bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Simulation Study of Control Sampling Methods for Nested Case-Control Studies of Genetic and Molecular Biomarkers and Prostate Cancer Progression
Authors: Wang Ming-Hsi , Shugart Yin Yao , Cole Stephen R. , Platz Elizabeth A. 
Published: March 2009

Abstract
Background: Incidence density sampling is typically the least biased efficient method for control sampling in nested case-control studies. However, in studies of genetic variants and prostate cancer progression, some argue that controls should be sampled from men who did not progress by end of follow-up. Thus, we examined the validity of relative risk (RR) estimates of prostate cancer progression using three methods for control sampling from cohorts of men with prostate cancer generated by Monte Carlo simulation.
Methods: Data were simulated for nine scenarios for combinations of genotype frequency (10%, 30%, and 50%) and association (RR, 1.0, 1.5, and 2.0) using prostate progression rates from Johns Hopkins Hospital. RRs estimated from conditional logistic regression for the genetic association from case-control studies nested in the nine cohort scenarios using three control sampling methods, (a) incidence density sampling, (b) incidence density sampling without replacement of selected controls, and (c) “pure” control sampling (i.e., men who did not progress by end of long-term follow-up), were compared with the true RRs.
Results: Use of controls selected by incidence density sampling produced unbiased RR estimates of progression. In our setting, only a slight bias was produced by use of incidence density sampling without replacement. In contrast, use of controls selected by pure control sampling produced biased RR estimates, except when there was no association; extent of bias increased with increasing size of the association and duration of follow-up.
Conclusions: Nested case-control studies designed to estimate the association of genetic variants with risk of prostate cancer progression should use incidence density sampling to provide a valid RR estimate. (Cancer Epidemiol Biomarkers Prev 2009;18(3):706–11)
Candidate Gene Analysis Using Imputed Genotypes: Cell Cycle Single-Nucleotide Polymorphisms and Ovarian Cancer Risk
Authors: Goode Ellen L. , Fridley Brooke L. , Vierkant Robert A. , Cunningham Julie M. , Phelan Catherine M. , Anderson Stephanie , Rider David N. , White Kristin L. , Pankratz V. Shane , Song Honglin , Hogdall Estrid , Kjaer Susanne K. , Whittemore Alice S. , DiCioccio Richard , Ramus Susan J. , Gayther Simon A. , Schildkraut Joellen M. , Pharaoh Paul P.D. , Sellers Thomas A. 
Published: March 2009

Abstract
Polymorphisms in genes critical to cell cycle control are outstanding candidates for association with ovarian cancer risk; numerous genes have been interrogated by multiple research groups using differing tagging single-nucleotide polymorphism (SNP) sets. To maximize information gleaned from existing genotype data, we conducted a combined analysis of five independent studies of invasive epithelial ovarian cancer. Up to 2,120 cases and 3,382 controls were genotyped in the course of two collaborations at a variety of SNPs in 11 cell cycle genes (CDKN2C, CDKN1A, CCND3, CCND1, CCND2, CDKN1B, CDK2, CDK4, RB1, CDKN2D, and CCNE1) and one gene region (CDKN2A-CDKN2B). Because of the semi-overlapping nature of the 123 assayed tagging SNPs, we performed multiple imputation based on fastPHASE using data from White non-Hispanic study participants and participants in the international HapMap Consortium and National Institute of Environmental Health Sciences SNPs Program. Logistic regression assuming a log-additive model was done on combined and imputed data. We observed strengthened signals in imputation-based analyses at several SNPs, particularly CDKN2A-CDKN2B rs3731239; CCND1 rs602652, rs3212879, rs649392, and rs3212891; CDK2 rs2069391, rs2069414, and rs17528736; and CCNE1 rs3218036. These results exemplify the utility of imputation in candidate gene studies and lend evidence to a role of cell cycle genes in ovarian cancer etiology, suggest a reduced set of SNPs to target in additional cases and controls. (Cancer Epidemiol Biomarkers Prev 2009;18(3):935–44)
Long-Term Dietary Acrylamide Intake and Risk of Epithelial Ovarian Cancer in a Prospective Cohort of Swedish Women
Authors: Larsson Susanna C. , Åkesson Agneta , Wolk Alicja 
Published: March 2009

Abstract
Background: Acrylamide, a probable human carcinogen, can be formed in carbohydrate-rich foods cooked at high temperatures. Whether dietary acrylamide intake is associated with the risk of cancer in humans is uncertain. We aimed to assess the relation between dietary acrylamide intake and the incidence of epithelial ovarian cancer.
Methods: The Swedish Mammography Cohort is a population-based prospective study of 61,057 Swedish women. Diet was assessed with a food-frequency questionnaire at baseline in 1987-1990 and again in 1997.
Results: During a mean follow-up of 17.5 years, we ascertained 368 incident cases of ovarian cancer. We observed no association between acrylamide intake and the risk of ovarian cancer. Compared with the lowest quartile of acrylamide intake (mean intake, 16.9 μg/day), the multivariable rate ratios for the highest quartile (mean intake, 32.5 μg/day) were 0.86 (95% confidence interval, 0.63-1.16) for total ovarian cancer and 1.05 (95% confidence interval, 0.68-1.63) for serous ovarian cancer (n = 182 cases).
Conclusions: The results from this prospective study provide no evidence that dietary acrylamide in amounts typically consumed by Swedish women is associated with the risk of ovarian cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(3):994–7)
CpG Island Tumor Suppressor Promoter Methylation in Non-BRCA-Associated Early Mammary Carcinogenesis
Authors: Vasilatos Shauna N. , Broadwater Gloria , Barry William T. , Baker Joseph C. , Lem Siya , Dietze Eric C. , Bean Gregory R. , Bryson Andrew D. , Pilie Patrick G. , Goldenberg Vanessa , Skaar David , Paisie Carolyn , Torres-Hernandez Alejandro , Grant Tracey L. , Wilke Lee G. , Ibarra-Drendall Catherine , Ostrander Julie H. , D'Amato Nicholas C. , Zalles Carola , Jirtle Randy , Weaver Valerie M. , Seewaldt Victoria L. 
Published: March 2009

Abstract
Background: Only 5% of all breast cancers are the result of BRCA1/2 mutations. Methylation silencing of tumor suppressor genes is well described in sporadic breast cancer; however, its role in familial breast cancer is not known.
Methods: CpG island promoter methylation was tested in the initial random periareolar fine-needle aspiration sample from 109 asymptomatic women at high risk for breast cancer. Promoter methylation targets included RARB (M3 and M4), ESR1, INK4a/ARF, BRCA1, PRA, PRB, RASSF1A, HIN-1, and CRBP1.
Results: Although the overall frequency of CpG island promoter methylation events increased with age (P &lt; 0.0001), no specific methylation event was associated with age. In contrast, CpG island methylation of RARB M4 (P = 0.051), INK4a/ARF (P = 0.042), HIN-1 (P = 0.044), and PRA (P = 0.032), as well as the overall frequency of methylation events (P = 0.004), was associated with abnormal Masood cytology. The association between promoter methylation and familial breast cancer was tested in 40 unaffected premenopausal women in our cohort who underwent BRCA1/2 mutation testing. Women with BRCA1/2 mutations had a low frequency of CpG island promoter methylation (15 of 15 women had ≤4 methylation events), whereas women without a mutation showed a high frequency of promoter methylation events (24 of 25 women had 5-8 methylation events; P &lt; 0.0001). Of women with a BRCA1/2 mutation, none showed methylation of HIN-1 and only 1 of 15 women showed CpG island methylation of RARB M4, INK4a/ARF, or PRB promoters.
Conclusions: This is the first evidence of CpG island methylation of tumor suppressor gene promoters in non-BRCA1/2 familial breast cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(3):901–14)
Reproductive Variables, Soy Intake, and Lung Cancer Risk among Nonsmoking Women in the Singapore Chinese Health Study
Authors: Seow Adeline , Koh Woon-Puay , Wang Renwei , Lee Hin-Peng , Yu Mimi C. 
Published: March 2009

Abstract
Lung cancer among nonsmokers has emerged as a distinct clinicopathologic entity for which the etiology is still poorly understood, but which accounts for a significant proportion of the lung cancers among women. Although estrogens have been shown to have mitogenic effects in lung cells and interact with growth factor pathways in tumorigenesis, epidemiologic evidence for a link between reproductive hormones and lung cancer is sparse and inconsistent. We examined the effect of parity, age at menarche/menopause, cycle length and use of exogenous hormones, and dietary soy and soy isoflavonoid intake on lung cancer risk in a prospective cohort of middle-aged and elderly Chinese women in Singapore among whom 91% were lifetime nonsmokers. Among 35,298 women (mean follow-up time, 9.6 years), 298 cases of incident lung cancer were recorded, of which 189 (63.4%) occurred in nonsmokers. Compared with nulliparous women, those with one to two, three to four, and more than five livebirths had relative risks of between 0.49 and 0.59 (P for trend &lt; 0.01) for all lung cancers, and between 0.32 and 0.42 (P for trend &lt; 0.001) for adenocarcinomas. This relationship was observed in both smokers and nonsmokers. Age at menarche and menopause did not seem to influence risk. Dietary soy isoflavonoid intake was associated with a statistically significant inverse trend among nonsmokers only (relative risks, 0.59 for highest versus lower quartile; P for trend, 0.021). These findings add support for the role of hormonal factors in the etiology of lung cancer among nonsmoking women, and are consistent with emerging experimental evidence in this regard. (Cancer Epidemiol Biomarkers Prev 2009;18(3):821–7)
DNA Promoter Methylation in Breast Tumors: No Association with Genetic Polymorphisms in MTHFR and MTR
Authors: Tao Meng Hua , Shields Peter G. , Nie Jing , Marian Catalin , Ambrosone Christine B. , McCann Susan E. , Platek Mary , Krishnan Shiva S. , Xie Bin , Edge Stephen B. , Winston Janet , Vito Dominica , Trevisan Maurizio , Freudenheim Jo L. 
Published: March 2009

Abstract
Aberrant promoter methylation is recognized as an important feature of breast carcinogenesis. We hypothesized that genetic variation of genes for methylenetetrahydrofolate reductase (MTHFR) and methionine synthase (MTR), two critical enzymes in the one-carbon metabolism, may alter DNA methylation levels and thus influence DNA methylation in breast cancer. We evaluated case-control association of MTHFR C677T, A1298C, and MTR A2756G polymorphisms for cases strata-defined by promoter methylation status for each of three genes, E-cadherin, p16, and RAR-β2 in breast cancer; in addition, we evaluated case-case comparisons of the likelihood of promoter methylation in relation to genotypes using a population-based case-control study conducted in Western New York State. Methylation was evaluated with real-time methylation-specific PCRs for 803 paraffin-embedded breast tumor tissues from women with primary, incident breast cancer. We applied unordered polytomous regression and unconditional logistic regression to derive adjusted odds ratios and 95% confidence intervals. We did not find any association of MTHFR and MTR polymorphisms with breast cancer risk stratified by methylation status nor between polymorphisms and likelihood of promoter methylation of any of the genes. There was no evidence of difference within strata defined by menopausal status, estrogen receptor status, folate intake, and lifetime alcohol consumption. Overall, we found no evidence that these common polymorphisms of the MTHFR and MTR genes are associated with promoter methylation of E-cadherin, p16, and RAR-β2 genes in breast cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(3):998–1002)
Obesity and Weight Gain in Adulthood and Telomere Length
Authors: Kim Sangmi , Parks Christine G. , DeRoo Lisa A. , Chen Honglei , Taylor Jack A. , Cawthon Richard M. , Sandler Dale P. 
Published: March 2009

Abstract
Obesity and weight gain in adulthood are associated with an increased risk of several cancers. Telomeres play a critical role in maintaining genomic integrity and may be involved in carcinogenesis. Using data from 647 women ages 35 to 74 years in the United States and Puerto Rico (2003-2004), we examined the association between current and past anthropometric characteristics and telomere length in blood. In a multivariate linear regression model, higher current body mass index (BMI) and hip circumference were inversely associated with telomere length. Higher BMI in the 30s was associated with shorter telomere length among women ages ≥40 years (Ptrend &lt; 0.01). Weight gain since the age 30s (Ptrend = 0.07) and weight cycling (Ptrend = 0.04) were also inversely associated with telomere length. When current BMI and BMI at ages 30 to 39 years were considered together, the most marked decrease in telomere length was found for women who had overweight or obese BMI at both time points (mean telomere repeat copy number to single-copy gene copy number ratio = 1.26; 95% confidence interval, 1.21-1.30) compared with women who had normal BMI at both times (mean telomere repeat copy number to single-copy gene copy number ratio = 1.33; 95% confidence interval, 1.30-1.36). These findings support the hypothesis that obesity may accelerate aging, and highlight the importance of maintaining a desirable weight in adulthood. (Cancer Epidemiol Biomarkers Prev 2009;18(3):816–20)
Involuntary Tobacco Smoke Exposure and Urinary Levels of Polycyclic Aromatic Hydrocarbons in the United States, 1999 to 2002
Authors: Suwan-ampai Plernpit , Navas-Acien Ana , Strickland Paul T. , Agnew Jacqueline 
Published: March 2009

Abstract
Evidence supports active smoking as a major source of exposure to polycyclic aromatic hydrocarbons (PAH), compounds that are mutagenic and carcinogenic in humans. The influence of involuntary exposure to tobacco smoke on PAH exposure levels among nonsmokers, however, is unknown. This study evaluated the association between both active and involuntary tobacco smoke and biomarkers of PAH exposure in the general U.S. population. A cross-sectional analysis of 5,060 participants ≥6 years of age was done using data from the 1999-2002 National Health and Nutrition Examination Survey (NHANES). PAH exposure was measured by urinary concentrations of 23 monohydroxylated metabolites of nine PAH compounds. Tobacco smoke exposure was defined as no exposure, involuntary exposure, and active exposure by combining serum cotinine levels, smoking status, and presence of household smokers. PAH metabolite levels ranged from 33.9 ng/L for 9-hydroxyphenanthrene to 2,465.4 ng/L for 2-hydroxynaphthalene. After adjustment for age, sex, race/ethnicity, education, household income, and broiled/grilled food consumption, participants involuntarily and actively exposed to tobacco smoke had urinary metabolite concentrations that were increased by a factor of 1.1 to 1.4 and 1.5 to 6.9, respectively, compared with unexposed participants. Associations for involuntary smoking were stronger and statistically significant for 1-hydroxypyrene, 2-hydroxyfluorene, 3-hydroxyfluorene, 9-hydroxyfluorene, 1-hydroxyphenanthrene, 2-hydroxyphenanthrene, and 3-hydroxyphenanthrene compared with other metabolites. Involuntary exposure to tobacco smoke was associated with elevated urinary concentrations of most PAH metabolites in a representative sample of the U.S. population. Policy and educational efforts must continue to minimize PAH exposure through active and involuntary tobacco smoke exposure. (Cancer Epidemiol Biomarkers Prev 2009;18(3):884–93)
Etiologic Heterogeneity for Cervical Carcinoma by Histopathologic Type, Using Comparative Age-Period-Cohort Models
Authors: Reimers Laura L. , Anderson William F. , Rosenberg Philip S. , Henson Donald E. , Castle Philip E. 
Published: March 2009

Abstract
Background: Cervical carcinomas comprise two main histopathologic types, squamous cell carcinomas and adenocarcinomas. Human papillomavirus (HPV) infections are causative for both types but the respective tumors may have different carcinogenic pathways.
Methods: To assess potential etiologic heterogeneity of cervical cancer by histopathologic type, we examined invasive squamous cell carcinomas and adenocarcinoma cervical cancer incidence rates in the National Cancer Institute's Surveillance, Epidemiology, and End Results database. We complemented standard descriptive epidemiology with comparative age-period-cohort (APC) models fitted to each histopathologic type.
Results: Squamous cell tumors (n = 25,219) were nearly 5-fold more common than adenocarcinomas (n = 5,451). Age-adjusted incidence trends decreased for squamous cell carcinomas but increased for adenocarcinomas. Cross-sectional age-specific incidence rates increased more rapidly for squamous cell carcinomas than adenocarcinomas in adolescents and young adults then leveled off for both types. APC models confirmed that secular trends and age-specific rates differed for the two types (P = 0 for the null hypothesis of no difference). For squamous cell carcinoma, the APC “fitted” age-at-onset rate curve peaked before age 40 years then declined; for adenocarcinoma, the fitted curve increased rapidly until age 40 years then rose more slowly.
Conclusions: Despite the necessary role of HPV infection in both squamous cell carcinomas and adenocarcinomas of the cervix, secular trends and age-related natural histories differed for the two tumor types, consistent with etiologic heterogeneity. Future analytic and clinical studies should consider the interaction (effect modification) of HPV infection and other cervical carcinoma risk factors by histopathologic type, time, and age. (Cancer Epidemiol Biomarkers Prev 2009;18(3):792–800)
Total and Unopposed Estrogen Exposure across Stages of the Transition to Menopause
Authors: O'Connor Kathleen A. , Ferrell Rebecca J. , Brindle Eleanor , Shofer Jane , Holman Darryl J. , Miller Rebecca C. , Schechter Deborah E. , Singer Burton , Weinstein Maxine 
Published: March 2009

AbstractDetailed characterization of estrogen dynamics during the transition to menopause is an important step toward understanding its potential implications for reproductive cancers developing in the transition years. We conducted a 5-year prospective study of endogenous levels of total and unopposed estrogen. Participants (n = 108; ages 25-58 years) collected daily urine specimens for 6 months in each of 5 consecutive years. Specimens were assayed for estrone-3-glucuronide (E1G) and pregnanediol-3-glucuronide. Linear mixed-effects models were used to estimate exposure to total and unopposed estrogen by age and reproductive stage. Reproductive stage was estimated using menstrual cycle length variance. E1G mean area under the curve and mean E1G 5th and 95th percentiles represented total estrogen exposure. An algorithm identifying days of above-baseline E1G that coincided with the days of baseline pregnanediol-3-glucuronide was used to identify days of unopposed estrogen. Mean E1G area under the curve increased with age in the pretransition and early transition and decreased in the late transition. Ninety-fifth percentile E1G levels did not decline until after menopause, whereas 5th percentile levels declined from the early transition to the postmenopause. The number of days of unopposed estrogen was significantly higher during the transition compared with the pretransition. Given the length of time women spend in the transition, they are exposed to more total and unopposed estrogen than has been previously appreciated. Coupled with epidemiologic evidence on lifetime exposure to estrogen, these results suggest that variation in the amount of time spent in the transition may be an important risk factor for reproductive cancers. (Cancer Epidemiol Biomarkers Prev 2009;18(3):828–36)
The mediating effect of job satisfaction and organizational commitment on self-reported performance: more robust evidence of the PSM—performance relationship
Authors: Vandenabeele Wouter 
Published: March 2009

Public service motivation (PSM) has been linked to various outcome variables, but as more and more public administration research is devoted to improving performance, the possible link between PSM and performance is increasingly of interest. The current study contributes to this literature by investigating whether this relationship is present in a dataset of Belgian civil servants. The results corroborate the general thesis and demonstrate a mediation effect (to some extent) of job satisfaction and organizational commitment on this relationship. By doing so, the present study partly unveils the mechanisms upon which the PSM—performance relationship is based. Points for practitioners The findings of this study should urge public managers and decision-makers to value the effect of PSM in a public sector environment. First, as individual PSM apparently correlates with performance, this might provide some ideas about how to manage human resources in an effectiveness and efficiency driven public sector. Considering PSM in recruitment, retention and training may engender better individual performance. Next to this, the mediating role of job satisfaction and organizational commitment should enable public managers to find more openings to harness PSM effectively. After all, it embeds PSM better into vested theory and practices, with which practitioners may be more familiar.
How to fully exploit the results of e-government user surveys: the case of Slovenia
Authors: Kunstelj Mateja , Jukić Tina , Vintar Mirko 
Published: March 2009

The article presents users' views on the development of e-government, addressing two interrelated questions that have not been sufficiently answered thus far: (1) How to increase the current low level of e-government use, and (2) How to advance the current practice of analyzing data from e-government satisfaction surveys in order to arrive at guidelines for decision-makers when shaping future actions of e-government development. For this purpose, a cause-and-effect model was developed and operationalized by a set of indicators observed by a citizen satisfaction survey carried out in Slovenia between 2005 and 2006. The model was then estimated using the PLS (Partial Least Squares) regression method. Finally, an improvement-priority matrix was applied to prioritize significant factors. The proposed manner of analyzing data from user surveys offers a universal tool for analyzing drivers and consequences of user satisfaction and the use of e-government, and prioritizing them in order to assist decision-makers in preparing future strategies, action plans, or guidelines for further developments. Points for practitioners 1. Methodological implications: • guidelines on how to conduct e-government user satisfaction surveys; • guidelines on how to analyze user survey data in order to formulate guidelines for future development of e-government. 2. Empirical implications: •results of e-government user satisfaction survey in Slovenia and other countries; • guidelines for future development of e-government services in Slovenia and beyond.