Null Results in Brief Dietary Factors and Cancers of the Renal Pelvis and Ureter Kaye E. Brock, 1 Gloria Gridley, 2 Linda Morris Brown, 2 Mimi C. Yu, 3 Janet B. Schoenberg, 4 Charles F. Lynch, 5 and Joseph K. McLaughlin 6 1 Department of Behavioural and Community Health Sciences, Faculty of Heath Sciences, University of Sydney, Sydney, New South Wales, Australia; 2 Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda, Maryland; 3 Cancer Center, MMC 806, University of Minnesota, Minneapolis, Minnesota; 4 New Jersey Department of Health and Senior Services, Trenton, New Jersey; 5 Department of Epidemiology, College of Public Health, University of Iowa, Iowa City, Iowa; and 6 International Epidemiology Institute, Rockville, Maryland Introduction In the United States, cancers of the renal pelvis and ureter (primarily transitional cell carcinomas) are rare and epidemi- ologic studies are infrequent compared with renal cell cancer (renal parenchyma) of the kidney (primarily adenocarcinomas) or bladder carcinomas [primarily transitional cell carcinomas; (1, 2)]. In this article, we used data from a large case-control study of cancers of the renal pelvis and ureter to examine dietary, anthropometric, and beverage associations. Most previous studies that investigated dietary risk factors for these tumors were combined with cancers of the kidney or bladder primarily due to their anatomic proximity. Earlier publications from this study investigated risks associated with smoking, analgesics, and hypertension (3-6). The strongest risk factor was cigarette smoking [ever smoked odds ratio (OR), 3.1] with long-term smokers having a 7-fold increased risk (6). Materials and Methods Detailed methods for case and control selection have been described elsewhere (6). In brief, eligible cases were white men and women ages 20 to 79 years in New Jersey, Iowa, or Los Angeles County, California, with microscopically confirmed cancers of the renal pelvis or ureter newly diagnosed between 1983 and 1986. Interviews were obtained for 498 cases (328 male and 170 female), including 306 with renal pelvis cancer and 192 with ureter cancer. Noninterviewed cases were slightly older than interviewed cases but had a similar distribution by sex and cancer site (6). Population-based controls were obtained by frequency matching to the cases based on age, gender, and geographic area. Controls younger than 65 years were chosen by random digit dialing (7), whereas older controls were selected from Medicare files of the then Health Care Financing Administration. The interviewer-administered questionnaire gathered information on demographic, anthro- pometric, and occupational factors as well as smoking, medication, beverage, and dietary history. Body mass index (BMI), (weight (usual) in kilograms/height in meters 2 ) was requested from individuals for a time period just before their diagnosis/interview and at age 20 years (BMI20). Subjects were classified as underweight (BMI <18.5), normal (BMI 18.5-24.9), overweight (BMI 25-29.9), and obese (BMI z30), based on NIH guidelines (8). Usual dietary intake was estimated from a 36-item food frequency questionnaire. Micronutrient levels were estimated by linking these foods to the nutrient density estimates derived from the U.S. Department of Agriculture food composition tables (9) and a U.S. Department of Agricul- ture-National Cancer Institute carotenoid food composition database (10). Food groups and nutrients were analyzed using quartiles based on the intake distribution of the controls. Unconditional logistic modeling [OR and 95% confidence interval (95% CI)] included adjustment for age, gender, study site, and pack-years of cigarette smoking in eight categories. Risk estimates for renal pelvis and ureter cancers were similar; thus, data are presented for both cancers combined. All P values are two-sided. There was 80% power to detect an OR of z1.4 for the highest versus the lowest quartile of intake (a = 0.05). Results There were no significant associations of cancer risk with being underweight or overweight, vitamin supplement use, or ever use and amount consumed of coffee, tea, or alcohol (Table 1). There were, however, surprising significant trends for number of years drank coffee and tea that reached 1.9 (95% CI, 1.1-3.5) for those who drank coffee for z51 years, and 1.5 (1.0-2.2) for those who drank tea for z46 years, despite no corresponding trends in other indicators of caffeine consumption. There was also a small nonsignificant association with cancer risk of drinking more than one glass of water. Similar findings were seen in smokers and nonsmokers separately (data not shown). Table 2 presents ORs for food groups and nutrients in quartiles of intake from low to high. There were no significant trends seen for intake of food groups or nutrients for all participants, all nonsmokers, or male smokers (data not shown). However, in female smokers (120 cases, 94 controls), high intakes of fruits (P trend = 0.001; highest quartile OR, 0.4; 95% CI, 0.2-0.8), dark yellow vegetables (P trend = 0.06; highest quartile OR, 0.4; 95% CI, 0.1-0.9), and h-cryptoxanthin (P trend = 0.01; highest quartile OR, 0.4; 95% CI, 0.2-0.9) were associated with reduced cancer risk. Discussion In our study of renal pelvis and ureter cancers, we found no consistent cancer risk associated with beverage intake, vita- min supplement use, or BMI. These findings are in agreement 1051 Cancer Epidemiol Biomarkers Prev 2006;15(5). May 2006 Cancer Epidemiol Biomarkers Prev 2006;15(5):1051 – 3 Received 1/24/06; accepted 3/2/06. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Requests for reprints: Gloria Gridley, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services, Executive Plaza South, Room 8024, 6120 Executive Boulevard, MSC 7244, Bethesda, MD 20892-7244. Phone: 301-4963-3344; Fax: 301-402-0081. E-mail: gridleyg@mail.nih.gov Copyright D 2006 American Association for Cancer Research. doi:10.1158/1055-9965.EPI-06-0056 Research. on January 10, 2022. © 2006 American Association for Cancer cebp.aacrjournals.org Downloaded from