This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Murta-Nascimento, C. Articles by Malats, N. Search for Related Content PubMed PubMed Citation Articles by Murta-Nascimento, C. Articles by Malats, N.

Risk of Bladder Cancer Associated with Family History of Cancer: Do Low-Penetrance Polymorphisms Account for the Increase in Risk?

¹ Institut Municipal d'Investigació Mèdica; ² Centre de Recerca en Epidemiologia Ambiental; ³ Universitat Pompeu Fabra, Barcelona, Spain; ⁴ Division of Cancer Epidemiology and Genetics, National Cancer Institute, Department of Health and Human Services, Bethesda, Maryland; ⁵ Universidad de Oviedo, Oviedo, Spain; ⁶ Unidad de Investigación, Hospital Universitario de Canarias, La Laguna, Spain; ⁷ Consorci Hospitalari Parc Taulí, Sabadell, Spain; and ⁸ Hospital General de Elche, Elche, Spain

Requests for reprints: Núria Malats, Centre de Recerca en Epidemiologia Ambiental (CREAL), Institut Municipal d'Investigació Mèdica (IMIM), Carrer del Dr. Aiguader 88, E-08003, Barcelona, Spain. Phone: 34-933-160-671; Fax: 34-933-160-575. E-mail: nuria{at}imim.es

The relationship between family history of cancer in first-degree relatives and risk of bladder cancer was examined in the Spanish Bladder Cancer Study. Information on family history of cancer was obtained for 1,158 newly diagnosed bladder cancer cases and 1,244 controls included in 18 hospitals between 1998 and 2001. A total of 464 (40.1%) cases and 436 (35.1%) controls reported a family history of cancer in 1 relative [odds ratio (OR), 1.32; 95% confidence interval (95% CI), 1.11-1.59]; the OR was 1.23 (95% CI, 1.01-1.50) among those with only one relative affected and 1.67 (95% CI, 1.23-2.29) among those with 2 affected relatives (P_trend = 0.0004). A greater risk of bladder cancer was observed among those diagnosed at age 45 years (OR, 2.67; 95% CI, 1.10-6.50) compared with those diagnosed over age 45 years (OR, 1.27; 95% CI, 1.06-1.52). The OR of bladder cancer among subjects reporting a family history of cancer of the bladder was 2.34 (95% CI, 0.95-5.77). Statistically significant associations emerged between bladder cancer risk and family history of cancer of the esophagus, lung, prostate, and brain. The OR of bladder cancer for those reporting family history of bladder cancer was 4.76 (95% CI, 1.25-18.09) among NAT2-slow acetylators and 1.17 (95% CI, 0.17-7.86) among NAT2-rapid/intermediate acetylators (P_interaction = 0.609). Among individuals with GSTM1 null and present genotypes, the corresponding ORs were 2.91 (95% CI, 0.44-19.09) and 4.21 (95% CI, 1.26-14.14), respectively (P_interaction = 0.712). Limitations of our study are small sample size in subgroup analyses, reliability of family history data, and possible residual confounding by shared environmental exposures. Overall, our findings support the hypothesis that genetic factors play a role in bladder cancer etiology. Whether these correspond to low-penetrance cancer-predisposing polymorphisms acting together and/or interacting with environmental factors warrants further research. (Cancer Epidemiol Biomarkers Prev 2007;16(8):1595–600)