bluuebunny/crossref_metadata_2025_split huggingface dataset:
Flaxseed Supplementation (Not Dietary Fat Restriction) Reduces Prostate Cancer Proliferation Rates in Men Presurgery
Authors: Demark-Wahnefried Wendy , Polascik Thomas J. , George Stephen L. , Switzer Boyd R. , Madden John F. , Ruffin Mack T. , Snyder Denise C. , Owzar Kouros , Hars Vera , Albala David M. , Walther Philip J. , Robertson Cary N. , Moul Judd W. , Dunn Barbara K. , Brenner Dean , Minasian Lori , Stella Philip , Vollmer Robin T. 
Published: December 2008

Abstract
Background: Prostate cancer affects one of six men during their lifetime. Dietary factors are postulated to influence the development and progression of prostate cancer. Low-fat diets and flaxseed supplementation may offer potentially protective strategies.
Methods: We undertook a multisite, randomized controlled trial to test the effects of low-fat and/or flaxseed-supplemented diets on the biology of the prostate and other biomarkers. Prostate cancer patients (n = 161) scheduled at least 21 days before prostatectomy were randomly assigned to one of the following arms: (a) control (usual diet), (b) flaxseed-supplemented diet (30 g/d), (c) low-fat diet (&lt;20% total energy), or (d) flaxseed-supplemented, low-fat diet. Blood was drawn at baseline and before surgery and analyzed for prostate-specific antigen, sex hormone-binding globulin, testosterone, insulin-like growth factor-I and binding protein-3, C-reactive protein, and total and low-density lipoprotein cholesterol. Tumors were assessed for proliferation (Ki-67, the primary endpoint) and apoptosis.
Results: Men were on protocol an average of 30 days. Proliferation rates were significantly lower (P &lt; 0.002) among men assigned to the flaxseed arms. Median Ki-67-positive cells/total nuclei ratios (×100) were 1.66 (flaxseed-supplemented diet) and 1.50 (flaxseed-supplemented, low-fat diet) versus 3.23 (control) and 2.56 (low-fat diet). No differences were observed between arms with regard to side effects, apoptosis, and most serologic endpoints; however, men on low-fat diets experienced significant decreases in serum cholesterol (P = 0.048).
Conclusions: Findings suggest that flaxseed is safe and associated with biological alterations that may be protective for prostate cancer. Data also further support low-fat diets to manage serum cholesterol. (Cancer Epidemiol Biomarkers Prev 2008;17(12):3577–87)
Psychosocial Factors Associated with an Increased Frequency of Prostate Cancer Screening in Men Ages 40 to 79 Years: The Olmsted County Study
Authors: Wallner Lauren P. , Sarma Aruna V. , Lieber Michael M. , St. Sauver Jennifer L. , Jacobson Debra J. , McGree Michaela E. , Gowan Monica E. , Jacobsen Steven J. 
Published: December 2008

Abstract
Prostate cancer is the second leading cause of cancer deaths among U.S. men. Early detection is associated with drastically improved 5-year survival rates. It is unclear, however, what psychosocial factors motivate or discourage men from taking advantage of both prostate-specific antigen (PSA) testing and digital rectal examination (DRE). The goal of the current study was to identify psychosocial factors that influence screening behavior for prostate cancer in a cohort of 2,447 men. In 1990, a randomly selected cohort of Caucasian men, ages 40 to 79 years, from Olmsted County, Minnesota, were enrolled in the study. These men completed a questionnaire containing queries on family history of prostate cancer, concern about getting prostate cancer, and marital status. Medical and laboratory records were reviewed to determine the number DREs (1989-1996) and PSA tests (1989-1998). Frequent screening was defined as the upper 25th percentile for number of DREs (&gt;4) or PSAs (&gt;3). Men who have a family history and men who worry or have concern about prostate cancer were more likely [odds ratio (OR), 1.5; 95% confidence interval (95% CI), 1.2-2.0 and OR, 1.9; 95% CI, 1.4-2.5] to seek screening compared with those without a family history or worry. The association between family history and frequent screening was similar in men who were married or living with someone (OR, 1.7; 95% CI, 1.2-2.2); however, it was reduced among men who live alone (OR, 0.6; 95% CI, 0.2-1.8). These data suggest that psychosocial factors such as family history, worry, or concern about prostate cancer and marital status may play an important role in men's decisions about prostate cancer screening. (Cancer Epidemiol Biomarkers Prev 2008;17(12):3588–92)
Effects on Chinese Restaurant Workers of Exposure to Cooking Oil Fumes: A Cautionary Note on Urinary 8-Hydroxy-2′-Deoxyguanosine
Authors: Pan Chih-Hong , Chan Chang-Chuan , Wu Kuen-Yuh 
Published: December 2008

Abstract
This study evaluates oxidative DNA damage in workers who are exposed to cooking oil fumes (COFs) in Chinese restaurants. The study participants were 387 nonsmoking Chinese restaurant workers, 202 kitchen staff, and 185 service staff at 23 Chinese restaurants in Taiwan. Airborne particulate matter and particulate polycyclic aromatic hydrocarbon levels were monitored in kitchens and dining areas. Urinary 1-hydroxypyrene (1-OHP) was used as an internal dose of exposure to COFs, and urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) was used as an oxidative DNA damage marker. The relationship between workers' 8-OHdG and 1-OHP levels was estimated using linear mixed-effects models. Airborne particulate matter and polycyclic aromatic hydrocarbons levels in kitchens significantly exceeded those in dining areas. The kitchen staff's geometric mean levels of urinary 8-OHdG (7.9 μg/g creatinine) and 1-OHP (4.5 μg/g creatinine) were significantly higher than those of the service staff, which were 5.4 and 2.7 μg/g creatinine, respectively. Urinary 1-OHP level, work in kitchens, gender, and work hours per day were four significant predictors of urinary 8-OHdG levels after adjustments are made for covariates. Oxidative DNA damage was associated with exposure of Chinese restaurant workers to COFs. Female restaurant workers had a greater oxidative stress response to COFs than male restaurant workers, providing additional evidence of the link between lung cancer in Chinese women and exposure to COFs. (Cancer Epidemiol Biomarkers Prev 2008;17(12):3351–7)
DJ-1 Could Predict Worse Prognosis in Esophageal Squamous Cell Carcinoma
Authors: Yuen Hiu-Fung , Chan Yuen-Piu , Law Simon , Srivastava Gopesh , El-tanani Mohamed , Mak Tak-Wah , Chan Kwok-Wah 
Published: December 2008

Abstract
Recent studies have revealed an oncogenic role of DJ-1 through its ability to transform normal cells, prevent oxidative damage, and inhibit apoptosis. However, its role in esophageal squamous cell carcinoma (ESCC) is unknown. In this study, by immunohistochemistry, we analyzed the expression of DJ-1 in 81 ESCC tumors, 31 paired nonneoplastic esophageal epithelia, and 19 paired ESCC lymph node metastases. We found that cytoplasmic DJ-1 expression was significantly higher in ESCC and ESCC lymph node metastases than in nonneoplastic esophageal epithelium. ESCC specimens with high distant metastatic potential also had a significantly higher level of nuclear DJ-1 expression (P = 0.018). By Kaplan-Meier analysis, we found that a high level of nuclear DJ-1 was significantly associated with poorer patient survival in our cohort (P = 0.028). To investigate whether DJ-1 promotes ESCC progression through phosphatidylinositol 3-kinase pathway and modulation of apoptosis, we performed immunohistochemistry of pAkt and Daxx. We found that DJ-1 expression was significantly associated with pAkt, whereas nuclear DJ-1 expression was significantly correlated with nuclear expression of Daxx. These results suggest that phosphatidylinositol 3-kinase pathway and Daxx-regulated apoptosis might be important in DJ-1-mediated ESCC progression. By using multivariate Cox regression, we further showed that T4 stage (P = 0.003) and DJ-1 (P = 0.034) are independent predictors of patient survival. In conclusion, our results suggest that DJ-1 plays a very important role in transformation and progression of ESCC and may be used as a prognostic marker in ESCC. (Cancer Epidemiol Biomarkers Prev 2008;17(12):3593–602)
Hyaluronan-Mediated Motility Receptor Gene Single Nucleotide Polymorphisms and Risk of Breast Cancer
Authors: Kalmyrzaev Bolot , Pharoah Paul D.P. , Easton Douglas F. , Ponder Bruce A.J. , Dunning Alison M. ,   for the SEARCH Team
Published: December 2008

Abstract
A recent study used a network modeling strategy to generate a set of genes linked by potential functional associations. The hyaluronan-mediated motility receptor (HMMR) gene was identified as being as functionally associated with BRCA1 and thus a candidate breast cancer gene. SNPs rs10515860, rs299290, and rs7712023 were reported to be significantly associated with breast cancer in a joint analysis of two small case-control studies. We have examined the association of these single nucleotide polymorphisms, together with others tagging the HMMR gene, in a larger, European case-control study and find no association of any of them with risk of breast cancer: rs10515860 [odds ratio (OR; AA/GG), 0.85; 95% confidence interval (CI), 0.65-1.12; Ptrend = 0.9], rs299290 [OR (CC/TT), 1.00; 95% CI, 0.87-1.15; Ptrend = 0.7], rs3756648 (rs7712023) [OR (TT/CC), 0.93; 95% CI, 0.84-1.02; Ptrend = 0.1], rs299284 [OR (TT/CC), 1.01; 95% CI, 0.76-1.35; Ptrend = 0.5], and rs13183712 [OR (TT/GG), 1.04; 95% CI, 0.88-1.23; Ptrend = 0.6]. (Cancer Epidemiol Biomarkers Prev 2008;17(12):3618–20)
Target Sequence Polymorphism of Human Manganese Superoxide Dismutase Gene and Its Association with Cancer Risk: A Review
Authors: Bag Arundhati , Bag Niladri 
Published: December 2008

AbstractIn normal state of a cell, endogenous antioxidant enzyme system maintains the level of reactive oxygen species generated by mitochondrial respiratory chain. Mitochondrial superoxide dismutase [SOD; manganese SOD (MnSOD) or SOD2] neutralizes highly reactive superoxide radical (O•-2), the first member in the plethora of mitochondrial reactive oxygen species. A polymorphism in the target sequence of MnSOD enzyme, Val16Ala, is known to disrupt proper targeting of the enzyme from cytosol to mitochondrial matrix where it acts on O•-2 to dismutate it to hydrogen peroxide (H2O2). A change in the level of O•-2 and of H2O2 in mitochondria modulates the molecular mechanisms of apoptosis, cellular adhesion, and cell proliferation and thus play key role in cancer development. Previous studies investigating the association between MnSOD Val16Ala polymorphism and cancer risk have revealed inconsistent results. We conducted a meta-analysis on these studies. Our meta-analysis on total of 7,366 cancer cases and 9,102 controls from 13 published case-control studies showed no overall association of this polymorphism either with breast cancer risk or for cancer risk as such (for Ala homozygous odds ratio, 0.98; 95% confidence interval, 0.90-1.07 and odds ratio, 1.02; 95% confidence interval, 0.91-1.14, respectively). Also, there was no major effect in either recessive or dominant model for the MnSOD Val16Ala. However, a proper evaluation of this polymorphism with cancer link demands experiments involving large sample size, cross-tabulation of gene-gene, gene-environment interactions, and linkage studies, as cell biological experiments clearly correlate critical levels of mitochondrial O•-2 and H2O2 to carcinogenesis. (Cancer Epidemiol Biomarkers Prev 2008;17(12):3298–305)
Nicotine Intake in Cigarette Smokers in England: Distribution and Demographic Correlates
Authors: Fidler Jennifer A. , Jarvis Martin J. , Mindell Jennifer , West Robert 
Published: December 2008

Abstract
Documenting smoke intake by objective biochemical markers is important for quantification of exposure to toxins. The aim of this report is to show the most definitive distribution of the nicotine metabolite, cotinine, yet available from English smokers in the period before implementation of the legislation banning smoking in indoor public areas. A total of 6,423 cigarette smokers, ages 16 years and above, taking part in the Health Survey for England between 1998 and 2003 provided a saliva cotinine value. Data on cigarette consumption, age, gender, social class, deprivation (as indicated by manual or nonmanual occupation, car ownership, and housing tenure), marital status, and region were collected. Cotinine concentrations showed no overall trend over the study period. The mean value was 289.15 ng/mL (SD 174.43); excluding those who had not smoked in the past 24 hours, the mean value was 302.08 ng/mL (SD 168.78). A higher cotinine concentration was associated with being middle-aged (peaking at 40 years), being male, being single, greater economic deprivation, and not living in London. After adjusting for cigarette consumption, higher values were associated with middle age, being male, and greater deprivation. This study provides the most complete picture yet of the smoke intake of cigarette smokers in England. The fact that cotinine peaks at around the age of 40 years raises the possibility that nicotine intake continues to increase decades after a person starts to smoke. Greater nicotine intake in more deprived smokers could explain why they find it harder to stop smoking. (Cancer Epidemiol Biomarkers Prev 2008;17(12):3331–6)
Exposure to a Tobacco-Specific Lung Carcinogen in Adolescent versus Adult Smokers
Authors: Hertsgaard Louise A. , Hanson Karen , Hecht Stephen S. , Lindgren Bruce R. , Luo Xianghua , Carmella Steven G. , Riley William T. , Zylla Emily B. , Murphy Sharon E. , Hatsukami Dorothy K. 
Published: December 2008

Abstract
Background: Previous studies with adult smokers have shown an association between number of cigarettes smoked per day (CPD) and levels of biomarkers of exposure to the tobacco-specific lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). This study compared carcinogen and nicotine exposure in adolescent and adult smokers across categories of CPD.
Method: Baseline smoking history and biomarker data were merged from six studies to make two samples: one of adolescent smokers and one of adult smokers. Metabolites of NNK, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), and its glucuronides (NNAL-Gluc) and total cotinine were quantified in urine.
Results: CPD was stratified into categories of 5 to 10, 11 to 15, and 16 to 20 CPD. Adolescents tended to have lower mean levels of NNAL plus NNAL-Glucs (total NNAL) compared with adults, although differences were not significant overall. Adolescent mean levels of NNAL/CPD were significantly lower than adult levels only in the 11 to 15 CPD category (P = 0.045). However, a significant positive relationship was observed for total NNAL/CPD by age. No significant differences between adolescents and adults were found in mean levels of total cotinine or cotinine/CPD. A subsample of urines from adolescents and adults were analyzed for NNAL-Glucs and NNAL. Adolescents and adults did not significantly differ in the ratio of NNAL-Glucs to NNAL.
Conclusions: Adolescent uptake of NNK and nicotine tends to be lower although not statistically different from adults. The lack of significant differences may be due to the wide variation in exposure in adolescents. Some adolescent smokers are exposed to lung carcinogens at levels similar to those of adults. (Cancer Epidemiol Biomarkers Prev 2008;17(12):3337–43)
Reproducibility and Correlations of Multiplex Cytokine Levels in Asymptomatic Persons
Authors: Wong Hui-Lee , Pfeiffer Ruth M. , Fears Thomas R. , Vermeulen Roel , Ji Shaoquan , Rabkin Charles S. 
Published: December 2008

AbstractRationale: Cytokines are humoral regulatory molecules that act together in immunologic pathways underlying pathogenesis. Grossly elevated blood levels characterize certain diseases; variations within physiologic ranges could also have significance. We therefore evaluated the performance characteristics of a multiplex cytokine immunoassay.Methods: We used a fluorescent bead-based (Luminex) immunoassay kit to simultaneously measure interleukin (IL) 1β, IL2, IL4, IL5, IL6, IL7, IL8, IL10, IL12p70, IL13, IFNγ, granulocyte colony-stimulating factor, and tumor necrosis factor-α. We tested identical aliquots of serum from 38 asymptomatic individuals on three different days and matched sets of serum, heparinized plasma, and acid citrate dextrose plasma from an additional 38 healthy donors expected to have low cytokine concentrations. We applied multiple imputation to calculate unbiased reproducibility estimates for measurements below the limits of detection. Correlations among the cytokines were assessed by Spearman rank order coefficients and principal components analyses.Results: Of the 13 cytokines, 3 were undetectable (IL1β, IL2, IL5) in more than half of the serum samples. Coefficients of variation for replicate serum measurements ranged from 18% to 44%, with intraclass correlation coefficients ranging from 55% to 98%. Only IL4, IL6, and IL8 had statistically significant correlations (Spearman ρ, 0.42-0.94) between serum and acid citrate dextrose or heparin plasma levels.Conclusions: Interindividual differences outweigh substantial laboratory variation for these assays, yielding high intraclass correlation coefficients despite unimpressive coefficients of variation. Plasma measurements generally are not reflective of serum levels and hence are not interchangeable. With their small volume, low cost per test, and multiplex capacity, Luminex-based cytokine assays have potential utility for epidemiologic studies. (Cancer Epidemiol Biomarkers Prev 2008;17(12):3450–6)
Alcohol Consumption and Mutations or Promoter Hypermethylation of thevon Hippel–LindauGene in Renal Cell Carcinoma
Authors: Schouten Leo J. , van Dijk Boukje A.C. , Oosterwijk Egbert , van Engeland Manon , Hulsbergen–van de Kaa Christina A. , Kiemeney Lambertus A.L.M. , Goldbohm Royle Alexandra , Kester Arnold , de Vogel Stefan , Schalken Jack A. , van den Brandt Piet A. 
Published: December 2008

AbstractAlcohol consumption has been associated with a decreased risk for renal cell cancer in several studies. We investigated whether alcohol is associated with (epi)genetic changes of the von Hippel–Lindau (VHL) gene in renal cell cancer. The Netherlands Cohort Study (NLCS) on Diet and Cancer started in 1986 (n = 120,852) and uses the case-cohort method. After 11.3 years of follow-up, 314 renal cell cancer cases and 4,511 subcohort members were available for analysis. DNA was isolated from paraffin-embedded tumor tissue from 235 cases. VHL mutations were analyzed by sequencing, whereas VHL promoter methylation was analyzed using methylation-specific PCR. In multivariate analysis, hazard ratios of renal cell cancer for cohort members who consumed up to 5, 15, 30, and ≥30 g of alcohol per day were 0.72, 0.64, 0.81, and 0.69, respectively, compared with nondrinkers [95% confidence interval (95% CI) for the ≥30 category, 0.44-1.07; P for trend, 0.17]. Alcohol intake from beer, wine, and liquor was associated with decreased risks for renal cell cancer, although not statistically significant. Hazard ratios were not different for clear-cell renal cell cancer with and without VHL mutations, except for alcohol from beer, which was associated with an increased risk for clear-cell renal cell cancer without VHL mutations (hazard ratio for ≥5 g of alcohol from beer compared with nondrinkers, 2.74; 95% CI, 1.35-5.57). Alcohol was associated with a decreased risk for clear-cell renal cell cancer without VHL gene promoter methylation (hazard ratio for &gt;15 g compared with nondrinkers, 0.58; 95% CI, 0.34-0.99). In this study, a not statistically significant inverse association was observed between alcohol and renal cell cancer. There was no statistical significant heterogeneity by VHL mutation or methylation status. (Cancer Epidemiol Biomarkers Prev 2008;17(12):3543–50)
Anthocyanin/Polyphenolic–Rich Fruit Juice Reduces Oxidative Cell Damage in an Intervention Study with Patients on Hemodialysis
Authors: Spormann Thomas M. , Albert Franz W. , Rath Thomas , Dietrich Helmut , Will Frank , Stockis Jean-Pierre , Eisenbrand Gerhard , Janzowski Christine 
Published: December 2008

Abstract
Hemodialysis patients face an elevated risk of cancer, arteriosclerosis, and other diseases, ascribed in part to increased oxidative stress. Red fruit juice with high anthocyanin/polyphenol content had been shown to reduce oxidative damage in healthy probands. To test its preventive potential in hemodialysis patients, 21 subjects in a pilot intervention study consumed 200 mL/day of red fruit juice (3-week run-in; 4-week juice uptake; 3-week wash-out). Weekly blood sampling was done to monitor DNA damage (comet assay ± formamidopyrimidine-DNA glycosylase enzyme), glutathione, malondialdehyde, protein carbonyls, trolox equivalent antioxidant capacity, triglycerides, and DNA binding capacity of the transcription factor nuclear factor-κB. Results show a significant decrease of DNA oxidation damage (P &lt; 0.0001), protein and lipid peroxidation (P &lt; 0.0001 and P &lt; 0.001, respectively), and nuclear factor-κB binding activity (P &lt; 0.01), and an increase of glutathione level and status (both P &lt; 0.0001) during juice uptake. We attribute this reduction in oxidative (cell) damage in hemodialysis patients to the especially high anthocyanin/polyphenol content of the juice. This provides promising perspectives into the prevention of chronic diseases such as cancer and cardiovascular disease in population subgroups exposed to enhanced oxidative stress like hemodialysis patients. (Cancer Epidemiol Biomarkers Prev 2008;17(12):3372–80)
Mammographic Breast Density—Evidence for Genetic Correlations with Established Breast Cancer Risk Factors
Authors: Douglas Julie A. , Roy-Gagnon Marie-Hélène , Zhou Chuan , Mitchell Braxton D. , Shuldiner Alan R. , Chan Heang-Ping , Helvie Mark A. 
Published: December 2008

AbstractPrevious twin and family studies indicate that the familial aggregation of breast density is due (in part) to genetic factors. Whether these genetic influences are shared with other breast cancer risk factors, however, is not known. Using standard film-screen mammography, we screened 550 women, including 611 pairs of sisters, from the Old Order Amish population of Lancaster County, Pennsylvania. We digitized mammograms and quantified the dense and nondense areas of the breast using a computer-assisted method. Information about other breast cancer risk factors was collected via questionnaires and a physical exam. Using pedigree-based variance component methods, we estimated the genetic contributions to several breast cancer risk factors, including breast density, and evaluated the evidence for shared genetic influences between them. After adjusting for covariates, genetic effects accounted for &gt;33% of the total variance of each risk factor (P &lt; 0.001), including breast density, and the dense and nondense areas of the breast were significantly genetically correlated with parity [genetic correlation (ρG) = -0.47; P = 0.013] and age at menarche (ρG = -0.38; P = 0.008), respectively. The nondense area of the breast and, in turn, breast density, expressed as a ratio of dense area to total area, were also genetically correlated with most measures of adiposity but in opposite directions (ρG ≥ 0.75; P &lt; 10−7 for nondense area). We conclude that the genetic components that influence breast density are not independent of the genetic components that influence other breast cancer risk factors. This shared genetic architecture should be considered in future genetic studies of breast density. (Cancer Epidemiol Biomarkers Prev 2008;17(12):3509–16)