bluuebunny/crossref_metadata_2025_split huggingface dataset:
Perinatal Risk Factors for Cancer of the Esophagus and Gastric Cardia: A Nested Case-Control Study
Authors: Akre Olof , Forssell Lina , Kaijser Magnus , Norén-Nilsson Ingrid , Lagergren Jesper , Nyrén Olof , Ekbom Anders 
Published: May 2006

AbstractBackground: We have previously hypothesized that preterm birth or impaired fetal growth may cause esophageal adenocarcinomas through gastroesophageal reflux early in life. In this study, we aimed to test if there is an association between gestational duration and birth weight on the one hand, and risk of esophageal and cardia adenocarcinoma on the other.Methods: We conducted a nested case-control study of 67 cases of esophageal adenocarcinoma and 93 cases of cardia adenocarcinoma, whereas 50 cases of squamous cell carcinoma were studied for comparison. Birth records of cases were traced. Three matched controls per case were randomly selected. Perinatal data were extracted from birth records.Results: Long gestational duration was associated with a decreased risk of cardia adenocarcinoma (Ptrend = 0.001) and a nonsignificant decreased risk of esophageal adenocarcinoma (P = 0.07), whereas no such association was found for esophageal squamous cell carcinoma (P = 0.96). Birth weight was not associated with risk of any of the studied cancers. Compared with lower maternal age (≤24 years) at giving birth, maternal age of 25 to 29 years were associated with a decreased risk of esophageal adenocarcinoma and squamous cell carcinoma (odds ratio, 0.4; 95% confidence interval, 0.2-0.9 and odds ratio, 0.3; 95% confidence interval, 0.1-0.8, respectively).Conclusions: Numerical constraints hamper inference, but our results are somewhat consistent with the idea that future risk of esophageal and cardia cancer may in part be determined already perinatally or in infancy and give some limited support to the hypothesis that timing of birth influences risk. (Cancer Epidemiol Biomarkers Prev 2006;15(5):867–71)
4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanol and its Glucuronides in the Urine of Infants Exposed to Environmental Tobacco Smoke
Authors: Hecht Stephen S. , Carmella Steven G. , Le Ky-Anh , Murphy Sharon E. , Boettcher Angela J. , Le Chap , Koopmeiners Joseph , An Larry , Hennrikus Deborah J. 
Published: May 2006

Abstract
Biomarkers of carcinogen uptake could provide important information pertinent to the question of exposure to environmental tobacco smoke (ETS) in childhood and cancer development later in life. Previous studies have focused on exposures before birth and during childhood, but carcinogen uptake from ETS in infants has not been reported. Exposures in infants could be higher than in children or adults because of their proximity to parents who smoke. Therefore, we quantified 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucuronides (total NNAL) in the urine of 144 infants, ages 3 to 12 months, who lived in homes with parents who smoked. Total NNAL is an accepted biomarker of uptake of the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone. Cotinine and its glucuronide (total cotinine) and nicotine and its glucuronide (total nicotine) were also quantified. Total NNAL was detectable in 67 of 144 infants (46.5%). Mean levels of total NNAL in the 144 infants were 0.083 ± 0.200 pmol/mL, whereas those of total cotinine and total nicotine were 0.133 ± 0.190 and 0.069 ± 0.102 nmol/mL, respectively. The number of cigarettes smoked per week in the home or car by any family member when the infant was present was significantly higher (P &lt; 0.0001) when NNAL was detected than when it was not (76.0 ± 88.1 versus 27.1 ± 38.2). The mean level of NNAL detected in the urine of these infants was higher than in most other field studies of ETS exposure. The results of this study show substantial uptake of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in infants exposed to ETS and support the concept that persistent ETS exposure in childhood could be related to cancer later in life. (Cancer Epidemiol Biomarkers Prev 2006;15(5):988–92)
DNMT3b Polymorphism and Hereditary Nonpolyposis Colorectal Cancer Age of Onset
Authors: Jones J. Shawn , Amos Christopher I. , Pande Mala , Gu Xiangjun , Chen Jinyun , Campos Imelda M. , Wei Qingyi , Rodriguez-Bigas Miguel , Lynch Patrick M. , Frazier Marsha L. 
Published: May 2006

Abstract
Hereditary nonpolyposis colorectal cancer (HNPCC) is an autosomal dominant syndrome of familial malignancies resulting from germ-line mutations in DNA mismatch repair genes. Colorectal and endometrial cancers are most frequently observed. A polymorphic C-to-T change in the promoter region of the DNMT3b gene, −149 bp from the transcription start site, is reported to greatly increase promoter activity and is associated with increased risk for lung cancer and decreased postsurgical survival in patients with small cell carcinoma of the head and neck. We studied the influence of this DNMT3b polymorphism on HNPCC age of onset. We determined the DNMT3b genotype of 146 mismatch repair mutation carriers from 72 families. Of these, 74 participants had colorectal cancer. The participants were genotyped by single-strand conformational polymorphism analysis and DNA sequencing. We tested the association between age of onset and DNMT3b genotypes by comparing Kaplan-Meier survival curves, evaluating the homogeneity of the curves using the log-rank test, Wilcoxon's test, and Fleming-Harrington test and estimating the strength and direction of the association using the Cox proportional hazards regression model adjusting for potential demographic and genetic confounding factors. HNPCC patients carrying one or two copies of the DNMT3b variant T allele developed their colorectal cancer significantly earlier than HNPCC patients who were homozygous for the wild-type DNMT3b allele. Combining knowledge of an individual's DNMT3b genotype with information on other genetic and environmental risk factors may improve risk estimates and help to identify individuals who are genetically susceptible to developing HNPCC at an earlier age. (Cancer Epidemiol Biomarkers Prev 2006;15(5):886–91)
A Comparison of Carotenoids, Retinoids, and Tocopherols in the Serum and Buccal Mucosa of Chronic Cigarette Smokers versus Nonsmokers
Authors: Gabriel Helen E. , Liu Zhenhua , Crott Jimmy W. , Choi Sang-Woon , Song Byeng Chun , Mason Joel B. , Johnson Elizabeth J. 
Published: May 2006

Abstract
Background: Cigarette smoking, a major risk factor for oropharyngeal cancer, is reported to alter oral levels of carotenoids and tocopherols. Such effects may be important because these nutrients, as well as retinoids, are putative chemoprotective agents.
Objectives: To determine whether chronic smoking is associated with altered concentrations of these nutrients in serum and buccal mucosa; to distinguish whether such effects are ascribable to diet; and to determine whether oral concentrations of these nutrients correlate with a putative biomarker of oral cancer risk.
Methods: Serum and buccal mucosal cells (BMC) were analyzed for these nutrients and for BMC micronuclei in smokers (n = 35) and nonsmokers (n = 21).
Results: General linear regression with adjustments for dietary intake showed that smokers possess lower serum concentrations of β- and α-carotene, cryptoxanthin, lutein, and zeaxanthin (P ≤ 0.01) and a significantly higher serum γ-tocopherol (P = 0.03). In BMCs, smokers had significantly lower concentrations of β- and α-carotene, lycopene, and α-tocopherol (P &lt; 0.05) but significantly higher γ-tocopherol (P &lt; 0.01). Among nonsmokers, many serum carotenoid concentrations correlated with concentrations of the corresponding nutrient in BMCs whereas no such correlations existed among smokers. BMC micronuclei did not correlate with the oral concentration of any micronutrient.
Conclusions: Chronic cigarette smokers have lower concentrations of many dietary antioxidants in serum and BMCs compared with nonsmokers, an effect which is not entirely ascribable to diet. Nevertheless, the lack of concordance between oral concentrations of these nutrients and genetic damage in the BMCs of smokers does not support a protective role for these nutrients in oral carcinogenesis. (Cancer Epidemiol Biomarkers Prev 2006:15(5):993–9)
Incidence of Colorectal Cancer in Relation to Glycemic Index and Load in a Cohort of Women
Authors: McCarl Mary , Harnack Lisa , Limburg Paul J. , Anderson Kristin E. , Folsom Aaron R. 
Published: May 2006

Abstract
Background: Dietary glycemic index (GI) and glycemic load (GL) affect circulating insulin concentrations. Elevated circulating insulin concentrations can increase insulin-like growth factor-1, and both of these hormones may have growth-promoting effects within the colorectum.
Methods: We examined associations of GI and GL with colorectal cancer (CRC) among participants in the Iowa Women's Health Study (n = 35,197; ages 55-69 years at baseline in 1986). Over 15 years of follow-up, we identified 757 cases of colon cancer and 209 cases of rectal cancer (954 CRC cases).
Results: Overall, neither GI nor GL were significantly associated with incident CRC. However, among obese women (baseline body mass index ≥30 kg/m2) CRC incidence was increased in the highest versus lowest quintiles of GI (relative risk, 1.66; 95% confidence intervals, 1.13-2.43; P for trend = 0.02) and GL (relative risk, 1.79; 95% confidence intervals, 1.19-2.70; P for trend &lt; 0.01). This pattern of increased risk for obese women with high GI or GL tended to hold for both colon cancer and rectal cancer, and for nondiabetic women as well. No statistically significant associations were observed between GI or GL and CRC among subjects whose baseline body mass index was &lt;30 kg/m2.
Conclusion: Our findings suggest that high GI or GL are not major CRC risk factors among older women in general, but may increase CRC risk among women who are obese. (Cancer Epidemiol Biomarkers Prev 2006;15(5):392–6)
Mammographic Density as a Surrogate Marker for the Effects of Hormone Therapy on Risk of Breast Cancer
Authors: Boyd Norman F. , Martin Lisa J. , Li Qing , Sun Limei , Chiarelli Anna M. , Hislop Greg , Yaffe Martin J. , Minkin Salomon 
Published: May 2006

Abstract
Background: Some types of hormone therapy increase both risk of breast cancer and mammographic density, a risk factor for the disease, suggesting that mammographic density may be a surrogate marker for the effects of hormones on risk of breast cancer. This research was undertaken to determine whether the effect of hormone therapy on breast cancer risk is mediated by its effect on mammographic density.
Methods: Individually matched cases and controls from three nested case-control studies in breast screening populations were studied. Cases had developed invasive breast cancer at least 12 months after the initial screen. Information was collected on hormone use and other risk factors at the time of the baseline mammogram, and percent density was measured by a computer-assisted method.
Results: There were 1,748 postmenopausal women, of whom 426 (24.4%) were using hormones at the time of their initial screening mammogram. Current use of hormone therapy was associated with an increased risk of breast cancer (odds ratio, 1.26; 95% confidence interval, 1.0-1.6) that was little changed by adjustment for percent density in the baseline mammogram (odds ratio, 1.19; 95% confidence interval, 0.9-1.5). Percent density in the baseline mammogram was among cases greater in current users of hormones that in never-users (difference = 5.0%, P &lt; 0.001), but the difference was smaller and nonsignificant in controls (difference = 1.6%, P = 0.3).
Conclusion: Although the effects of hormone therapy on mammographic density were greater in cases than controls, we did not find evidence that these effects were causally related to risk of breast cancer. (Cancer Epidemiol Biomarkers Prev 2006;15(5):961–6)
Plasma Antibodies against Trichomonas vaginalis and Subsequent Risk of Prostate Cancer
Authors: Sutcliffe Siobhan , Giovannucci Edward , Alderete John F. , Chang Te-Hung , Gaydos Charlotte A. , Zenilman Jonathan M. , De Marzo Angelo M. , Willett Walter C. , Platz Elizabeth A. 
Published: May 2006

Abstract
Background: Although several previous case-control studies have investigated associations between sexually transmitted infections (STI) and prostate cancer, most have focused on gonorrhea and syphilis, two well-recognized, symptomatic STIs. Another STI of interest for prostate carcinogenesis is trichomonosis, a less well recognized and frequently asymptomatic STI with known prostate involvement. We investigated this infection in relation to incident prostate cancer in a nested case-control study within the Health Professionals Follow-up Study.
Methods: Prostate cancer cases were men diagnosed with prostate cancer between the date of blood draw (1993-1995) and 2000 (n = 691). Controls were men who had had at least one prostate-specific antigen test and who were free of prostate cancer and alive at the time of case diagnosis. One control was individually matched to each case by age (n = 691). Serologic evidence of a history of trichomonosis was assessed by a recombinant Trichomonas vaginalis α-actinin IgG ELISA.
Results: Thirteen percent of cases and 9% of controls were seropositive for trichomonosis (adjusted odds ratio, 1.43; 95% confidence interval, 1.00-2.03). This association persisted after additional adjustment for such factors as a history of other STIs, and was strongest among men who used aspirin infrequently over the course of their lives (odds ratio, 2.05; 95% confidence interval, 1.05-4.02, Pinteraction = 0.11).
Conclusions: Serologic evidence of a history of trichomonosis was positively associated with incident prostate cancer in this large, nested case-control study of male health professionals. As this study is the first, to our knowledge, to investigate associations between T. vaginalis serology and prostate cancer, additional studies are necessary before conclusions can be made. (Cancer Epidemiol Biomarkers Prev 2006;15(5):939–45)
Associations of Classic Kaposi Sarcoma with Common Variants in Genes that Modulate Host Immunity
Authors: Brown Elizabeth E. , Fallin Daniele , Ruczinski Ingo , Hutchinson Amy , Staats Brian , Vitale Francesco , Lauria Carmela , Serraino Diego , Rezza Giovanni , Mbisa Georgina , Whitby Denise , Messina Angelo , Goedert James J. , Chanock Stephen J. ,   Kaposi Sarcoma Working Group
Published: May 2006

AbstractClassic Kaposi sarcoma (CKS) is an inflammatory-mediated neoplasm primarily caused by Kaposi sarcoma–associated herpesvirus (KSHV). Kaposi sarcoma lesions are characterized, in part, by the presence of proinflammatory cytokines and growth factors thought to regulate KSHV replication and CKS pathogenesis. Using genomic DNA extracted from 133 CKS cases and 172 KSHV-latent nuclear antigen-positive, population-based controls in Italy without HIV infection, we examined the risk of CKS associated with 28 common genetic variants in 14 immune-modulating genes. Haplotypes were estimated for IL1A, IL1B, IL4, IL8, IL8RB, IL10, IL12A, IL13, and TNF. Compared with controls, CKS risk was decreased with 1235T/−1010G–containing diplotypes of IL8RB (odds ratio, 0.49; 95% confidence interval, 0.30-0.78; P = 0.003), whereas risk was increased with diplotypes of IL13 containing the promoter region variant 98A (rs20541, alias +130; odds ratio, 1.88; 95% confidence interval, 1.15-3.08; P = 0.01) when considered in multivariate analysis. Risk estimates did not substantially vary by age, sex, incident disease, or disease burden. Our data provide preliminary evidence for variants in immune-modulating genes that could influence the risk of CKS. Among KSHV-seropositive Italians, CKS risk was associated with diplotypes of IL8RB and IL13, supporting laboratory evidence of immune-mediated pathogenesis. (Cancer Epidemiol Biomarkers Prev 2006;15(5):926–34)
A Reproducibility Study for a Fluoride Assay in Bone
Authors: Medina Nancy , Douglass Chester W. , Whitford Gary M. , Hoover Robert N. , Fears Thomas R. 
Published: May 2006

Abstract
Osteosarcoma is a rare malignancy of largely unknown etiology. Although there is no consistent evidence for an association between fluoridation and cancer, some concerns remain about osteosarcoma. As part of the design of a collaborative study, bone samples were collected to allow for an evaluation of the association between osteosarcoma risk and individual fluoride exposure measured by levels of fluoride in bone. In this report, we provide the results of pilot experiments to consider issues that arose during the study design and to assess the reliability of the bone assays. Correlations of fluoride levels between normal bone near the affected area and iliac crest bone were strong and positive. The day-to-day laboratory analysis of fluoride in human and deer jaw bone yielded acceptable average coefficients of variation below 10% and an overall estimate of 5%. The intraclass correlation (ICC) is of particular importance to epidemiologists because it indicates the effect of measurement error on study results. Here, the estimated ICC is 0.86, and the estimated downward bias is only 14%. Hence, the ICC is strong enough so that the estimates of the relative risk will suffer little attenuation from lab measurements. (Cancer Epidemiol Biomarkers Prev 2006;15(5):1035–7)
Anthropometry, Physical Activity, and the Risk of Pancreatic Cancer in the European Prospective Investigation into Cancer and Nutrition
Authors: Berrington de González Amy , Spencer Elizabeth A. , Bueno-de-Mesquita H. Bas , Roddam Andrew , Stolzenberg-Solomon Rachel , Halkjær Jytte , Tjønneland Anne , Overvad Kim , Clavel-Chapelon Francoise , Boutron-Ruault Marie-Christine , Boeing Heiner , Pischon Tobias , Linseisen Jakob , Rohrmann Sabine , Trichopoulou Antonia , Benetou Vassiliki , Papadimitriou Aristoteles , Pala Valeria , Palli Domenico , Panico Salvatore , Tumino Rosario , Vineis Paolo , Boshuizen Hendriek C. , Ocke Marga C. , Peeters Petra H. , Lund Eiliv , Gonzalez Carlos A. , Larrañaga Nerea , Martinez-Garcia Carmen , Mendez Michelle , Navarro Carmen , Quirós J. Ramón , Tormo María-José , Hallmans Göran , Ye Weimin , Bingham Sheila A. , Khaw Kay-Tee , Allen Naomi , Key Tim J. , Jenab Mazda , Norat Teresa , Ferrari Pietro , Riboli Elio 
Published: May 2006

Abstract
Tobacco smoking is the only established risk factor for pancreatic cancer. Results from several epidemiologic studies have suggested that increased body mass index and/or lack of physical activity may be associated with an increased risk of this disease. We examined the relationship between anthropometry and physical activity recorded at baseline and the risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition (n = 438,405 males and females age 19-84 years and followed for a total of 2,826,070 person-years). Relative risks (RR) were calculated using Cox proportional hazards models stratified by age, sex, and country and adjusted for smoking and self-reported diabetes and, where appropriate, height. In total, there were 324 incident cases of pancreatic cancer diagnosed in the cohort over an average of 6 years of follow-up. There was evidence that the RR of pancreatic cancer was associated with increased height [RR, 1.74; 95% confidence interval (95% CI), 1.20-2.52] for highest quartile compared with lowest quartile (Ptrend = 0.001). However, this trend was primarily due to a low risk in the lowest quartile, as when this group was excluded, the trend was no longer statistically significant (P = 0.27). A larger waist-to-hip ratio and waist circumference were both associated with an increased risk of developing the disease (RR per 0.1, 1.24; 95% CI, 1.04-1.48; Ptrend = 0.02 and RR per 10 cm, 1.13; 95% CI, 1.01-1.26; Ptrend = 0.03, respectively). There was a nonsignificant increased risk of pancreatic cancer with increasing body mass index (RR, 1.09; 95% CI, 0.95-1.24 per 5 kg/m2), and a nonsignificant decreased risk with total physical activity (RR, 0.82; 95% CI, 0.50-1.35 for most active versus inactive). Future studies should consider including measurements of waist and hip circumference, to further investigate the relationship between central adiposity and the risk of pancreatic cancer. (Cancer Epidemiol Biomarkers Prev 2006;15(5):879–85)
The Influence of Statin Use on Breast Density
Authors: Boudreau Denise M. , Rutter Carolyn M. , Buist Diana S.M. 
Published: May 2006

Abstract
Objective: To evaluate if 3-hydroxy-3-methylglutaryl CoA reductase reductase inhibitor use (statins) alters mammography measured breast density.
Methods: Cohort study of women ages 50 to 80 years with two mammography screenings. Changes in BI-RADS breast density between screenings was compared for nonusers, initiators, discontinuers, continuers, and any users of statins.
Results: Statin use was not associated with increases or decreases in breast density compared with nonusers after adjusting for age, body mass index, change in body mass index, hormone therapy use, and time between screenings. Cumulative days of statin use during the year before screening was not associated with changes in breast density in any of the groups of statin users. When hormone therapy users were excluded, any statin use was associated with an increase in breast density compared with nonusers (odds ratio, 1.2; 95% confidence interval, 1.0-1.5).
Conclusions: We found no association between statin use and change in breast density in general, but statin use may be associated with increases in breast density among nonusers of hormone therapy. (Cancer Epidemiol Biomarkers Prev 2006;15(5):1026–9)
Estimating the Effect of Human Base Excision Repair Protein Variants on the Repair of Oxidative DNA Base Damage
Authors: Sokhansanj Bahrad A. , Wilson David M. 
Published: May 2006

Abstract
Epidemiologic studies have revealed a complex association between human genetic variance and cancer risk. Quantitative biological modeling based on experimental data can play a critical role in interpreting the effect of genetic variation on biochemical pathways relevant to cancer development and progression. Defects in human DNA base excision repair (BER) proteins can reduce cellular tolerance to oxidative DNA base damage caused by endogenous and exogenous sources, such as exposure to toxins and ionizing radiation. If not repaired, DNA base damage leads to cell dysfunction and mutagenesis, consequently leading to cancer, disease, and aging. Population screens have identified numerous single-nucleotide polymorphism variants in many BER proteins and some have been purified and found to exhibit mild kinetic defects. Epidemiologic studies have led to conflicting conclusions on the association between single-nucleotide polymorphism variants in BER proteins and cancer risk. Using experimental data for cellular concentration and the kinetics of normal and variant BER proteins, we apply a previously developed and tested human BER pathway model to (i) estimate the effect of mild variants on BER of abasic sites and 8-oxoguanine, a prominent oxidative DNA base modification, (ii) identify ranges of variation associated with substantial BER capacity loss, and (iii) reveal nonintuitive consequences of multiple simultaneous variants. Our findings support previous work suggesting that mild BER variants have a minimal effect on pathway capacity whereas more severe defects and simultaneous variation in several BER proteins can lead to inefficient repair and potentially deleterious consequences of cellular damage. (Cancer Epidemiol Biomarkers Prev 2006;15(5):1000–8)