Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Urinary Bladder Neoplasms: HELP
Articles by Mariana Carla Stern
Based on 15 articles published since 2010
(Why 15 articles?)
||||

Between 2010 and 2020, Mariana C. Stern wrote the following 15 articles about Urinary Bladder Neoplasms.
 
+ Citations + Abstracts
1 Article A Data Mining Approach to Investigate Food Groups related to Incidence of Bladder Cancer in the BLadder cancer Epidemiology and Nutritional Determinants International Study. 2020

Yu, Evan Y W / Wesselius, Anke / Sinhart, Christoph / Wolk, Alicja / Stern, Mariana Carla / Jiang, Xuejuan / Tang, Li / Marshall, James / Kellen, Eliane / van den Brandt, Piet / Lu, Chih-Ming / Pohlabeln, Hermann / Steineck, Gunnar / Allam, Mohamed Farouk / Karagas, Margaret R / La Vecchia, Carlo / Porru, Stefano / Carta, Angela / Golka, Klaus / Johnson, Kenneth C / Benhamou, Simone / Zhang, Zuo-Feng / Bosetti, Cristina / Taylor, Jack A / Weiderpass, Elisabete / Grant, Eric J / White, Emily / Polesel, Jerry / Zeegers, Maurice P A. ·Department of Complex Genetics and Epidemiology, School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands. · DKE Scientific staff, Data Science & Knowledge Engineering, Faculty of Science and Engineering. · Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institute,Stockholm, Sweden. · Department of Preventive Medicine, University of Southern California, Los Angeles, CA, USA. · Department of Cancer Prevention and Control, Roswell Park Cancer Institute, Buffalo, NY, USA. · Leuven University Centre for Cancer Prevention (LUCK), Leuven, Belgium. · Department of Epidemiology, Schools for Oncology and Developmental Biology and Public Health and Primary Care, Maastricht University Medical Centre, Maastricht, The Netherlands. · Department of Urology, Buddhist Dalin Tzu Chi General Hospital, Dalin Township 62247, Chiayi County, Taiwan. · Leibniz Institute for Prevention Research and Epidemiology-BIPS, Bremen, Germany. · Department of Oncology and Pathology, Division of Clinical Cancer Epidemiology, Karolinska Hospital, Stockholm, Sweden. · Department of Preventive Medicine and Public Health, Faculty of Medicine, University of Cordoba, Cordoba, Spain. · Department of Epidemiology, Geisel School of Medicine at Dartmouth, Hanover, NH, USA. · Department of Clinical Medicine and Community Health, University of Milan, Milan, Italy. · Department of Diagnostics and Public Health, Section of Occupational Health, University of Verona, Italy. · University Research Center "Integrated Models for Prevention and Protection in Environmental and Occupational Health" MISTRAL, University of Verona, Milano Bicocca and Brescia, Italy. · Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, University of Brescia, Italy. · Leibniz Research Centre for Working Environment and Human Factors at TU Dortmund, Dortmund, Germany. · Department of Epidemiology and Community Medicine, University of Ottawa, Ottawa, ON, Canada. · INSERM U946, Variabilite Genetique et Maladies Humaines, Fondation Jean Dausset/CEPH, Paris, France. · Departments of Epidemiology, UCLA Center for Environmental Genomics, Fielding School of Public Health, University of California, Los Angeles (UCLA), Los Angeles, CA, USA. · Department of Oncology, Istituto di Ricerche Farmacologiche Mario Negri-IRCCS, Milan, Italy. · Epidemiology Branch, and Epigenetic and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, USA. · International Agency for Research on Cancer (IARC), World Health Organization, Lyon, France. · Department of Epidemiology Radiation Effects Research Foundation, Hiroshima, Japan. · Fred Hutchinson Cancer Research Center, Seattle, WA, USA. · Unit of Cancer Epidemiology, Centro di Riferimento Oncologico di Aviano (CRO) IRCCS, Italy. · CAPHRI School for Public Health and Primary Care, University of Maastricht, Maastricht, The Netherlands. · School of Cancer Sciences, University of Birmingham, Birmingham, UK. ·Br J Nutr · Pubmed #32321598.

ABSTRACT: At present, the analysis of diet and bladder cancer (BC) is mostly based on the intake of individual foods. The examination of food combinations provides a scope to deal with the complexity and unpredictability of the diet and aims to overcome the limitations of the study of nutrients and foods in isolation. This article aims to demonstrate the usability of supervised data mining methods to extract the food groups related to BC. In order to derive key food groups associated with BC risk, we applied the data mining technique C5.0 with 10-fold cross validation in the BLadder cancer Epidemiology and Nutritional Determinants (BLEND) study, including data from 18 case-control and 1 nested case-cohort study, compromising 8,320 BC cases out of 31,551 participants. Dietary data, on the 11 main food groups of the Eurocode 2 Core classification codebook and relevant non-diet data (i.e. sex, age and smoking status) were available. Primarily, five key food groups were extracted; in order of importance: beverages (non-milk); grains and grain products; vegetables and vegetable products; fats, oils and their products; meats and meat products were associated with BC risk. Since these food groups are corresponded with previously proposed BC related dietary factors, data mining seems to be a promising technique in the field of nutritional epidemiology and deserves further examination.

2 Article The association between coffee consumption and bladder cancer in the bladder cancer epidemiology and nutritional determinants (BLEND) international pooled study. 2019

Yu, Evan Yi-Wen / Wesselius, Anke / van Osch, Frits / Stern, Mariana Carla / Jiang, Xuejuan / Kellen, Eliane / Lu, Chih-Ming / Pohlabeln, Hermann / Steineck, Gunnar / Marshall, James / Allam, Mohamed Farouk / La Vecchia, Carlo / Johnson, Kenneth C / Benhamou, Simone / Zhang, Zuo-Feng / Bosetti, Cristina / Taylor, Jack A / Zeegers, Maurice P. ·NUTRIM School for Nutrition and Translational Research in Metabolism, University of Maastricht, Universiteitssingel 40 (Room C5.564), 6229 ER, Maastricht, The Netherlands. evan.yu@maastrichtuniversity.nl. · CAPHRI School for Public Health and Primary Care, University of Maastricht, Maastricht, The Netherlands. evan.yu@maastrichtuniversity.nl. · NUTRIM School for Nutrition and Translational Research in Metabolism, University of Maastricht, Universiteitssingel 40 (Room C5.564), 6229 ER, Maastricht, The Netherlands. · Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK. · Department of Preventive Medicine, University of Southern California, Los Angeles, CA, USA. · Leuven University Centre for Cancer Prevention (LUCK), Louvain, Belgium. · Department of Urology, Buddhist Dalin Tzu Chi General Hospital, Dalin Township, Chiayi County, Taiwan. · Leibniz Institute for Prevention Research and Epidemiology-BIPS, Bremen, Germany. · Clinical Cancer Epidemiology, Department of Oncology, Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. · Department of Cancer Prevention and Control, Roswell Park Cancer Institute, Buffalo, NY, USA. · Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, Section of Public Health and Human Sciences, University of Brescia, Brescia, Italy. · Department of Clinical Medicine and Community Health, University of Milan, Milan, Italy. · Department of Epidemiology and Community Medicine, University of Ottawa, Ottawa, ON, Canada. · INSERM U946, Variabilite Genetique et Maladies Humaines, Fondation Jean Dausset/CEPH, Paris, France. · Departments of Epidemiology, UCLA Center for Environmental Genomics, Fielding School of Public Health, University of California, Los Angeles (UCLA), Los Angeles, CA, USA. · Laboratory of Oncology, Istituto di Ricerche Farmacologiche "Mario Negri" IRCCS, Milan, Italy. · Epidemiology Branch and Epigenetic and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, USA. · CAPHRI School for Public Health and Primary Care, University of Maastricht, Maastricht, The Netherlands. ·Cancer Causes Control · Pubmed #31147895.

ABSTRACT: BACKGROUND: Inconsistent results for coffee consumption and bladder cancer (BC) risk have been shown in epidemiological studies. This research aims to increase the understanding of the association between coffee consumption and BC risk by bringing together worldwide case-control studies on this topic. METHODS: Data were collected from 13 case-control comprising of 5,911 cases and 16,172 controls. Pooled multivariate odds ratios (ORs), with corresponding 95% confidence intervals (CIs), were obtained using multilevel logistic regression models. Furthermore, linear dose-response relationships were examined using fractional polynomial models. RESULTS: No association of BC risk was observed with coffee consumption among smokers. However, after adjustment for age, gender, and smoking, the risk was significantly increased for never smokers (ever vs. never coffee consumers: OR CONCLUSION: This research suggests that positive associations between coffee consumption and BC among never smokers but not smokers.

3 Article Modeling the Complex Exposure History of Smoking in Predicting Bladder Cancer: A Pooled Analysis of 15 Case-Control Studies. 2019

van Osch, Frits H M / Vlaanderen, Jelle / Jochems, Sylvia H J / Bosetti, Cristina / Polesel, Jerry / Porru, Stefano / Carta, Angela / Golka, Klaus / Jiang, Xuejuan / Stern, Mariana C / Zhong, Wei-De / Kellen, Eliane / Pohlabeln, Hermann / Tang, Li / Marshall, James / Steineck, Gunnar / Karagas, Margaret R / Johnson, Kenneth C / Zhang, Zuo-Feng / Taylor, Jack A / La Vecchia, Carlo / Bryan, Richard T / van Schooten, Frederik J / Wesselius, Anke / Zeegers, Maurice P. ·From the Department of Complex Genetics, Nutrition and Translational Research in Metabolism (School NUTRIM), Maastricht University, Maastricht, The Netherlands. · Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, United Kingdom. · Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands. · Unit of Cancer Epidemiology, Department of Oncology, IRCCS - Istituto di Ricerche Farmacologiche Mario Negri Via Giuseppe La Masa, Milan, Italy. · Unit of Cancer Epidemiology, CRO Aviano National Cancer Institute, Aviano (PN), Italy. · Department of Diagnostics and Public Health, Section of Occupational Health, University of Verona, Italy. · University Research Center "Integrated Models for Prevention and Protection in Environmental and Occupational Health" MISTRAL, University of Brescia, Italy. · Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, University of Brescia, Italy. · Leibniz Research Centre for Working Environment and Human Factors, Sektion Lebenswissenschaften Dortmund, Germany. · Department of Preventive Medicine, University of Southern California, Los Angeles, CA. · Department of Ophthalmology, University of Southern California, Los Angeles, CA. · Department of Urology, Guangzhou First People's Hospital, the Second Affiliated Hospital of South China University of Technology, Guangzhou, China. · Leuven University Centre for Cancer Prevention (LUCK), Leuven, Belgium. · Leibniz Institute for Prevention Research and Epidemiology - BIPS, Bremen, Germany. · Department of Cancer Prevention and Control, Roswell Park Cancer Institute, Buffalo, NY. · Department of Oncology & Pathology, Division of Clinical Cancer Epidemiology, Karolinska Hospital, Stockholm, Sweden. · Department of Epidemiology, Geisel School of Medicine at Dartmouth, Hanover, NH. · Department of Epidemiology and Community Medicine, University of Ottawa, ON, Canada. · Departments of Epidemiology, UCLA Center for Environmental Genomics, Fielding School of Public Health, University of California, Los Angeles (UCLA), Los Angeles, CA. · Epidemiology Branch, and Epigenetic and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC. · Department of Clinical Medicine and Community Health - Università degli Studi di Milano, Milan, Italy. · Department of Pharmacology and Toxicology, NUTRIM School for Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, The Netherlands. · Department of Complex Genetics, Public Health and Primary Care (School CAPHRI), Maastricht University, Maastricht, The Netherlands. ·Epidemiology · Pubmed #30601243.

ABSTRACT: BACKGROUND: Few studies have modeled smoking histories by combining smoking intensity and duration to show what profile of smoking behavior is associated with highest risk of bladder cancer. This study aims to provide insight into the association between smoking exposure history and bladder cancer risk by modeling both smoking intensity and duration in a pooled analysis. METHODS: We used data from 15 case-control studies included in the bladder cancer epidemiology and nutritional determinants study, including a total of 6,874 cases and 17,727 controls. To jointly interpret the effects of intensity and duration of smoking, we modeled excess odds ratios per pack-year by intensity continuously to estimate the risk difference between smokers with long duration/low intensity and short duration/high intensity. RESULTS: The pattern observed from the pooled excess odds ratios model indicated that for a fixed number of pack-years, smoking for a longer duration at lower intensity was more deleterious for bladder cancer risk than smoking more cigarettes/day for a shorter duration. We observed similar patterns within individual study samples. CONCLUSIONS: This pooled analysis shows that long duration/low intensity smoking is associated with a greater increase in bladder cancer risk than short duration/high intensity smoking within equal pack-year categories, thus confirming studies in other smoking-related cancers and demonstrating that reducing exposure history to a single metric such as pack-years was too restrictive.

4 Article The 19q12 bladder cancer GWAS signal: association with cyclin E function and aggressive disease. 2014

Fu, Yi-Ping / Kohaar, Indu / Moore, Lee E / Lenz, Petra / Figueroa, Jonine D / Tang, Wei / Porter-Gill, Patricia / Chatterjee, Nilanjan / Scott-Johnson, Alexandra / Garcia-Closas, Montserrat / Muchmore, Brian / Baris, Dalsu / Paquin, Ashley / Ylaya, Kris / Schwenn, Molly / Apolo, Andrea B / Karagas, Margaret R / Tarway, McAnthony / Johnson, Alison / Mumy, Adam / Schned, Alan / Guedez, Liliana / Jones, Michael A / Kida, Masatoshi / Hosain, G M Monawar / Malats, Nuria / Kogevinas, Manolis / Tardon, Adonina / Serra, Consol / Carrato, Alfredo / Garcia-Closas, Reina / Lloreta, Josep / Wu, Xifeng / Purdue, Mark / Andriole, Gerald L / Grubb, Robert L / Black, Amanda / Landi, Maria T / Caporaso, Neil E / Vineis, Paolo / Siddiq, Afshan / Bueno-de-Mesquita, H Bas / Trichopoulos, Dimitrios / Ljungberg, Börje / Severi, Gianluca / Weiderpass, Elisabete / Krogh, Vittorio / Dorronsoro, Miren / Travis, Ruth C / Tjønneland, Anne / Brennan, Paul / Chang-Claude, Jenny / Riboli, Elio / Prescott, Jennifer / Chen, Constance / De Vivo, Immaculata / Govannucci, Edward / Hunter, David / Kraft, Peter / Lindstrom, Sara / Gapstur, Susan M / Jacobs, Eric J / Diver, W Ryan / Albanes, Demetrius / Weinstein, Stephanie J / Virtamo, Jarmo / Kooperberg, Charles / Hohensee, Chancellor / Rodabough, Rebecca J / Cortessis, Victoria K / Conti, David V / Gago-Dominguez, Manuela / Stern, Mariana C / Pike, Malcolm C / Van Den Berg, David / Yuan, Jian-Min / Haiman, Christopher A / Cussenot, Olivier / Cancel-Tassin, Geraldine / Roupret, Morgan / Comperat, Eva / Porru, Stefano / Carta, Angela / Pavanello, Sofia / Arici, Cecilia / Mastrangelo, Giuseppe / Grossman, H Barton / Wang, Zhaoming / Deng, Xiang / Chung, Charles C / Hutchinson, Amy / Burdette, Laurie / Wheeler, William / Fraumeni, Joseph / Chanock, Stephen J / Hewitt, Stephen M / Silverman, Debra T / Rothman, Nathaniel / Prokunina-Olsson, Ludmila. ·Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. · Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. · Clinical Research Directorate/Clinical Monitoring Research Program, SAIC-Frederick, Inc., Frederick National Laboratory for Cancer Research, Frederick, Maryland. · Division of Genetics and Epidemiology, Institute of Cancer Research, London, United Kingdom. · Laboratory of Pathology, Center of Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. · Maine Cancer Registry, Augusta, Maine. · Genitourinary Malignancy Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. · Geisel School of Medicine at Dartmouth, Lebanon, New Hampshire. · Vermont Cancer Registry, Burlington, Vermont. · Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. · Department of Pathology and Laboratory Medicine, Maine Medical Center, Portland, Maine. · Department of Pathology, University of Vermont College of Medicine, Burlington, Vermont. · New Hampshire State Cancer Registry, Concord, New Hampshire. · Spanish National Cancer Research Centre, Madrid, Spain. · Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain. Hospital del Mar Medical Research Institute (IMIM), Barcelona, Spain. National School of Public Health, Athens, Greece. CIBER Epidemiologia y Salud Pública (CIBERESP), Barcelona, Spain. · CIBER Epidemiologia y Salud Pública (CIBERESP), Barcelona, Spain. Instituto Universitario de Oncología, Universidad de Oviedo, Oviedo, Spain. · CIBER Epidemiologia y Salud Pública (CIBERESP), Barcelona, Spain. Universitat Pompeu Fabra, Barcelona, Spain. · Ramón y Cajal Hospital, Madrid, Spain. · Unidad de Investigación, Hospital Universitario de Canarias, La Laguna, Spain. · Hospital del Mar-IMIM, Univesitat Pompeu Fabra, Barcelona, Spain. · Department of Epidemiology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas. · Division of Urologic Surgery, Washington University School of Medicine, St. Louis, Missouri. · School of Public Health, Imperial College London, London, United Kingdom. Human Genetics Foundation (HuGeF), Torino, Italy. · School of Public Health, Imperial College London, London, United Kingdom. · National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands. Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, the Netherlands. Department of Epidemiology and Biostatistics, The School of Public Health, Imperial College London, London, United Kingdom. Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia. · Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts. Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece. Hellenic Health Foundation, Athens, Greece. · Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden. · Human Genetics Foundation (HuGeF), Torino, Italy. Cancer Epidemiology Centre, Cancer Council Victoria, Melbourne, Australia. Centre for Epidemiology and Biostatistics, University of Melbourne, Australia. · Department of Community Medicine, Faculty of Health Sciences, University of Tromsø, The Arctic University of Norway, Tromsø, Norway. Department of Research, Cancer Registry of Norway, Oslo, Norway. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. Samfundet Folkhälsan, Helsinki, Finland. · Fondazione IRCCS Istituto Nazionale dei Tumori, Milano, Italy. · Public Health Division of Gipuzkoa, Basque Regional Health Department and Ciberesp-Biodonostia, San Sebastian, Spain. · Cancer Epidemiology Unit, University of Oxford, Oxford, United Kingdom. · Danish Cancer Society Research Center, Copenhagen, Denmark. · International Agency for Research on Cancer, Lyon, France. · Division of Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts. Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts. · Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts. · Department of Nutrition and Epidemiology, Harvard School of Public Health, Boston, Massachusetts. · Epidemiology Research Program, American Cancer Society, Atlanta, Georgia. · National Institute for Health and Welfare, Helsinki, Finland. · Fred Hutchinson Cancer Research Center, Division of Public Health Sciences, Seattle, Washington. · Department of Obstetrics and Gynecology, Keck School of Medicine of USC, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, California. Department of Preventive Medicine, Keck School of Medicine of USC, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, California. · Department of Preventive Medicine, Keck School of Medicine of USC, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, California. · Genomic Medicine Group, Galician Foundation of Genomic Medicine, Complejo Hospitalario Universitario de Santiago, Servicio Galego de Saude (SERGAS), Instituto de Investigación Sanitaria de Santiago (IDIS), Santiago de Compostela, Spain. · Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, New York. · University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania. · AP-HP, Hopital Tenon, GHU-Est, Department of Urology, Paris, France. Centre de Recherche sur les Pathologies Prostatiques, Paris, France. UPMC Univ Paris 06, ONCOTYPE-URO, Paris, France. · Centre de Recherche sur les Pathologies Prostatiques, Paris, France. UPMC Univ Paris 06, ONCOTYPE-URO, Paris, France. · Centre de Recherche sur les Pathologies Prostatiques, Paris, France. UPMC Univ Paris 06, ONCOTYPE-URO, Paris, France. AP-HP, Hopital Pitie-Salpetriere, GHU-Est, Departments of Urology and Pathology, Paris, France. · Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, University of Brescia, Brescia, Italy. · Department of Cardiac, Thoracic and Vascular Sciences, University of Padova, Padua, Italy. · Department of Urology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas. · Cancer Genomics Research Laboratory, SAIC-Frederick, Inc., Frederick National Laboratory for Cancer Research, Frederick, Maryland. · Information Management Services, Rockville, Maryland. · Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. prokuninal@mail.nih.gov. ·Cancer Res · Pubmed #25320178.

ABSTRACT: A genome-wide association study (GWAS) of bladder cancer identified a genetic marker rs8102137 within the 19q12 region as a novel susceptibility variant. This marker is located upstream of the CCNE1 gene, which encodes cyclin E, a cell-cycle protein. We performed genetic fine-mapping analysis of the CCNE1 region using data from two bladder cancer GWAS (5,942 cases and 10,857 controls). We found that the original GWAS marker rs8102137 represents a group of 47 linked SNPs (with r(2) ≥ 0.7) associated with increased bladder cancer risk. From this group, we selected a functional promoter variant rs7257330, which showed strong allele-specific binding of nuclear proteins in several cell lines. In both GWASs, rs7257330 was associated only with aggressive bladder cancer, with a combined per-allele OR = 1.18 [95% confidence interval (CI), 1.09-1.27, P = 4.67 × 10(-5)] versus OR = 1.01 (95% CI, 0.93-1.10, P = 0.79) for nonaggressive disease, with P = 0.0015 for case-only analysis. Cyclin E protein expression analyzed in 265 bladder tumors was increased in aggressive tumors (P = 0.013) and, independently, with each rs7257330-A risk allele (P(trend) = 0.024). Overexpression of recombinant cyclin E in cell lines caused significant acceleration of cell cycle. In conclusion, we defined the 19q12 signal as the first GWAS signal specific for aggressive bladder cancer. Molecular mechanisms of this genetic association may be related to cyclin E overexpression and alteration of cell cycle in carriers of CCNE1 risk variants. In combination with established bladder cancer risk factors and other somatic and germline genetic markers, the CCNE1 variants could be useful for inclusion into bladder cancer risk prediction models.

5 Article Genome-wide interaction study of smoking and bladder cancer risk. 2014

Figueroa, Jonine D / Han, Summer S / Garcia-Closas, Montserrat / Baris, Dalsu / Jacobs, Eric J / Kogevinas, Manolis / Schwenn, Molly / Malats, Nuria / Johnson, Alison / Purdue, Mark P / Caporaso, Neil / Landi, Maria Teresa / Prokunina-Olsson, Ludmila / Wang, Zhaoming / Hutchinson, Amy / Burdette, Laurie / Wheeler, William / Vineis, Paolo / Siddiq, Afshan / Cortessis, Victoria K / Kooperberg, Charles / Cussenot, Olivier / Benhamou, Simone / Prescott, Jennifer / Porru, Stefano / Bueno-de-Mesquita, H Bas / Trichopoulos, Dimitrios / Ljungberg, Börje / Clavel-Chapelon, Françoise / Weiderpass, Elisabete / Krogh, Vittorio / Dorronsoro, Miren / Travis, Ruth / Tjønneland, Anne / Brenan, Paul / Chang-Claude, Jenny / Riboli, Elio / Conti, David / Gago-Dominguez, Manuela / Stern, Mariana C / Pike, Malcolm C / Van Den Berg, David / Yuan, Jian-Min / Hohensee, Chancellor / Rodabough, Rebecca / Cancel-Tassin, Geraldine / Roupret, Morgan / Comperat, Eva / Chen, Constance / De Vivo, Immaculata / Giovannucci, Edward / Hunter, David J / Kraft, Peter / Lindstrom, Sara / Carta, Angela / Pavanello, Sofia / Arici, Cecilia / Mastrangelo, Giuseppe / Karagas, Margaret R / Schned, Alan / Armenti, Karla R / Hosain, G M Monawar / Haiman, Chris A / Fraumeni, Joseph F / Chanock, Stephen J / Chatterjee, Nilanjan / Rothman, Nathaniel / Silverman, Debra T. ·Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA, Institute for Cancer Research, London, UK, Epidemiology Research Program, American Cancer Society, Atlanta, GA, USA, Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain, Municipal Institute of Medical Research, Barcelona, Spain, CIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain, National School of Public Health, Athens, Greece, Maine Cancer Registry, Augusta, ME, USA, Spanish National Cancer Research Centre (CNIO), Madrid, Spain, Vermont Cancer Registry, Burlington, VT, USA, Center for Genomics Research, SAIC-Frederick, Inc., National Cancer Institute-Frederick, Frederick, MD, USA, Information Management Services, Inc., Rockville, MD, USA, Imperial College London, London, UK, Department of Preventive Medicine and Department of Obstetrics & Gynecology, Keck School of Medicine of USC, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA, Fred Hutchinson Cancer Research Center, Division of Public Health Sciences, Seattle, WA, USA, Department of Urology, Assistance Publique-Hôpitaux de Paris, Tenon Hospital, Paris, France, Centre de Recherche sur les Pathologies Prostatiques, Paris, France, Institut national de la sante et de la recherche medicale, U946, Foundation Jean Dausset Centre d'Etude du Polymorphisme Humain (CEPH), Paris, France, Centre National de la Receherche Scientifique, UMR8200, Institut Gustave-Roussy, Villejuif, France, Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA, Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA, Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, University of Brescia, Brescia, Italy, National Institute for Public Health and the Environment (RIVM), Biltho · Institute for Cancer Research, London, UK. · Epidemiology Research Program, American Cancer Society, Atlanta, GA, USA. · Maine Cancer Registry, Augusta, ME, USA. · Spanish National Cancer Research Centre (CNIO), Madrid, Spain. · Vermont Cancer Registry, Burlington, VT, USA. · Center for Genomics Research, SAIC-Frederick, Inc., National Cancer Institute-Frederick, Frederick, MD, USA. · Information Management Services, Inc., Rockville, MD, USA. · Imperial College London, London, UK. · Department of Preventive Medicine and Department of Obstetrics & Gynecology, Keck School of Medicine of USC, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA. · Fred Hutchinson Cancer Research Center, Division of Public Health Sciences, Seattle, WA, USA. · Department of Urology, Assistance Publique-Hôpitaux de Paris, Tenon Hospital, Paris, France, Centre de Recherche sur les Pathologies Prostatiques, Paris, France. · Institut national de la sante et de la recherche medicale, U946, Foundation Jean Dausset Centre d'Etude du Polymorphisme Humain (CEPH), Paris, France, Centre National de la Receherche Scientifique, UMR8200, Institut Gustave-Roussy, Villejuif, France. · Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA, Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA. · Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, University of Brescia, Brescia, Italy. · Imperial College London, London, UK, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands, Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, The Netherlands. · Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden. · Fondazione IRCCS Istituto Nazionale dei Tumori, Milano, Italy. · CIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain, Public Health Division of Gipuzkoa, BioDonostia Research Institute, Health Department of Basque Region, San Sebastian, Spain. · Cancer Epidemiology Unit, University of Oxford, Oxford, UK. · Danish Cancer Society Research Center, Copenhagen, Denmark. · International Agency for Research on Cancer, Lyon, France. · DKFZ, Heidelberg, Germany. · Genomic Medicine Group, Galician Foundation of Genomic Medicine, Complejo Hospitalario Universitario de Santiago, Servicio Galego de Saude (SERGAS), Instituto de Investigación Sanitaria de Santiago (IDIS), Santiago de Compostela, Spain. · Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. · UPMC Univ Paris 06, GRC n°5,ONCOTYPE-URO, Paris, France. · Department of Urology, Assistance Publique-Hôpitaux de Paris, Tenon Hospital, Paris, France, Centre de Recherche sur les Pathologies Prostatiques, Paris, France, UPMC Univ Paris 06, GRC n°5,ONCOTYPE-URO, Paris, France. · Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA. · Department of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA, USA. · Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA, Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA, Broad Institute of Harvard and MIT, Cambridge, MA, USA. · Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA, Department of Biostatistics, Harvard School of Public Health, Boston, MA, USA. · Department of Cardiac, Thoracic and Vascular Sciences, University of Padova, Padova, Italy; · Geisel School of Medicine at Dartmouth, Lebanon, NH, USA. · New Hampshire Department of Health and Human Services, Concord, NH, USA and. · Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA. ·Carcinogenesis · Pubmed #24662972.

ABSTRACT: Bladder cancer is a complex disease with known environmental and genetic risk factors. We performed a genome-wide interaction study (GWAS) of smoking and bladder cancer risk based on primary scan data from 3002 cases and 4411 controls from the National Cancer Institute Bladder Cancer GWAS. Alternative methods were used to evaluate both additive and multiplicative interactions between individual single nucleotide polymorphisms (SNPs) and smoking exposure. SNPs with interaction P values < 5 × 10(-) (5) were evaluated further in an independent dataset of 2422 bladder cancer cases and 5751 controls. We identified 10 SNPs that showed association in a consistent manner with the initial dataset and in the combined dataset, providing evidence of interaction with tobacco use. Further, two of these novel SNPs showed strong evidence of association with bladder cancer in tobacco use subgroups that approached genome-wide significance. Specifically, rs1711973 (FOXF2) on 6p25.3 was a susceptibility SNP for never smokers [combined odds ratio (OR) = 1.34, 95% confidence interval (CI) = 1.20-1.50, P value = 5.18 × 10(-) (7)]; and rs12216499 (RSPH3-TAGAP-EZR) on 6q25.3 was a susceptibility SNP for ever smokers (combined OR = 0.75, 95% CI = 0.67-0.84, P value = 6.35 × 10(-) (7)). In our analysis of smoking and bladder cancer, the tests for multiplicative interaction seemed to more commonly identify susceptibility loci with associations in never smokers, whereas the additive interaction analysis identified more loci with associations among smokers-including the known smoking and NAT2 acetylation interaction. Our findings provide additional evidence of gene-environment interactions for tobacco and bladder cancer.

6 Article Comprehensive analyses of DNA repair pathways, smoking and bladder cancer risk in Los Angeles and Shanghai. 2014

Corral, Roman / Lewinger, Juan Pablo / Van Den Berg, David / Joshi, Amit D / Yuan, Jian-Min / Gago-Dominguez, Manuela / Cortessis, Victoria K / Pike, Malcolm C / Conti, David V / Thomas, Duncan C / Edlund, Christopher K / Gao, Yu-Tang / Xiang, Yong-Bing / Zhang, Wei / Su, Yu-Chen / Stern, Mariana C. ·Department of Preventive Medicine, Keck School of Medicine of USC, University of Southern California, Los Angeles, CA; Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA. ·Int J Cancer · Pubmed #24382701.

ABSTRACT: Tobacco smoking is a bladder cancer risk factor and a source of carcinogens that induce DNA damage to urothelial cells. Using data and samples from 988 cases and 1,004 controls enrolled in the Los Angeles County Bladder Cancer Study and the Shanghai Bladder Cancer Study, we investigated associations between bladder cancer risk and 632 tagSNPs that comprehensively capture genetic variation in 28 DNA repair genes from four DNA repair pathways: base excision repair (BER), nucleotide excision repair (NER), non-homologous end-joining (NHEJ) and homologous recombination repair (HHR). Odds ratios (ORs) and 95% confidence intervals (CIs) for each tagSNP were corrected for multiple testing for all SNPs within each gene using pACT and for genes within each pathway and across pathways with Bonferroni. Gene and pathway summary estimates were obtained using ARTP. We observed an association between bladder cancer and POLB rs7832529 (BER) (pACT = 0.003; ppathway = 0.021) among all, and SNPs in XPC (NER) and OGG1 (BER) among Chinese men and women, respectively. The NER pathway showed an overall association with risk among Chinese males (ARTP NER p = 0.034). The XRCC6 SNP rs2284082 (NHEJ), also in LD with SREBF2, showed an interaction with smoking (smoking status interaction pgene = 0.001, ppathway = 0.008, poverall = 0.034). Our findings support a role in bladder carcinogenesis for regions that map close to or within BER (POLB, OGG1) and NER genes (XPC). A SNP that tags both the XRCC6 and SREBF2 genes strongly modifies the association between bladder cancer risk and smoking.

7 Article Genome-wide association study identifies multiple loci associated with bladder cancer risk. 2014

Figueroa, Jonine D / Ye, Yuanqing / Siddiq, Afshan / Garcia-Closas, Montserrat / Chatterjee, Nilanjan / Prokunina-Olsson, Ludmila / Cortessis, Victoria K / Kooperberg, Charles / Cussenot, Olivier / Benhamou, Simone / Prescott, Jennifer / Porru, Stefano / Dinney, Colin P / Malats, Núria / Baris, Dalsu / Purdue, Mark / Jacobs, Eric J / Albanes, Demetrius / Wang, Zhaoming / Deng, Xiang / Chung, Charles C / Tang, Wei / Bas Bueno-de-Mesquita, H / Trichopoulos, Dimitrios / Ljungberg, Börje / Clavel-Chapelon, Françoise / Weiderpass, Elisabete / Krogh, Vittorio / Dorronsoro, Miren / Travis, Ruth / Tjønneland, Anne / Brenan, Paul / Chang-Claude, Jenny / Riboli, Elio / Conti, David / Gago-Dominguez, Manuela / Stern, Mariana C / Pike, Malcolm C / Van Den Berg, David / Yuan, Jian-Min / Hohensee, Chancellor / Rodabough, Rebecca / Cancel-Tassin, Geraldine / Roupret, Morgan / Comperat, Eva / Chen, Constance / De Vivo, Immaculata / Giovannucci, Edward / Hunter, David J / Kraft, Peter / Lindstrom, Sara / Carta, Angela / Pavanello, Sofia / Arici, Cecilia / Mastrangelo, Giuseppe / Kamat, Ashish M / Lerner, Seth P / Barton Grossman, H / Lin, Jie / Gu, Jian / Pu, Xia / Hutchinson, Amy / Burdette, Laurie / Wheeler, William / Kogevinas, Manolis / Tardón, Adonina / Serra, Consol / Carrato, Alfredo / García-Closas, Reina / Lloreta, Josep / Schwenn, Molly / Karagas, Margaret R / Johnson, Alison / Schned, Alan / Armenti, Karla R / Hosain, G M / Andriole, Gerald / Grubb, Robert / Black, Amanda / Ryan Diver, W / Gapstur, Susan M / Weinstein, Stephanie J / Virtamo, Jarmo / Haiman, Chris A / Landi, Maria T / Caporaso, Neil / Fraumeni, Joseph F / Vineis, Paolo / Wu, Xifeng / Silverman, Debra T / Chanock, Stephen / Rothman, Nathaniel. ·Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA. ·Hum Mol Genet · Pubmed #24163127.

ABSTRACT: Candidate gene and genome-wide association studies (GWAS) have identified 11 independent susceptibility loci associated with bladder cancer risk. To discover additional risk variants, we conducted a new GWAS of 2422 bladder cancer cases and 5751 controls, followed by a meta-analysis with two independently published bladder cancer GWAS, resulting in a combined analysis of 6911 cases and 11 814 controls of European descent. TaqMan genotyping of 13 promising single nucleotide polymorphisms with P < 1 × 10(-5) was pursued in a follow-up set of 801 cases and 1307 controls. Two new loci achieved genome-wide statistical significance: rs10936599 on 3q26.2 (P = 4.53 × 10(-9)) and rs907611 on 11p15.5 (P = 4.11 × 10(-8)). Two notable loci were also identified that approached genome-wide statistical significance: rs6104690 on 20p12.2 (P = 7.13 × 10(-7)) and rs4510656 on 6p22.3 (P = 6.98 × 10(-7)); these require further studies for confirmation. In conclusion, our study has identified new susceptibility alleles for bladder cancer risk that require fine-mapping and laboratory investigation, which could further understanding into the biological underpinnings of bladder carcinogenesis.

8 Article Dietary sources of N-nitroso compounds and bladder cancer risk: findings from the Los Angeles bladder cancer study. 2014

Catsburg, Chelsea E / Gago-Dominguez, Manuela / Yuan, Jian-Min / Castelao, J Esteban / Cortessis, Victoria K / Pike, Malcolm C / Stern, Mariana C. ·Department of Preventive Medicine, Keck School of Medicine, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA. ·Int J Cancer · Pubmed #23775870.

ABSTRACT: N-Nitroso compounds (NOCs) have been proposed as possible bladder carcinogens. The main sources of exogenous exposure to NOCs are cigarette smoke and diet, particularly processed (i.e., nitrite-treated) meats. Perhaps more importantly, NOCs can be formed endogenously from dietary precursors such as nitrate, nitrite and amines. Heme has been shown to increase endogenous nitrosation. We examined the role of dietary sources of NOCs and NOC precursors as potential bladder cancer risk factors using data from the Los Angeles Bladder Cancer Study, a population-based case-control study. Dietary and demographic information was collected from 1,660 bladder cancer cases and 1,586 controls via a structured questionnaire. Intake of liver and of salami/pastrami/corned beef, were both statistically significantly associated with risk of bladder cancer in this study, particularly among nonsmokers. Heme intake was also statistically significantly associated with risk of bladder cancer among nonsmokers only. When considering NOC precursors, risk was consistently higher among subjects with concurrent high intake of nitrate and high intake of the different meats (sources of amines and nitrosamines). Results of this study are consistent with a role of dietary sources of NOC precursors from processed meats in bladder cancer risk, suggesting consumption of meats with high amine and heme content such as salami and liver as a risk factor for bladder cancer. In addition, any effect of consuming these meats may be greater when accompanied by high nitrate intake.

9 Article Elevated 4-aminobiphenyl and 2,6-dimethylaniline hemoglobin adducts and increased risk of bladder cancer among lifelong nonsmokers--The Shanghai Bladder Cancer Study. 2013

Tao, Li / Day, Billy W / Hu, Bibin / Xiang, Yong-Bing / Wang, Renwei / Stern, Mariana C / Gago-Dominguez, Manuela / Cortessis, Victoria K / Conti, David V / Van Den Berg, David / Pike, Malcolm C / Gao, Yu-Tang / Yu, Mimi C / Yuan, Jian-Min. ·Cancer Prevention Institute of California, Fremont, CA, USA. ·Cancer Epidemiol Biomarkers Prev · Pubmed #23539508.

ABSTRACT: BACKGROUND: 4-Aminobiphenyl (ABP) is an established human bladder carcinogen, with tobacco smoke being a major source of human exposure. Other arylamine compounds, including 2,6-dimethylaniline (2,6-DMA), have been implicated as possible human bladder carcinogens. Hemoglobin adducts of 4-ABP and 2,6-DMA are validated biomarkers of exposure to those compounds in humans. METHODS: The Shanghai Bladder Cancer Study enrolled 581 incident bladder cancer cases and 604 population controls. Each participant was solicited for his/her history of tobacco use and other lifestyle factors and donation of blood and urine specimens. Red blood cell lysates were used to quantify both hemoglobin adducts of 4-ABP and 2,6-DMA. Urine samples were used to quantify total cotinine. ORs and 95% confidence intervals (CI) for bladder cancer were estimated using unconditional logistic regression methods. RESULTS: Among lifelong nonsmokers, ORs (95% CIs) of bladder cancer for low (below median of positive values) and high versus undetectable levels of 2,6-DMA hemoglobin adducts were 3.87 (1.39-10.75) and 6.90 (3.17-15.02), respectively (Ptrend < 0.001). Similarly, among lifelong nonsmokers, ORs (95% CIs) of bladder cancer for third and fourth versus first/second quartiles of 4-ABP hemoglobin adducts was 1.30 (0.76-2.22) and 2.29 (1.23-4.24), respectively (Ptrend = 0.009). The two associations were independent of each other. CONCLUSION: Hemoglobin adducts of 4-ABP and 2,6-DMA were significantly and independently associated with increased bladder cancer risk among lifelong nonsmokers in Shanghai, China. IMPACT: The findings of the present study in China with previous data in Los Angeles, California strongly implicate arylamines as potential causal agents of human bladder cancer.

10 Article Cigarette smoking and subtypes of bladder cancer. 2012

Jiang, Xuejuan / Castelao, J Esteban / Yuan, Jian-Min / Stern, Mariana C / Conti, David V / Cortessis, Victoria K / Pike, Malcolm C / Gago-Dominguez, Manuela. ·Department of Preventive Medicine, Keck School of Medicine, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA. xuejuanj@usc.edu ·Int J Cancer · Pubmed #21412765.

ABSTRACT: There is little information regarding associations between suspected bladder cancer risk factors and tumor subtypes at diagnosis. Some, but not all, studies have found that bladder cancer among smokers is often more invasive than it is among nonsmokers. This population-based case-control study was conducted in Los Angeles, California, involving 1,586 bladder cancer patients and their individually matched controls. Logistic regression was used to conduct separate analyses according to tumor subtypes defined by stage and grade. Cigarette smoking increased risk of both superficial and invasive bladder cancer, but the more advanced the stage, the stronger the effect. The odds ratios associated with regular smokers were 2.2 (95% confidence intervals, 1.8-2.8), 2.7 (2.1-3.6) and 3.7 (2.5-5.5) for low-grade superficial, high-grade superficial and invasive tumors respectively. This pattern was consistently observed regardless of the smoking exposure index under examination. Women had higher risk of invasive bladder cancer than men even they smoked comparable amount of cigarettes as men. There was no gender difference in the association between smoking and risk of low-grade superficial bladder cancer. The heterogeneous effect of cigarette smoking was attenuated among heavy users of NSAIDs. Our results indicate that cigarette smoking was more strongly associated with increased risk of invasive bladder cancer than with low-grade superficial bladder cancer.

11 Article Lower risk in parous women suggests that hormonal factors are important in bladder cancer etiology. 2011

Davis-Dao, Carol A / Henderson, Katherine D / Sullivan-Halley, Jane / Ma, Huiyan / West, Dee / Xiang, Yong-Bing / Gago-Dominguez, Manuela / Stern, Mariana C / Castelao, J Esteban / Conti, David V / Pike, Malcolm C / Bernstein, Leslie / Cortessis, Victoria K. ·Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA. ·Cancer Epidemiol Biomarkers Prev · Pubmed #21493870.

ABSTRACT: BACKGROUND: Urinary bladder cancer is two to four times more common among men than among women, a difference in risk not fully explained by established risk factors. Our objective was to determine whether hormonal and reproductive factors are involved in female bladder cancer. METHODS: We analyzed data from two population-based studies: the Los Angeles-Shanghai Bladder Cancer Study, with 349 female case-control pairs enrolled in Los Angeles and 131 female cases and 138 frequency-matched controls enrolled in Shanghai, and the California Teachers Study (CTS), a cohort of 120,857 women with 196 incident cases of bladder urothelial carcinoma diagnosed between 1995 and 2005. We also conducted a meta-analysis summarizing associations from our primary analyses together with published results. RESULTS: In primary data analyses, parous women experienced at least 30% reduced risk of developing bladder cancer compared with nulliparous women (Shanghai: OR = 0.38, 95% CI: 0.13-1.10; CTS: RR = 0.69, 95% CI: 0.50-0.95) consistent with results of a meta-analysis of nine studies (summary RR = 0.73, 95% CI: 0.63-0.85). The CTS, which queried formulation of menopausal hormone therapy (HT), revealed a protective effect for use of combined estrogen and progestin compared with no HT (RR = 0.60, 95% CI: 0.37-0.98). Meta-analysis of three studies provided a similar effect estimate (summary RR = 0.65, 95% CI: 0.48-0.88). CONCLUSIONS: A consistent pattern of reduced bladder cancer risk was found among parous women and those who used estrogen and progestin for HT. IMPACT: These results suggest that more research is warranted to investigate hormonal and reproductive factors as possible contributors to bladder cancer risk.

12 Article Genetic variations on chromosomes 5p15 and 15q25 and bladder cancer risk: findings from the Los Angeles-Shanghai bladder case-control study. 2011

Gago-Dominguez, Manuela / Jiang, Xuejuan / Conti, David V / Castelao, Jose Esteban / Stern, Mariana C / Cortessis, Victoria K / Pike, Malcolm C / Xiang, Yong-Bing / Gao, Yu-Tang / Yuan, Jian-Min / Van Den Berg, David J. ·Department of Preventive Medicine, Keck School of Medicine, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089-9175, USA. mgago@usc.edu ·Carcinogenesis · Pubmed #21081471.

ABSTRACT: Genome-wide association studies have associated common variations at chromosomes 5p15 and 15q25 with lung cancer risk. The 5p15 locus has also been associated with increased bladder cancer risk in a recent report. The 15q25 locus has been associated with nicotine dependence and self-reported number of cigarettes smoked per day in some studies and it was proposed that its association with lung cancer may be mediated through differences in smoking behavior. Here, we investigated the roles of variations at 5p15 (rs401681, rs402710, rs2736098 and rs2736100) and 15q25 (rs1051730 and rs8034191) in bladder cancer etiology in two case-control studies conducted separately in Los Angeles County, CA, USA (498 cases and 588 controls) and in Shanghai, China (506 cases and 530 controls). We replicated the association between the 5p15 locus and bladder cancer among non-Hispanic whites (NHW) in Los Angeles [for rs2736100, per C allele odds ratio (OR) = 1.23; 95% confidence interval (CI), 1.02-1.48; P = 0.029] and among Chinese in Shanghai (OR = 1.22; 95% CI, 1.02-1.47; P = 0.033). Both rs1051730 and rs8034191 at 15q25 were rare among Chinese. Among NHW, a significant association was found between rs8034191 and bladder cancer which persisted after adjustment for cigarette smoking status, number of cigarettes smoked per day and number of years of smoking (per C allele OR = 1.26; 95% CI, 1.04-1.54; P = 0.017). Our results support 5p15 and 15q25 as susceptibility regions for bladder cancer risk.

13 Article Risk of urinary bladder cancer is associated with 8q24 variant rs9642880[T] in multiple racial/ethnic groups: results from the Los Angeles-Shanghai case-control study. 2010

Cortessis, Victoria K / Yuan, Jian-Min / Van Den Berg, David / Jiang, Xuejuan / Gago-Dominguez, Manuela / Stern, Mariana C / Castelao, Jose E / Xiang, Yong-Bing / Gao, Yu-Tang / Pike, Malcolm C / Conti, David V. ·Department of Preventive Medicine, Keck School of Medicine, Norris Comprehensive Cancer Center, University of Southern California, 1441 Eastlake Ave, MC-9175, Los Angeles, CA 90089, USA. cortessi@usc.edu ·Cancer Epidemiol Biomarkers Prev · Pubmed #21051319.

ABSTRACT: BACKGROUND: Multiple chromosome 8q24 genotypic variants are strongly implicated in several cancers. Recent genome-wide association studies of urinary bladder cancer report risk to be associated with the T allele of rs9642880 on 8q24 among individuals of European descent. METHODS: We examined associations between bladder cancer risk and genotypes defined by rs9642880 and each of 8 additional 8q24 variants associated with risk of other cancers, in both high-risk non-Hispanic white and low-risk Chinese participants enrolled in a large population-based case-control study conducted in Los Angeles County and Shanghai. RESULTS: We confirmed association of rs9642880 T with bladder cancer risk not only among non-Hispanic whites but also among Chinese participants [overall per-allele relative risk estimate 1.32 (95% CI, 1.16-1.50; P = 0.000024)]. Subgroup analyses suggested that effects of rs9642880 are largely confined to nonsmokers and former smokers, and may be particularly important in the etiology of noninvasive papillary tumors. There was little indication that 8q24 SNPs associated with other cancer types--rs7008482, rs7000448, rs6983561, rs6983267, rs13281615, rs13254738, or rs10090154--are associated with bladder cancer risk. CONCLUSIONS: Bladder cancer risk is associated specifically with variation in the discrete 8q24 region containing rs9642880. Factors other than rs9642880 genotypes seem to underlie differences in bladder cancer risk between non-Hispanic whites and Chinese. IMPACT: Characterization of functional consequences of genetic variation in the discrete region including rs9642880 is needed to understand biological basis of this bladder cancer-specific 8q24 association in these racial/ethnic groups characterized by both high and low risk of bladder cancer.

14 Article A multi-stage genome-wide association study of bladder cancer identifies multiple susceptibility loci. 2010

Rothman, Nathaniel / Garcia-Closas, Montserrat / Chatterjee, Nilanjan / Malats, Nuria / Wu, Xifeng / Figueroa, Jonine D / Real, Francisco X / Van Den Berg, David / Matullo, Giuseppe / Baris, Dalsu / Thun, Michael / Kiemeney, Lambertus A / Vineis, Paolo / De Vivo, Immaculata / Albanes, Demetrius / Purdue, Mark P / Rafnar, Thorunn / Hildebrandt, Michelle A T / Kiltie, Anne E / Cussenot, Olivier / Golka, Klaus / Kumar, Rajiv / Taylor, Jack A / Mayordomo, Jose I / Jacobs, Kevin B / Kogevinas, Manolis / Hutchinson, Amy / Wang, Zhaoming / Fu, Yi-Ping / Prokunina-Olsson, Ludmila / Burdett, Laurie / Yeager, Meredith / Wheeler, William / Tardón, Adonina / Serra, Consol / Carrato, Alfredo / García-Closas, Reina / Lloreta, Josep / Johnson, Alison / Schwenn, Molly / Karagas, Margaret R / Schned, Alan / Andriole, Gerald / Grubb, Robert / Black, Amanda / Jacobs, Eric J / Diver, W Ryan / Gapstur, Susan M / Weinstein, Stephanie J / Virtamo, Jarmo / Cortessis, Victoria K / Gago-Dominguez, Manuela / Pike, Malcolm C / Stern, Mariana C / Yuan, Jian-Min / Hunter, David J / McGrath, Monica / Dinney, Colin P / Czerniak, Bogdan / Chen, Meng / Yang, Hushan / Vermeulen, Sita H / Aben, Katja K / Witjes, J Alfred / Makkinje, Remco R / Sulem, Patrick / Besenbacher, Soren / Stefansson, Kari / Riboli, Elio / Brennan, Paul / Panico, Salvatore / Navarro, Carmen / Allen, Naomi E / Bueno-de-Mesquita, H Bas / Trichopoulos, Dimitrios / Caporaso, Neil / Landi, Maria Teresa / Canzian, Federico / Ljungberg, Borje / Tjonneland, Anne / Clavel-Chapelon, Francoise / Bishop, David T / Teo, Mark T W / Knowles, Margaret A / Guarrera, Simonetta / Polidoro, Silvia / Ricceri, Fulvio / Sacerdote, Carlotta / Allione, Alessandra / Cancel-Tassin, Geraldine / Selinski, Silvia / Hengstler, Jan G / Dietrich, Holger / Fletcher, Tony / Rudnai, Peter / Gurzau, Eugen / Koppova, Kvetoslava / Bolick, Sophia C E / Godfrey, Ashley / Xu, Zongli / Sanz-Velez, José I / D García-Prats, María / Sanchez, Manuel / Valdivia, Gabriel / Porru, Stefano / Benhamou, Simone / Hoover, Robert N / Fraumeni, Joseph F / Silverman, Debra T / Chanock, Stephen J. ·Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA. ·Nat Genet · Pubmed #20972438.

ABSTRACT: We conducted a multi-stage, genome-wide association study of bladder cancer with a primary scan of 591,637 SNPs in 3,532 affected individuals (cases) and 5,120 controls of European descent from five studies followed by a replication strategy, which included 8,382 cases and 48,275 controls from 16 studies. In a combined analysis, we identified three new regions associated with bladder cancer on chromosomes 22q13.1, 19q12 and 2q37.1: rs1014971, (P = 8 × 10⁻¹²) maps to a non-genic region of chromosome 22q13.1, rs8102137 (P = 2 × 10⁻¹¹) on 19q12 maps to CCNE1 and rs11892031 (P = 1 × 10⁻⁷) maps to the UGT1A cluster on 2q37.1. We confirmed four previously identified genome-wide associations on chromosomes 3q28, 4p16.3, 8q24.21 and 8q24.3, validated previous candidate associations for the GSTM1 deletion (P = 4 × 10⁻¹¹) and a tag SNP for NAT2 acetylation status (P = 4 × 10⁻¹¹), and found interactions with smoking in both regions. Our findings on common variants associated with bladder cancer risk should provide new insights into the mechanisms of carcinogenesis.

15 Article Hypertension, diuretics and antihypertensives in relation to bladder cancer. 2010

Jiang, Xuejuan / Castelao, J Esteban / Yuan, Jian-Min / Groshen, Susan / Stern, Mariana C / Conti, David V / Cortessis, Victoria K / Coetzee, Gerhard A / Pike, Malcolm C / Gago-Dominguez, Manuela. ·Department of Preventive Medicine, Keck School of Medicine, Norris Comprehensive Cancer Center, University of Southern California, 1441 Eastlake Avenue, Los Angeles, CA 90089, USA. xuejuanj@usc.edu ·Carcinogenesis · Pubmed #20732908.

ABSTRACT: The aim of this study is to investigate the relationships between hypertension, hypertension medication and bladder cancer risk in a population-based case-control study conducted in Los Angeles. Non-Asians between the ages of 25 and 64 years with histologically confirmed bladder cancers diagnosed between 1987 and 1996 were identified through the Los Angeles County Cancer Surveillance Program. A total of 1585 cases and their age-, gender- and race-matched neighborhood controls were included in the analyses. Conditional logistic regression models were used to examine the relationship between history of hypertension, medication use and bladder cancer risk. A history of hypertension was not related to bladder cancer; however, among hypertensive individuals, there was a significant difference in bladder cancer risk related to the use of diuretics or antihypertensive drugs (P for heterogeneity = 0.004). Compared with individuals without hypertension, hypertensive individuals who regularly used diuretics/antihypertensives had a similar risk [odds ratio (OR) 1.06; 95% confidence interval (CI) 0.86-1.30], whereas untreated hypertensive subjects had a 35% reduction in risk (OR: 0.65; 95% CI: 0.48-0.88). A greater reduction in bladder cancer risk was observed among current-smokers (OR: 0.43; 95% CI: 0.27-0.71) and carriers of GSTM1-null (homozygous absence) genotypes (OR: 0.43; 95% CI: 0.22-0.85). Similarly, among smokers with GSTM1-null genotype, levels of 4-aminobiphenyl-hemoglobin adducts were significantly lower among untreated hypertensive individuals (45.7 pg/g Hb) compared with individuals without hypertension (79.8 pg/g Hb) (P = 0.009). In conclusion, untreated hypertension was associated with a reduced risk of bladder cancer.