2009). Many of these studies have shown a positive association with a family history of cancer (Goldgar et al, 1994;Mellemgaard et al, 1994;Schlehofer et al, 1996;Gago-Dominguez et al, 2001), particularly when the affected relative is a sibling (Czene and Hemminki, 2002;Gudbjartsson et al, 2002;Negri et al, 2006;Hung et al, 2007;Clague et al, 2009).…”

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confidence: 99%

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Family history of cancer and renal cell cancer risk in Caucasians and African Americans

et al. 2010

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BACKGROUND:The association between renal cell carcinoma (RCC) risk and family history of cancer has not been examined with an adequate number of African Americans (AAs). METHODS: In a population-based case -control study, unconditional logistic regression was used to calculate the association between RCC risk and a family history of cancer among 1217 RCC cases and 1235 controls. RESULTS: Increased RCC risk was shown for subjects with at least one first-degree relative with kidney cancer (odds ratio ¼ 2.29; 95% confidence interval ¼ 1.31 -4.00). No differences in risk were observed when analyses were stratified by race. For Caucasians, excess risk was observed among those reporting a sibling with kidney cancer, whereas for AAs, increased risk occurred among subjects reporting either a sibling or parent affected with the disease. A family history of non-renal cancers, and those related to smoking or to the von Hippel -Lindau syndrome, revealed no association with RCC risk. CONCLUSION: The RCC risk associated with a family history of kidney cancer is similar among Caucasians and AAs.

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Section: Discussionmentioning

confidence: 96%

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confidence: 99%

Family history of cancer and renal cell cancer risk in Caucasians and African Americans

et al. 2010

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“…[31][32][33][34] There is a significantly increased risk of bladder cancer among firstdegree relatives of individuals who have bladder cancer, with an earlier age of disease onset. [35][36][37] In a large twin study, environmental factors were estimated to contribute a significant 69% to bladder cancer risk, whereas inherited genetic factors contributed a nonsignificant 31% of risk. 38 Attention has been given to the NAT2 slow acetylator and GSTM1-null genotypes as potential familial risk factors.…”

Section: Bladder Cancer Carcinogenesismentioning

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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“…Table 4 summarizes pertinent details of 9 case-control and 4 cohort studies in which family history of TCCUT was quantitatively evaluated as a bladder cancer risk factor. [12][13][14][15][16][17][18][19][20][21][22][23][24] These studies varied widely in sample size, quality of design and analysis, inclusion/exclusion of upper urinary tract sites, and the extent to which reported cancers were objectively documented, but are surprisingly similar in their estimated risk ratios. These range from 1.2 to 6.1 among male and female cases combined, with most of the results clustering between 1.4 and 1.9.…”

Section: Case Reports Of Familial Tccutmentioning

confidence: 99%

“…[2,7] Common variants in low-penetrance genes involved in the metabolism of environmental toxins have been shown to modify individual susceptibility to bladder carcinogens. [2] Furthermore, a genetic predisposition to bladder cancer is suggested by the occurrence of TCCUT in several Mendelian disorders [8][9][10][11], epidemiologic studies showing that a positive TCCUT family history increases bladder cancer risk [12][13][14][15][16][17][18][19][20][21][22][23][24], and a limited number of case reports describing multiple-case TCCUT families. [25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41] Therefore, both genetic and environmental factors play a role in the development of bladder and related urinary tract cancers.…”

Section: Introductionmentioning

confidence: 99%

Familial and genetic risk of transitional cell carcinoma of the urinary tract

Mueller¹,

Caporaso²,

Greene³

2008

Urologic Oncology: Seminars and Original Investigations

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Environmental exposures, including tobacco smoke and occupational exposure to aromatic amines, have been implicated in bladder cancer etiology. However, the pathogenesis of urinary bladder transitional cell carcinoma remains incompletely defined. In epidemiologic studies, family history confers a two-fold increase in bladder cancer risk, but it is uncertain whether this represents evidence of a genetic and/or a shared environmental basis for familial aggregation. Polymorphisms in genes involved in the metabolism of environmental toxins (e.g., NAT2) clearly modify individual susceptibility to bladder cancer. A genetic predisposition has also been suggested by case reports describing multiple-case families, and the development of bladder cancer in association with several well-described Mendelian disorders (e.g., HNPCC, retinoblastoma). Here we update a previouslyreported family, report a new multiple-case kindred, critically review previously-reported bladder cancer families and the epidemiologic literature related to family history of transitional cell carcinoma of the urinary tract (TCCUT) as a risk factor, as well as provide a brief summary of genetic factors that have been implicated in TCCUT risk. We conclude that familial TCCUT is either very uncommon or significantly under-reported, perhaps on the assumption that this is an environmental rather than a genetic disorder. The interaction between multiple genetic and environmental factors has made it challenging to identify genetic components responsible for many common diseases; therefore, a proposed genome-wide association study (GWAS) for urinary bladder cancer may help to clarify the etiologic role of the candidate genetic pathways reviewed here, as well as characterize gene/environment interactions that contribute to TCCUT carcinogenesis.

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Family history of urogenital cancers in patients with bladder, renal cell and prostate cancers

Cited by 30 publications

References 43 publications

Family history of cancer and renal cell cancer risk in Caucasians and African Americans

Family history of cancer and renal cell cancer risk in Caucasians and African Americans

The origins of bladder cancer

Familial and genetic risk of transitional cell carcinoma of the urinary tract

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