bluuebunny/crossref_metadata_2025_split huggingface dataset:
Family History of Hemolymphopoietic and Other Cancers and Risk of Non-Hodgkin's Lymphoma
Authors: Negri Eva , Talamini Renato , Montella Maurizio , Dal Maso Luigino , Crispo Anna , Spina Michele , La Vecchia Carlo , Franceschi Silvia 
Published: March 2006

AbstractWe investigated the risk of lymphomas, hemolymphopoietic (HLP) cancers (including lymphomas), and non-HLP cancers in first-degree relatives of non-Hodgkin's lymphoma (NHL) cases in an Italian case-control study on 225 patients (median age, 59 years) with a new diagnosis of NHL and 504 hospital controls (median age, 63 years), admitted for a wide spectrum of acute, nonneoplastic, nonimmune conditions. We estimated odds ratios (OR) adjusted for sex, age, family size, and other potential confounders. We also built the cohort of all first-degree relatives and computed age and sex adjusted hazard ratios (HR) using proportional hazard models. A history of lymphoma in first-degree relatives was reported by 5 NHL cases and 3 controls [OR, 3.2; 95% confidence interval (95% CI), 0.7-14.4] whereas 14 cases and 11 controls reported a family history of HLP cancers (OR, 3.0; 95% CI, 1.2-7.0). The HR of relatives of NHL cases, compared with relatives of controls, was 4.5 (95% CI, 1.1-18.8) for lymphomas, 3.5 (95% CI, 1.5-7.4) for HLP cancers, 1.6 (95% CI, 1.3-2.0) for all cancers, and 1.0 (95% CI, 0.9-1.1) for all causes of deaths. The HRs were higher for relatives of NHL cases diagnosed before the age of 50 years: 7.1 for HLP cancers, 2.0 for all cancers, and 1.6 for all deaths. A family history of cancer of the liver (OR, 2.1; 95% CI, 1.0-4.2), breast (OR, 2.0; 95% CI, 1.0-3.6), and kidney (OR, 4.6; 95% CI, 1.0-20.9) increased NHL risk. The OR was also elevated for all cancer sites (OR, 1.7 95% CI, 1.2-2.4) and the risk increased with the number of affected relatives also when HLP cancers were excluded. (Cancer Epidemiol Biomarkers Prev 2006;15(2):245–50)
Residential Insecticide Use and Risk of Non-Hodgkin's Lymphoma
Authors: Colt Joanne S. , Davis Scott , Severson Richard K. , Lynch Charles F. , Cozen Wendy , Camann David , Engels Eric A. , Blair Aaron , Hartge Patricia 
Published: March 2006

Abstract
Previous studies have linked non-Hodgkin's lymphoma (NHL) with occupational exposure to insecticides, but residential use is largely unexplored. In this population-based case-control study, we examined NHL risk and use of insecticides in the home and garden. We identified NHL cases, uninfected with HIV, diagnosed between 1998 and 2000 among women and men ages 20 to 74 years in Iowa and the metropolitan areas of Los Angeles, Detroit, and Seattle. Controls were selected using random digit dialing or Medicare files. Computer-assisted personal interviews (1,321 cases and 1,057 controls) elicited data on insecticide use at each home occupied since 1970. Insecticide levels were measured in dust taken from used vacuum cleaner bags (682 cases and 513 controls). We previously reported a positive association with dichlorodiphenyldichloroethylene levels in carpet dust residues. Here, we focus on insecticides that were commonly used after 1970, the time period covered by our questionnaire. People whose homes were treated for termites had elevated NHL risk (odds ratio, 1.3; 95% confidence interval, 1.0-1.6). Risk was modestly, although not significantly, elevated in all but one study center and in all sexes and races. The elevation in risk was restricted to people whose homes were treated before the 1988 chlordane ban. There was a significant trend of increasing risk with increasing levels of α-chlordane residues in dust (Ptrend = 0.04) and a marginally significant trend for γ-chlordane (Ptrend = 0.06). We found no evidence of associations for insects overall, for specific types of insects other than termites, or for elevated residues of other insecticides. We concluded that chlordane treatment of homes for termites may increase residents' NHL risk. (Cancer Epidemiol Biomarkers Prev 2006;15(2):251–7)
A Prospective Study of Lycopene and Tomato Product Intake and Risk of Prostate Cancer
Authors: Kirsh Victoria A. , Mayne Susan T. , Peters Ulrike , Chatterjee Nilanjan , Leitzmann Michael F. , Dixon L. Beth , Urban Donald A. , Crawford E. David , Hayes Richard B. 
Published: March 2006

Abstract
Background: Dietary lycopene and tomato products may reduce risk of prostate cancer; however, uncertainty remains about this possible association.
Methods: We evaluated the association between intake of lycopene and specific tomato products and prostate cancer risk in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, a multicenter study designed to investigate cancer early detection methods and etiologic determinants. Participants completed both a general risk factor and a 137-item food frequency questionnaire at baseline. A total of 1,338 cases of prostate cancer were identified among 29,361 men during an average of 4.2 years of follow-up.
Results: Lycopene intake was not associated with prostate cancer risk. Reduced risks were also not found for total tomato servings or for most tomato-based foods. Statistically nonsignificant inverse associations were noted for pizza [all prostate cancer: relative risk (RR), 0.83; 95% confidence interval (95% CI), 0.67-1.03 for ≥1 serving/wk versus &lt; 0.5 serving/mo; Ptrend = 0.06 and advanced prostate cancer: RR, 0.79; 95% CI, 0.56-1.10; Ptrend = 0.12] and spaghetti/tomato sauce consumption (advanced prostate cancer: RR = 0.81, 95% CI, 0.57-1.16 for ≥2 servings/wk versus &lt; 1 serving/mo; Ptrend = 0.31). Among men with a family history of prostate cancer, risks were decreased in relation to increased consumption of lycopene (Ptrend = 0.04) and specific tomato-based foods commonly eaten with fat (spaghetti, Ptrend = 0.12; pizza, Ptrend = 0.15; lasagna, Ptrend = 0.02).
Conclusions: This large study does not support the hypothesis that greater lycopene/tomato product consumption protects from prostate cancer. Evidence for protective associations in subjects with a family history of prostate cancer requires further corroboration. (Cancer Epidemiol Biomarkers Prev 2006;15(1):92–8)
Human Papillomavirus 16, 18, and 33 Infections and Risk of Prostate Cancer: A Nordic Nested Case-Control Study
Authors: Korodi Zoltan , Dillner Joakim , Jellum Egil , Lumme Sonja , Hallmans Göran , Thoresen Steinar , Hakulinen Timo , Stattin Pär , Luostarinen Tapio , Lehtinen Matti , Hakama Matti 
Published: March 2006

Abstract
Epidemiologic evidence of sexual history has emerged as a consistently found risk factor for prostate cancer. Some studies have reported an association between human papillomavirus (HPV) infections and prostate cancer. We did a nested case-control study within cohorts of more than 200,000 men enrolled in three Nordic biobanking projects. Follow-up using cancer registry linkages identified 804 prospectively occurring prostate cancer cases. Four control subjects per case were randomly selected from eligible sets of matched subjects that were alive and free of cancer at the time of diagnosis of the corresponding case and were matched to cases on biobank cohort, age (±2 years), county of residence, and date of blood sampling (±2 months in the Finnish and Swedish cohorts, ±6 months in the Norwegian cohort). The serum samples were analyzed by standard ELISAs for the presence of immunoglobulin G antibodies against HPV types 16, 18, and 33. The joint HPV-16/HPV-18/HPV-33 seroprevalence in the joint cohort was 13.4% (107 of 799) among cases and 14.0% (363 of 2,596) among controls (odds ratio, 0.94; 95% confidence interval, 0.74-1.19). There were no noteworthy differences when the data were analyzed by different HPV type, country, or antibody levels. Our data do not support an association between serologic markers of HPV-16, HPV-18, and HPV-33 infections and risk of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2952–5)
Quantitative Analysis of Plasma TP53 249Ser-Mutated DNA by Electrospray Ionization Mass Spectrometry
Authors: Lleonart Matilde E. , Kirk Gregory D. , Villar Stephanie , Lesi Olufunmilayo A. , Dasgupta Abhijit , Goedert James J. , Mendy Maimuna , Hollstein Monica C. , Montesano Ruggero , Groopman John D. , Hainaut Pierre , Friesen Marlin D. 
Published: March 2006

Abstract
A mutation in codon 249 of the TP53 gene (249Ser), related to aflatoxin B1 exposure, has previously been associated with hepatocellular carcinoma risk. Using a novel internal standard plasmid, plasma concentrations of 249Ser-mutated DNA were quantified by electrospray ionization mass spectrometry in 89 hepatocellular carcinoma cases, 42 cirrhotic patients, and 131 nonliver diseased control subjects, all from highly aflatoxin-exposed regions of The Gambia. The hepatocellular carcinoma cases had higher median plasma concentrations of 249Ser (2,800 copies/mL; interquartile range: 500-11,000) compared with either cirrhotic (500 copies/mL; interquartile range: 500-2,600) or control subjects (500 copies/mL; interquartile range: 500-2,000; P &lt; 0.05). About half (52%) of the hepatocellular carcinoma cases had &gt;2,500 copies of 249Ser/mL plasma, corresponding to the prevalence of this mutation in liver tumors in The Gambia. In comparison, only 15% of control group and 26% of cirrhotic participants exceeded this level (P &lt; 0.05). Further subset analysis revealed a statistically significant, quantitative relation between diagnosis of hepatocellular carcinoma and levels of 249Ser detected at 2,501 to 10,000 copies/mL plasma (odds ratio, 3.8; 95% confidence interval, 1.3-10.9) and at &gt;10,000 copies/mL plasma (odds ratio, 62; 95% confidence interval, 4.7-820) when compared with control subjects and after adjusting for age, gender, recruitment site, hepatitis B and C serologic status, and total DNA concentration. Levels of &gt;10,000 copies of 249Ser/mL plasma were also significantly associated with the diagnosis of hepatocellular carcinoma (odds ratio, 15; 95% confidence interval, 1.6-140) when compared with cirrhotic patients. Potential applications for the quantification of 249Ser DNA in plasma include estimation of long-term, cumulative aflatoxin exposure and selection of appropriate high-risk individuals for targeted intervention. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2956–62)
Combined Effects of the p53 and p73 Polymorphisms on Lung Cancer Risk
Authors: Schabath Matthew B. , Wu Xifeng , Wei Qingyi , Li Guojun , Gu Jian , Spitz Margaret R. 
Published: March 2006

Abstract
Lung cancer is a multigenic disease where one variant single nucleotide polymorphism may have only a modest independent effect on the disease phenotype, yet in aggregate, multiple biologically relevant single nucleotide polymorphisms may provide a more accurate representation of risk. Polymorphisms in members of the p53 family, such as p53 and p73, that have a functional relevance would be predicted to contribute to the disease phenotype. In this analysis, we used genotype data from 863 lung cancer cases and 852 healthy controls to test for multigenetic effects of polymorphisms at p53 exon 4, introns 3 and 6, and at p73 exon 2. All individuals in this analysis were self-reported non–Hispanic Caucasians. When the p73 and p53 variant alleles were combined and analyzed as a continuous variable, there was a 13% increase [odds ratios (OR), 1.13; 95% confidence intervals (CI), 1.05-1.21] in lung cancer risk for each additional variant allele. Furthermore, when the number of variant alleles was categorized into three groups (zero, one to three, and four or more variants), there was evidence of a gene-dosage effect with increased risks for individuals with one to three variants (OR, 1.30; 95% CI, 1.05-1.61) and four or more variants (OR, 1.78; 95% CI, 1.23-2.56). When the data were stratified by smoking status, an increased risk for lung cancer was evident only in current (OR, 2.32; 95% CI, 1.25-4.33) and former smokers (OR, 1.73; 95% CI, 1.02-2.94) with four or more variants. Younger individuals with four or more variants were also at a significantly increased risk for lung cancer (OR, 3.15; 95% CI, 1.62-6.12). This study provides support for the multigenetic effects of variant alleles from p53 exon 4, and introns 3 and 6, and p73, and their interplay with smoking, resulting in a significantly increased risk for lung cancer in this Caucasian population. (Cancer Epidemiol Biomarkers Prev 2006;15(1):158–61)
Circulating Steroid Hormones and the Risk of Prostate Cancer
Authors: Severi Gianluca , Morris Howard A. , MacInnis Robert J. , English Dallas R. , Tilley Wayne , Hopper John L. , Boyle Peter , Giles Graham G. 
Published: March 2006

Abstract
Epidemiologic studies have failed to support the hypothesis that circulating androgens are positively associated with prostate cancer risk and some recent studies have even suggested that high testosterone levels might be protective particularly against aggressive cancer. We tested this hypothesis by measuring total testosterone, androstanediol glucuronide, androstenedione, DHEA sulfate, estradiol, and sex hormone–binding globulin in plasma collected at baseline in a prospective cohort study of 17,049 men. We used a case-cohort design, including 524 cases diagnosed during a mean 8.7 years follow-up and a randomly sampled subcohort of 1,859 men. The association between each hormone level and prostate cancer risk was tested using Cox models adjusted for country of birth. The risk of prostate cancer was ∼30% lower for a doubling of the concentration of estradiol but the evidence was weak (Ptrend = 0.07). None of the other hormones was associated with overall prostate cancer (Ptrend ≥ 0.3). None of the hormones was associated with nonaggressive prostate cancer (all Ptrend ≥ 0.2). The hazard ratio [HR; 95% confidence interval (95% CI)] for aggressive cancer almost halved for a doubling of the concentration of testosterone (HR, 0.55; 95% CI, 0.32-0.95) and androstenedione (HR, 0.51; 95% CI, 0.31-0.83), and was 37% lower for a doubling of the concentration of DHEA sulfate (HR, 0.63; 95% CI, 0.46-0.87). Similar negative but nonsignificant linear trends in risk for aggressive cancer were obtained for free testosterone, estradiol, and sex hormone–binding globulin (Ptrend = 0.06, 0.2, and 0.1, respectively). High levels of testosterone and adrenal androgens are thus associated with reduced risk of aggressive prostate cancer but not with nonaggressive disease. (Cancer Epidemiol Biomarkers Prev 2006;15(1):86–91)
Complementary Medicine Use before and 1 Year Following Genetic Testing for BRCA1/2 Mutations
Authors: DiGianni Lisa M. , Rue Montserrat , Emmons Karen , Garber Judy E. 
Published: March 2006

Abstract
Purpose: We explored change in complementary and alternative medicine (CAM) use by unaffected women and cancer survivors from enrollment into a randomized BRCA1/2 testing program to CAM use 1 year following results disclosure.
Methods: A cohort of 243 high-risk women completed questionnaires at enrollment into a BRCA1/2 randomized trial and 1 year post results disclosure. Uses of several CAMs for cancer prevention were explored, including ingestible, behavioral, and physical modalities. Assessment of the change in CAM use from baseline to 1 year follow-up was conducted using a repeated self-administered questionnaire. Correlates of the number of CAMs used at 1 year were explored using multivariable linear regression models.
Results: Among the subset of women who changed their CAM behavior from enrollment to 1 year following BRCA1/2 results disclosure, there was a significantly higher proportion who changed from no CAM use to CAM use among the overall cohort (P = 0.01), among women without cancer at enrollment (P = 0.003), among women found to be BRCA1/2 carriers (P = 0.03), and among women randomized to the genetic counseling intervention arm of the study (P = 0.009). Number of CAMs used at 1 year was positively associated with number of CAMs used at baseline, sunscreen use, and BRCA1/2 mutation status.
Conclusion: High-risk women who have received BRCA1/2 counseling and testing frequently adopt new CAM use in the first year after learning their genetic status. Mutation carriers frequently initiate CAM use after learning their genetic status as part of their cancer preventive regimen. Further studies are warranted to determine the efficacy of CAM-related strategies for cancer prevention. (Cancer Epidemiol Biomarkers Prev 2006;15(1):70–5)
Toxicokinetics of Acrylamide in Humans after Ingestion of a Defined Dose in a Test Meal to Improve Risk Assessment for Acrylamide Carcinogenicity
Authors: Fuhr Uwe , Boettcher Melanie I. , Kinzig-Schippers Martina , Weyer Alexandra , Jetter Alexander , Lazar Andreas , Taubert Dirk , Tomalik-Scharte Dorota , Pournara Panagiota , Jakob Verena , Harlfinger Stefanie , Klaassen Tobias , Berkessel Albrecht , Angerer Jürgen , Sörgel Fritz , Schömig Edgar 
Published: March 2006

Abstract
High amounts of acrylamide in some foods result in an estimated daily mean intake of 50 μg for a western style diet. Animal studies have shown the carcinogenicity of acrylamide upon oral exposure. However, only sparse human toxicokinetic data is available for acrylamide, which is needed for the extrapolation of human cancer risk from animal data. We evaluated the toxicokinetics of acrylamide in six young healthy volunteers after the consumption of a meal containing 0.94 mg of acrylamide. Urine was collected up to 72 hours thereafter. Unchanged acrylamide, its mercapturic acid metabolite N-acetyl-S-(2-carbamoylethyl)cysteine (AAMA), its epoxy derivative glycidamide, and the respective metabolite of glycidamide, N-acetyl-S-(2-hydroxy-2-carbamoylethyl)cysteine (GAMA), were quantified in the urine by liquid chromatography-mass spectrometry. Toxicokinetic variables were obtained by noncompartmental methods. Overall, 60.3 ± 11.2% of the dose was recovered in the urine. Although no glycidamide was found, unchanged acrylamide, AAMA, and GAMA accounted for urinary excretion of (mean ± SD) 4.4 ± 1.5%, 50.0 ± 9.4%, and 5.9 ± 1.2% of the dose, respectively. Apparent terminal elimination half-lives for the substances were 2.4 ± 0.4, 17.4 ± 3.9, and 25.1 ± 6.4 hours. The ratio of GAMA/AAMA amounts excreted was 0.12 ± 0.02. In conclusion, most of the acrylamide ingested with food is absorbed in humans. Conjugation with glutathione exceeds the formation of the reactive metabolite glycidamide. The data suggests an at least 2-fold and 4-fold lower relative internal exposure for glycidamide from dietary acrylamide in humans compared with rats or mice, respectively. This should be considered for quantitative cancer risk assessment. (Cancer Epidemiol Biomarkers Prev 2006;15(2):266–71)
Genetic Polymorphisms in Base-Excision Repair Pathway Genes and Risk of Breast Cancer
Authors: Zhang Yawei , Newcomb Polly A. , Egan Kathleen M. , Titus-Ernstoff Linda , Chanock Stephen , Welch Robert , Brinton Louise A. , Lissowska Jolanta , Bardin-Mikolajczak Alicja , Peplonska Beata , Szeszenia-Da̧browska Neonila , Zatonski Witold , Garcia-Closas Montserrat 
Published: March 2006

AbstractImpaired base-excision repair (BER) function can give rise to the accumulation of DNA damage and initiation of cancer. We evaluated whether genetic variation in six BER pathway genes (XRCC1, ADPRT, APEX1, OGG1, LIG3, and MUTYH) is associated with breast cancer risk in two large population-based case-control studies in the United States (3,368 cases and 2,880 controls) and Poland (1,995 cases and 2,296 controls). A detailed evaluation was first done in a subset of 1,898 cases and 1,514 controls with mouthwash DNA samples in the U.S. study. Significant findings were followed up in the remainder of the U.S. study population that provided cytobrush DNA samples and in the Polish study. Using data from U.S. study participants with mouthwash DNA, we found no significant overall association between breast cancer risk and XRCC1 R280H and R194W, ADPRT V726W, APEX1 D148E, OGG1 S326C, LIG3 R780H, or MUTYH 5′ untranslated region. These data suggested a decreased risk for XRCC1Q399R homozygous variants compared with homozygous wild-type in premenopausal women, but these findings were not confirmed when data from cytobrush DNA samples were added [combined odds ratio (OR), 0.8; 95% confidence interval (95% CI), 0.6-1.1] or in the Polish study (OR, 1.0; 95% CI, 0.7-1.5). Meta-analyses based on our data and published data from studies of two single nucleotide polymorphisms in XRCC1 showed no evidence of an overall association between breast cancer risk and homozygous variants versus wild-type for Q399R (OR, 1.1; 95% CI, 1.0-1.2) or R194W (OR, 1.0; 95% CI, 0.7-1.8), although there was a suggestion for an association in Asian populations for Q399R (OR, 1.6; 95% CI, 1.1-2.4; P = 0.02). In conclusion, our results do not support that the polymorphisms evaluated in six BER pathway genes play a major role in breast carcinogenesis, particularly in Caucasian populations. (Cancer Epidemiol Biomarkers Prev 2006;15(2):353–8)
Long-term Storage and Recovery of Buccal Cell DNA from Treated Cards
Authors: Sigurdson Alice J. , Ha Mina , Cosentino Mark , Franklin Tracie , Haque Kashif A. , Qi Ying , Glaser Cynthia , Reid Yvonne , Vaught Jim B. , Bergen Andrew W. 
Published: March 2006

Abstract
Economical methods for collecting and storing high-quality DNA are needed for large population-based molecular epidemiology studies. Buccal cell DNA collected via saliva and stored on treated filter paper cards could be an attractive method, but modest DNA yields and the potential for reduced recovery of DNA over time were unresolved impediments. Consequently, buccal cell DNA collection via oral mouthwash rinsing became the method of choice in epidemiologic studies. However, the amount of genomic DNA (gDNA) required for genotyping continues to decrease, and reliable whole genome amplification (WGA) methods further reduced the mass of gDNA needed for WGA to 10 ng, diminishing the obstacle of low DNA yields from cards. However, concerns about yield and DNA quality over time remained. We located and analyzed 42 buccal cell saliva samples collected and stored on treated cards for 7 years at room temperature, −20°C, and −80°C. We recovered DNA from the treated cards, estimated the concentration by a human-specific quantitative real-time PCR assay, and evaluated the quality by PCR amplification of 268-, 536-, and 989-bp fragments of the β-globin gene and by AmpFlSTR Identifiler assay analysis. Most DNA yields per 3-mm punch were &lt;10 ng, and most PCR amplicons failed to amplify, where size of the amplicon was negatively associated with successful amplification. Using these methods, treated cards did not consistently provide sufficient quantities of buccal cell gDNA after 7 years of storage for genotyping or WGA.(Cancer Epidemiol Biomarkers Prev 2006;15(2):385–8)