bluuebunny/crossref_metadata_2025_split huggingface dataset:
Serum Organochlorine Pesticide Residues and Risk of Testicular Germ Cell Carcinoma: A Population-Based Case-Control Study
Authors: Biggs Mary L. , Davis Mark D. , Eaton David L. , Weiss Noel S. , Barr Dana B. , Doody David R. , Fish Sherianne , Needham Larry L. , Chen Chu , Schwartz Stephen M. 
Published: August 2008

Abstract
Testicular germ cell carcinoma (TGCC) is the most common malignancy among men ages 20 to 34 years. Although the pathogenesis of TGCC is poorly understood, suboptimal androgen levels or impaired androgen signaling may play a role. Some persistent organochlorine pesticides commonly found in human tissue possess antiandrogenic properties. We examined whether the risk of TGCC is associated with serum levels of 11 organochlorine pesticides, including p,p′-DDE, and whether the p,p′-DDE-TGCC association is modified by CAG or GGN repeat polymorphisms in the androgen receptor gene. We conducted a population-based case-control study among 18- to 44-year-old male residents of three Washington State counties. Cases (n = 246) were diagnosed during 1999 to 2003 with a first, primary TGCC. Controls (n = 630) were men of similar age with no history of TGCC from the same population identified through random-digit telephone dialing. Questionnaires elicited information on demographic, medical, and lifestyle factors. A blood specimen provided serum for gas chromatography-high-resolution mass spectrometry analysis of organochlorine pesticide residues and DNA for genotyping. We observed no clear patterns between TGCC risk and concentrations of any of the organochlorines measured, nor did we observe that the risk associated with p,p′-DDE was modified by androgen receptor CAG (&lt;23 versus ≥23 repeats) or GGN (&lt;17 versus ≥17 repeats) genotype. This study does not provide support for the hypothesis that adult exposure to organochlorine pesticides is associated with risk of TGCC. Due to uncertainty regarding how well organochlorine levels measured in adulthood reflect exposures during early life, further research is needed using exposure measurements collected in utero or during infancy. (Cancer Epidemiol Biomarkers Prev 2008;17(8):2012–8)
Red Meat Consumption during Adolescence among Premenopausal Women and Risk of Breast Cancer
Authors: Linos Eleni , Willett Walter C. , Cho Eunyoung , Colditz Graham , Frazier Lindsay A. 
Published: August 2008

Abstract
Background: Adolescence may be a period of increased susceptibility to breast cancer due to regular division of undifferentiated cells that occurs between puberty and first birth. Red meat consumption during early adult life has been associated with breast cancer, but intake during adolescence has not been examined prospectively. We aimed to assess the relationship between red meat intake during adolescence and premenopausal breast cancer.
Methods: We examined the incidence of invasive premenopausal breast cancer prospectively within the Nurses' Health Study II. A total of 39,268 premenopausal women who completed a validated 124-item food frequency questionnaire on their diet during high school, were followed for 7 years, from 1998 to 2005. Cox proportional hazards regression was used to estimate relative risks (RR) and 95% confidence intervals (95% CI).
Results: 455 cases of invasive premenopausal breast cancer were diagnosed between 1998 and 2005. Compared with women in the lowest quintile of red meat intake during high school, the multivariate-adjusted RR for the highest quintile of intake was 1.34 (95% CI, 0.94-1.89; Ptrend = 0.05). A significant linear association was observed with every additional 100 g of red meat consumed per day (RR, 1.20; 95% CI, 1.00-1.43; P = 0.05). This association was more pronounced in hormone receptor–positive tumors (RR, 1.36; 95% CI, 1.08-1.70; P = 0.008) and was not significant in hormone receptor–negative tumors (RR, 0.99; 95% CI, 0.61-1.61, P = 0.97).
Conclusion: Higher red meat intake in adolescence may increase the risk of premenopausal breast cancer. (Cancer Epidemiol Biomarkers Prev 2008;17(8):2146–51)
Multiplex Genotyping as a Biomarker for Susceptibility to Carcinogenic Exposure in the FLEHS Biomonitoring Study
Authors: Ketelslegers Hans B. , Gottschalk Ralph W.H. , Koppen Gudrun , Schoeters Greet , Baeyens Willy F. , van Larebeke Nicolas A. , van Delft Joost H.M. , Kleinjans Jos C.S. 
Published: August 2008

Abstract
Cancer has been suggested to result from interactions between genetic and environmental factors, and certain subgroups in the general population may be at increased risk because of their relatively higher susceptibility to environmental carcinogens. The current study, part of a large biomonitoring study conducted in Flanders from 2002 to 2006 (The Flanders Environment and Health Survey), aims to determine these susceptible subpopulations based on multiple genotypic differences between individuals.
A random selection of 429 adolescents and 361 adults was genotyped for 36 polymorphisms in 23 genes selected because of their known role in carcinogen metabolism, DNA repair, and oxidative stress. In both age groups, relationships between endogenous exposure to organochloride substances (polychlorinated biphenyl, hexachlorobenzene, dichlorodiphenyl dichloroethane), metals (cadmium, lead), and urinary metabolites (1-hydroxypyrene, trans-trans muconic acid) versus genotoxic effects (Comet assay and micronuclei in lymphocytes, and urinary 8-hydroxydeoxyguanosine) were investigated. In addition, in the study among adults, the relationship of these exposures with several tumor markers (prostate-specific antigen, carcinoembryonic antigen, and p53) was tested. The impact of the genotype on established exposure-effect relationships was evaluated. Eight exposure-effect relationships were found, including three novel associations, with an impact of various genotypes, predominantly affecting biotransformation and oxidative stress response.
This study shows that at least part of the interindividual differences in relationships between carcinogen exposure and genotoxic effect can be explained by genotypic differences, enabling the identification of more susceptible subgroups for environmental cancer risks. This may be of relevance for environmental health policy setting. (Cancer Epidemiol Biomarkers Prev 2008;17(8):1902–12)
Psychologic Predictors of Cancer Information Avoidance among Older Adults: The Role of Cancer Fear and Fatalism
Authors: Miles Anne , Voorwinden Sanne , Chapman Sarah , Wardle Jane 
Published: August 2008

Abstract
Little is known about the correlates of cancer information avoidance and whether people with negative feelings and beliefs about cancer are more likely to avoid cancer information, allowing such thoughts and feelings to persist unchallenged. Using the Extended Parallel Processing Model as a theoretical guide, we tested the hypothesis that cancer fear and fatalism would predict cancer information avoidance but that part of this effect would be mediated via cancer-specific threat and efficacy beliefs. A community sample of older adults, ages 50 to 70 years (n = 1,442), completed a postal questionnaire that included the Powe Fatalism Inventory and the Champion Cancer Fear scale along with other measures of cancer-specific beliefs and demographic variables. Higher levels of cancer fear were positively associated with higher levels of cancer information avoidance, and part of this relationship was mediated via perceived cancer severity. The relationship between cancer fatalism and cancer information avoidance was partly mediated by severity and response-efficacy beliefs. This research shows that people with negative views about cancer are more likely to avoid cancer information. This means people with higher levels of cancer fear and fatalism are less likely to learn about positive developments made in the field of cancer control, allowing such negative feelings and views to continue. Research needs to focus on how to get positive messages about improvements in cancer prevention and control through to people who are fearful of and fatalistic about the disease. (Cancer Epidemiol Biomarkers Prev 2008;17(8):1872–9)
Disparities in Cervical Cancer Screening between Asian American and Non-Hispanic White Women
Authors: Wang Judy H. , Sheppard Vanessa B. , Schwartz Marc D. , Liang Wenchi , Mandelblatt Jeanne S. 
Published: August 2008

Abstract
Background: Asian American women have higher cervical cancer mortality rates than non-Hispanic White women, yet have lower Pap screening rates than their White counterparts. This study examined whether ethnic differences in the use of Pap screening were associated with differences in cultural views, controlling for demographic and access factors.
Methods: Cross-sectional survey data from the Commonwealth 2001 Health Care Quality Survey were used. Non-Hispanic White (n = 2,146) and Asian American women (including Chinese, Vietnamese, Korean, Filipino, and Japanese; n = 259) were included in this study. Eastern cultural views were measured by beliefs in the role of self-care and luck. Access factors (having health insurance, regular providers, and communication with providers) and demographics of patients and providers were measured. The outcome was receipt of a Pap test in the past 2 years.
Results: Asian American women had a lower rate of obtaining a recent Pap test (70%) than non-Hispanic White women (81%; P = 0.001). More Asians believed in the role of luck and self-care and experienced access barriers than Whites (P &lt; 0.0001). Women with less Eastern cultural views are more likely to be recently screened than women with more (odds ratio, 1.08; 95% confidence interval, 1.00-1.16; P &lt; 0.05). All access factors and provider gender types predicted the outcome. Within the Asian subgroups, Vietnamese women had lower screening rates (55%) and greater Eastern cultural views than their Asian counterparts.
Conclusion: More research is needed to understand cultural and other barriers to Pap screening in high-risk Asian women, and attention should be paid to within-group differences. (Cancer Epidemiol Biomarkers Prev 2008;17(8):1968–73)
Reproducibility of Serum Pituitary Hormones in Women
Authors: Arslan Alan A. , Gu Yian , Zeleniuch-Jacquotte Anne , Koenig Karen L. , Liu Mengling , Velikokhatnaya Lyudmila , Shore Roy E. , Toniolo Paolo , Linkov Faina , Lokshin Anna E. 
Published: August 2008

Abstract
Endogenous pituitary hormones are commonly used in clinical and epidemiologic studies and some of them are thought to influence the risk of several diseases in women. In most studies, endogenous levels of pituitary hormones are usually assessed at a single point in time, assuming that this single measurement represents the long-term biomarker status of the individual. Such an assumption is rarely tested and may not always be valid. This study examined the reproducibility of the following pituitary hormones: adrenocorticotropic hormone (ACTH), growth hormone, follicle-stimulating hormone (FSH), luteinizing hormone (LH), thyroid-stimulating hormone (TSH), and prolactin, measured using the Luminex xMap method in sera of healthy premenopausal and postmenopausal women. The study included 30 premenopausal women with three yearly samples and 35 postmenopausal women with two repeated yearly samples randomly selected from an existing prospective cohort. Analysis of intraclass correlation coefficients suggested higher reproducibility in postmenopausal women compared with premenopausal women for the following hormones: FSH (0.72 and 0.37, respectively), LH (0.83 and 0.44, respectively), and growth hormone (0.60 and 0.35, respectively). The intraclass correlation coefficients were relatively high and similar between postmenopausal and premenopausal women for ACTH (0.95 and 0.94, respectively), TSH (0.85 and 0.85, respectively), and prolactin (0.72 and 0.69, respectively). This study found that serum concentrations of FSH, LH, and growth hormone are stable in postmenopausal women and that ACTH, TSH, and prolactin are stable in both premenopausal and postmenopausal women, suggesting that a single measurement may reliably categorize average levels over at least a 2-year period. (Cancer Epidemiol Biomarkers Prev 2008;17(8):1880–3)
Genetic Polymorphisms in the Paraoxonase 1 Gene and Risk of Ovarian Epithelial Carcinoma
Authors: Lurie Galina , Wilkens Lynne R. , Thompson Pamela J. , McDuffie Katharine E. , Carney Michael E. , Terada Keith Y. , Goodman Marc T. 
Published: August 2008

Abstract
Oxidative stress during successive ovulations increases the opportunity for DNA damage to ovarian epithelial cells and the potential for malignant transformation. Paraoxonase 1 (PON1) is an endogenous free radical scavenger that reduces oxidative stress. The association of two common functional single nucleotide polymorphisms (SNP), rs854560 T&gt;A and rs662 A&gt;G, with the risk of epithelial ovarian cancer was examined in a population-based case-control study in Hawaii. A personal interview and blood specimens were collected from 274 women with histologically confirmed, primary ovarian cancer and 452 controls frequency matched on age and ethnicity. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated by unconditional logistic regression. Both PON1 SNPs were significantly associated with ovarian cancer risk. The ORs were 0.53 (95% CI, 0.35-0.79; P for allele-dose effect = 0.01) for women carrying the rs854560 T allele compared with women with the AA genotype and 0.65 (95% CI, 0.44-0.95; P for allele-dose effect = 0.03) for women carrying the rs662 A allele compared with women with the GG genotype. The association of the rs854560 T genotype with risk was stronger among smokers (OR, 0.33; 95% CI, 0.17-0.64; P for allele-dose effect = 0.0007) than among nonsmokers (OR, 0.68; 95% CI, 0.40-1.18; P for allele-dose effect = 0.53). The decreased risk associated with the rs854560 T allele was also stronger among obese women (OR, 0.19; 95% CI, 0.06-0.55; P for allele-dose effect = 0.007) than among nonobese women (OR, 0.62; 95% CI, 0.40-0.98; P for allele-dose effect = 0.16). Our study provides evidence for an association of two PON1 SNPs with the risk of epithelial ovarian cancer. Possible effect modification of these associations by tobacco smoking and obesity needs confirmation in other studies. (Cancer Epidemiol Biomarkers Prev 2008;17(8):2070–7)
The Human Papillomavirus Infection in Men Study: Human Papillomavirus Prevalence and Type Distribution among Men Residing in Brazil, Mexico, and the United States
Authors: Giuliano Anna R. , Lazcano-Ponce Eduardo , Villa Luisa L. , Flores Roberto , Salmeron Jorge , Lee Ji-Hyun , Papenfuss Mary R. , Abrahamsen Martha , Jolles Emily , Nielson Carrie M. , Baggio Maria Luisa , Silva Roberto , Quiterio Manuel 
Published: August 2008

Abstract
Male sexual behavior influences the rates of cervical dysplasia and invasive cervical cancer, as well as male human papillomavirus (HPV) infection and disease. Unfortunately, little is known regarding male HPV type distribution by age and across countries. In samples combined from the coronal sulcus, glans penis, shaft, and scrotum of 1,160 men from Brazil, Mexico, and the United States, overall HPV prevalence was 65.2%, with 12.0% oncogenic types only, 20.7% nononcogenic types only, 17.8% both oncogenic and nononcogenic, and 14.7% unclassified infections. Multiple HPV types were detected in 25.7% of study participants. HPV prevalence was higher in Brazil (72.3%) than in the United States (61.3%) and Mexico (61.9%). HPV16 (6.5%), HPV51 (5.3%), and HPV59 (5.3%) were the most commonly detected oncogenic infections, and HPV84 (7.7%), HPV62 (7.3%), and HPV6 (6.6%) were the most commonly detected nononcogenic infections. Overall HPV prevalence was not associated with age. However, significant associations with age were observed when specific categories of HPV, nononcogenic, and unclassified HPV infections were considered. Studies of HPV type distribution among a broad age range of men from multiple countries is needed to fill the information gap internationally with respect to our knowledge of HPV infection in men. (Cancer Epidemiol Biomarkers Prev 2008;17(8):2036–43)
Alcohol and Breast Cancer Risk Defined by Estrogen and Progesterone Receptor Status: A Case-Control Study
Authors: Deandrea Silvia , Talamini Renato , Foschi Roberto , Montella Maurizio , Dal Maso Luigino , Falcini Fabio , La Vecchia Carlo , Franceschi Silvia , Negri Eva 
Published: August 2008

Abstract
Background: Alcohol consumption increases breast cancer risk. Some studies suggested that this association is stronger or limited to tumors expressing estrogen receptors (ER).
Methods: We investigated the role of alcohol according to ER and progesterone receptor (PR) status in a case-control study on breast cancer conducted from 1991 to 1994 in three Italian areas. Cases were 989 women with incident, histologically confirmed breast cancer. Controls were 1,350 women admitted to hospitals in the same catchment areas for acute nonneoplastic diseases. A validated food-frequency questionnaire was used to collect information on dietary habits and lifetime consumption of various alcoholic beverages. Multiple logistic regression models were used to estimate odds ratios and 95% confidence interval (95% CI).
Results: Alcohol drinking was associated with ER+ tumors (odds ratio, 2.16; 95% CI, 1.68-2.76 for an intake of ≥13.8 g/d as compared with nondrinkers). The odds ratio was 1.13 (95% CI, 1.07-1.20) for a 10-g increase in daily intake. For ER- tumors, the relation with alcohol consumption was not significant (odds ratio, 1.36; 95% CI, 0.93-2.01). When breast cancers were further classified according to PR, the findings for ER+PR+ cancers were similar to those for all ER+ ones, with an odds ratio of 2.34 (95% CI, 1.81-3.04) for an intake of ≥13.8 g/d. No significant association emerged for ER-PR- tumors (odds ratio, 1.25; 95% CI, 0.81-1.94).
Conclusion: This study supports the hypothesis that alcohol is more strongly related to ER+ than to ER- breast tumors. (Cancer Epidemiol Biomarkers Prev 2008;17(8):2025–8)
Dietary Soy and Isoflavone Intake and Risk of Colorectal Cancer in the Japan Public Health Center–Based Prospective Study
Authors: Akhter Munira , Inoue Manami , Kurahashi Norie , Iwasaki Motoki , Sasazuki Shizuka , Tsugane Shoichiro ,   for the Japan Public Health Center-Based Prospective Study Group
Published: August 2008

Abstract
Several experimental studies have reported that the anticarcinogenic properties of dietary soy play an important role in preventing colorectal cancer. However, few epidemiologic studies have examined this association in general populations and their findings have been inconsistent. We investigated the association between dietary soy and isoflavone intake and incidence of colorectal cancer in a prospective cohort study of 83,063 Japanese men and women, ages 45 to 74 years. Dietary soy and isoflavone intake was measured through a validated food frequency questionnaire in 1995 and 1998. Throughout 2004, a total of 886 cases of colorectal cancer were newly identified (291 proximal colon, 286 distal colon, and 277 rectum). The hazard ratios and 95% confidence intervals (95% CIs) were estimated by fitting a Cox proportional hazards model. The intake of isoflavones, miso soup, and soy food was not associated with colorectal cancer in either men or women. By colorectal cancer subsite, the risk of proximal colon cancer in men decreased with increasing consumption of isoflavones, miso soup, and soy food. Compared with men in the lowest quartiles of isoflavones, miso soup, and soy food intake, the hazard ratios in the highest quartiles were 0.55 (95% CI, 0.33-0.92), 0.72 (95% CI, 0.43-1.21), and 0.51 (95% CI, 0.30-0.87), respectively. The results showed no association for distal colon and rectal cancer in men or for subsites of colorectal cancer in women. These findings suggest that the intake of isoflavones, miso soup, and soy food has no substantial effect on the risk of colorectal cancer in Japanese men and women. (Cancer Epidemiol Biomarkers Prev 2008;17(8):2128–35)
Body Size and Risk of Luminal, HER2-Overexpressing, and Triple-Negative Breast Cancer in Postmenopausal Women
Authors: Phipps Amanda I. , Malone Kathleen E. , Porter Peggy L. , Daling Janet R. , Li Christopher I. 
Published: August 2008

AbstractAlthough the clinical relevance of molecular subtypes of breast cancer has been documented, little is known about risk factors for different tumor subtypes, especially the HER2-overexpressing and the triple-negative subtypes that have poor prognoses. Obesity may be differentially related to the risk of different subtypes given the various potential mechanisms underlying its association with breast cancer. We pooled two population-based case-control studies of postmenopausal breast cancer for an analysis, including 1,447 controls and 1,008 luminal (hormone receptor positive), 39 HER2-overexpressing (hormone receptor negative, HER2 positive), and 77 triple-negative (hormone receptor and HER2 negative) cases. Associations between anthropometric factors and the risk of different breast cancer subtypes were evaluated using polytomous logistic regression. Among women not currently using menopausal hormone therapy, body mass index (BMI) and weight were associated with the risk of luminal tumors [odds ratio (OR) comparing highest versus lowest quartiles, 1.7; 95% confidence interval (95% CI), 1.2-2.4 and OR, 1.7; 95% CI, 1.2-2.4, respectively] and suggestively associated with risk of triple-negative tumors (OR, 2.7; 95% CI, 1.0-7.5 and OR, 5.1; 95% CI, 1.1-23.0, respectively). Neither BMI nor weight was associated with the risk of any tumor subtype among hormone therapy users. The positive relationship between BMI and luminal tumors among postmenopausal women not using hormone therapy is well characterized in the literature. Although our sample size was limited, body size may also be related to the risk of postmenopausal triple-negative breast cancer among nonusers of hormone therapy. Given the expanding obesity epidemic, the widespread cessation of hormone therapy use, and the poor prognosis of triple-negative tumors, this novel finding merits confirmation. (Cancer Epidemiol Biomarkers Prev 2008;17(8):2078–86)
Nested Case-Control Study of the Association of Circulating Levels of Serum Insulin-like Growth Factor I and Insulin-like Growth Factor Binding Protein 3 with Breast Cancer in Young Women in Norway
Authors: Vatten Lars J. , Holly Jeff M. , Gunnell David , Tretli Steinar 
Published: August 2008

AbstractBackground: High circulating levels of insulin-like growth factor (IGF-I) may elevate the risk of breast cancer in premenopausal women, possibly by increasing cell proliferation and reducing apoptosis.Methods: We conducted a nested case-control study among 35,105 Norwegian women who participated in a health screening survey, ages 40 to 42 years, and who were subsequently followed for a mean period of 4.3 years. During this period, 325 women were diagnosed with breast cancer; 647 women without breast cancer, matched on age and time of blood sampling, were selected as controls. Serum concentrations of IGF-I and its main binding protein (IGFBP-3) were measured with radioimmunoassay, and logistic regression analysis was used to adjust for relevant covariates.Results: The mean age at blood collection was 41.1 years in both groups, and the mean age at diagnosis for the cases was 45.4 years (range, 40-51 years). The median IGF-I level did not differ between cases (205 ng/mL) and controls (202 ng/mL). When analyzed by categories of serum IGF-I, the relative risk for women in the highest versus the lowest quintile was 1.46 (95% confidence interval, 0.93-2.32; Ptrend = 0.15) after adjusting for serum IGFBP-3, age, and year of blood collection. The exclusion of cases that were diagnosed within 2 years after blood collection did not materially affect the results.Conclusion: We found only a modest positive association between serum IGF-I levels and risk of breast cancer in women younger than 50 years of age. (Cancer Epidemiol Biomarkers Prev 2008;17(8):2097–100)