bluuebunny/crossref_metadata_2025_split huggingface dataset:
Are We Overemphasizing Sun Avoidance in Protection from Melanoma?
Authors: Wartman David , Weinstock Martin 
Published: March 2008

Abstract
The public health effect of melanoma in the United States is undeniable as ∼60,000 diagnoses of invasive melanoma and 8,000 deaths from melanoma are expected in 2007. Due to the poor outcomes associated with treating advanced cases of melanoma, substantial public health resources have been devoted to prevention efforts. Of the various factors involved in the pathogenesis of melanoma, including genetic predisposition, immunosuppression, and UV radiation, decreasing UV exposure has attracted the most attention for decreasing the public health effect of melanoma. Although sun avoidance may be an important measure for reducing the public health effect of melanocytic and keratinocytic malignancies, educational and media campaigns to encourage sun avoidance have failed to achieve the desired behavior changes in young people, have had limited effect on elderly patients who have already experienced decades of damaging sun exposure, and most importantly have failed to decrease the incidence of melanoma. We believe the best method to reduce deaths from melanoma is to emphasize early detection and treatment of suspicious lesions through combined efforts of both patients and providers. (Cancer Epidemiol Biomarkers Prev 2008;17(3):469–70)
Cyclin E Overexpression in Epithelial Ovarian Cancer Characterizes an Etiologic Subgroup
Authors: Schildkraut Joellen M. , Moorman Patricia G. , Bland Amy E. , Halabi Susan , Calingaert Brian , Whitaker Regina , Lee Paula S. , Elkins-Williams Tyler , Bentley Rex C. , Marks Jeffrey R. , Berchuck Andrew 
Published: March 2008

Abstract
Background: The objective of this study was to determine whether cyclin E overexpression defines an etiologically distinct subgroup of ovarian cancer.
Methods: We analyzed data from 538 epithelial ovarian cancer cases and 629 controls enrolled in a population-based case-control study. Cyclin E protein overexpression was assessed using immunohistochemistry. Case-control and case-case comparisons were done to evaluate the relationship between cyclin E overexpression and epidemiologic risk factors. Logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (95% CI) while adjusting for potential confounders.
Results: Case-control comparisons showed ovarian cancers with and without cyclin E overexpression have different associations with several epidemiologic risk factors. A dose-response relationship was observed between lifetime ovulatory cycles (LOC) and ovarian cancer that overexpressed cyclin E [OR, 1.8; 95% CI, 1.1-3.0 for moderately high LOC (265-390 cycles) and OR, 2.7; 95% CI, 1.6-4.5 for high LOC (&gt;390 cycles) compared with low LOC (&lt;265 cycles)], but no relationship was seen with cancers that lacked overexpression. The most important components of the LOC variable contributing to the differences in the association with the cyclin E subgroups of ovarian cancer were months of oral contraceptive use and months pregnant.
Conclusions: Cyclin E overexpression is associated with a high number of LOC, largely influenced by oral contraceptive use and pregnancy. This suggests that cyclin E overexpression is a molecular signature characteristic of ovarian cancer cases that may arise via a pathway that involves ovulation-induced alterations. (Cancer Epidemiol Biomarkers Prev 2008;17(3):585–93)
Issues of Diagnostic Review in Brain Tumor Studies: From the Brain Tumor Epidemiology Consortium
Authors: Davis Faith G. , Malmer Beatrice S. , Aldape Ken , Barnholtz-Sloan Jill S. , Bondy Melissa L. , Brännström Thomas , Bruner Janet M. , Burger Peter C. , Collins V. Peter , Inskip Peter D. , Kruchko Carol , McCarthy Bridget J. , McLendon Roger E. , Sadetzki Siegal , Tihan Tarik , Wrensch Margaret R. , Buffler Patricia A. 
Published: March 2008

AbstractEpidemiologists routinely conduct centralized single pathology reviews to minimize interobserver diagnostic variability, but this practice does not facilitate the combination of studies across geographic regions and institutions where diagnostic practices differ. A meeting of neuropathologists and epidemiologists focused on brain tumor classification issues in the context of protocol needs for consortial studies (http://epi.grants.cancer.gov/btec/). It resulted in recommendations relevant to brain tumors and possibly other rare disease studies. Two categories of brain tumors have enough general agreement over time, across regions, and between individual pathologists that one can consider using existing diagnostic data without further review: glioblastomas and meningiomas (as long as uniform guidelines such as those provided by the WHO are used). Prospective studies of these tumors benefit from collection of pathology reports, at a minimum recording the pathology department and classification system used in the diagnosis. Other brain tumors, such as oligodendroglioma, are less distinct and require careful histopathologic review for consistent classification across study centers. Epidemiologic study protocols must consider the study specific aims, diagnostic changes that have taken place over time, and other issues unique to the type(s) of tumor being studied. As diagnostic changes are being made rapidly, there are no readily available answers on disease classification issues. It is essential that epidemiologists and neuropathologists collaborate to develop appropriate study designs and protocols for specific hypothesis and populations. (Cancer Epidemiol Biomarkers Prev 2008;17(3):484–9)
UGT1A1 Genetic Polymorphisms, Endogenous Estrogen Exposure, Soy Food Intake, and Endometrial Cancer Risk
Authors: Deming Sandra L. , Zheng Wei , Xu Wang-Hong , Cai Qiuyin , Ruan Zhixian , Xiang Yong-Bing , Shu Xiao-Ou 
Published: March 2008

Abstract
Estrogen exposures play a critical role in the development of endometrial cancer. Genetic variation in the estrogen metabolism UGT1A1 gene may modify the effect of estrogenic exposures on endometrial cancer risk. We tested this hypothesis in a population-based case-control study of 1,047 endometrial cancer cases and 1,035 controls who completed an in-person interview and were genotyped for the UGT1A1 polymorphisms rs2070959 (A/G), rs887829 (G/A), and rs8175347 (6/7 TA repeats). Estrogen exposure-related factors evaluated include menstrual characteristics, oral contraceptive use, body mass index, waist-hip ratio, and soy food intake. Conditional logistic regression was used to calculate odds ratios and 95% confidence intervals. The homozygote variant genotype (G/G) of the rs2070959 polymorphism was significantly associated with a reduced risk of endometrial cancer (odds ratio, 0.5; 95% confidence interval, 0.3-0.8). No significant associations between endometrial cancer risk and genotype were seen for the rs887829 and rs8175347 polymorphisms. Analysis of the joint effects of genotype and markers of estrogen exposure found the lowest risk of endometrial cancer among those with the homozygous variant genotype of the rs2070959 polymorphism and who were postmenopausal, had low body mass index, and had low soy food intake, although a test for multiplicative interaction was not significant. Taken together, these data suggest that the G/G genotype (rs2070959) in the UGT1A1 gene may decrease the risk of endometrial cancer and that this effect is most evident among women with low levels of endogenous estrogen exposure or with low soy food intake. (Cancer Epidemiol Biomarkers Prev 2008;17(3):563–70)
Reproductive Steroid Hormones and Recurrence-Free Survival in Women with a History of Breast Cancer
Authors: Rock Cheryl L. , Flatt Shirley W. , Laughlin Gail A. , Gold Ellen B. , Thomson Cynthia A. , Natarajan Loki , Jones Lovell A. , Caan Bette J. , Stefanick Marcia L. , Hajek Richard A. , Al-Delaimy Wael K. , Stanczyk Frank Z. , Pierce and John P. ,   for the Women's Healthy Eating and Living Study Group
Published: March 2008

Abstract
Epidemiologic studies fairly consistently show in postmenopausal women that reproductive steroid hormones contribute to primary breast cancer risk, and this association is strongly supported by experimental studies using laboratory animals and model systems. Evidence linking sex hormone concentrations with risk for recurrence in women diagnosed with breast cancer is limited; however, beneficial effects of antiestrogenic therapy on recurrence-free survival suggest that these hormones affect progression and risk for recurrence. This study examined whether baseline serum concentrations of estradiol, testosterone, and sex hormone binding globulin were associated with recurrence-free survival in a nested case-control cohort of women from a randomized diet trial (Women's Healthy Eating and Living Study) who were followed for &gt;7 years after diagnosis. In 153 case-control pairs of perimenopausal and postmenopausal women in this analysis, total estradiol [hazard ratio (HR), 1.41 per unit increase in log concentration; 95% confidence interval (95% CI), 1.01-1.97], bioavailable estradiol (HR, 1.26; 95% CI, 1.03-1.53), and free estradiol (HR, 1.31; 95% CI, 1.03-1.65) concentrations were significantly associated with risk for recurrence. Recurred women had an average total estradiol concentration that was double that of nonrecurred women (22.7 versus 10.8 pg/mL; P = 0.05). Testosterone and sex hormone binding globulin concentrations did not differ between cases and controls and were not associated with risk for recurrence. Although genetic and metabolic factors likely modulate the relationship between circulating sex hormones and risk, results from this study provide evidence that higher serum estrogen concentration contributes to risk for recurrence in women diagnosed with early stage breast cancer. (Cancer Epidemiol Biomarkers Prev 2008;17(3):614–20)
Risk of Testicular Germ Cell Tumors and Polymorphisms in the Insulin-Like Growth Factor Genes
Authors: Chia Victoria M. , Sakoda Lori C. , Graubard Barry I. , Rubertone Mark V. , Chanock Stephen J. , Erickson Ralph L. , McGlynn Katherine A. 
Published: March 2008

AbstractBecause taller men are at increased risk of developing testicular germ cell tumors (TGCT), it is conceivable that factors that influence adult height could be related to risk of TGCT. Because common genetic variation in genes of the insulin-like growth factor (IGF) pathway could influence somatic growth, 43 single nucleotide polymorphisms in four IGF genes (IGF-1, IGF-1R, IGF-2, and IGFALS) were genotyped in 577 case and 707 control participants from the U.S. Servicemen's Testicular Tumor Environmental and Endocrine Determinants Study to assess relationships with TGCT risk; additionally, associations between polymorphisms and adult height were examined. Relationships between polymorphisms and adult height were assessed using adjusted linear regression models, and associations between polymorphisms and TGCT risk were determined by adjusted logistic regression models estimating odds ratios. Although four IGF-1R polymorphisms (rs907806, rs3743258, rs229765, and rs9282714) were associated with height (Ptrend &lt; 0.05), there were no relationships with any other polymorphism. Overall, there were no associations among polymorphisms or haplotypes in the IGF genes and TGCT risk, with odds ratios ranging from 0.55 to 1.50. Similarly, there was no association among the polymorphisms and risk of specific TGCT histologies (seminoma and nonseminoma). There was a suggestion, however, that adult height may modify the relationship between an IGF-1 haplotype and TGCT risk. These results suggest that, in aggregate, genetic variation in IGF loci is not associated with TGCT risk. (Cancer Epidemiol Biomarkers Prev 2008;17(3):721–6)
Coffee, Tea, Colas, and Risk of Epithelial Ovarian Cancer
Authors: Song Yoon Ju , Kristal Alan R. , Wicklund Kristine G. , Cushing-Haugen Kara L. , Rossing Mary Anne 
Published: March 2008

Abstract
Associations of coffee, tea, and other caffeinated beverages with ovarian cancer risk remain uncertain. In a population-based study in Washington State, 781 women with epithelial ovarian cancer diagnosed in 2002 to 2005 and 1,263 controls completed self-administered questionnaires detailing consumption of caffeinated and noncaffeinated coffee, teas, and colas and in-person interviews regarding reproductive and hormonal exposures. We assessed risk associated with coffee, tea, and cola drinking and with total caffeine consumption using logistic regression to calculate odds ratios and 95% confidence intervals. Neither caffeinated nor decaffeinated coffees were associated with ovarian cancer risk; also, we observed no association of total caffeine with risk using a combined index that summed intake from coffee, tea, and carbonated soft drinks. Among teas, neither herbal/decaffeinated nor black teas were associated with risk; however, women who reported drinking ≥1 cup/d of green tea had a 54% reduction in risk (Ptrend = 0.01). Associations of green tea with risk were similar when invasive and borderline cases were considered separately and when Asian women were excluded from analysis. Green tea, which is commonly consumed in countries with low ovarian cancer incidence, should be further investigated for its cancer prevention properties. (Cancer Epidemiol Biomarkers Prev 2008;17(3):712–6)
DNA Methylation in Tumor and Matched Normal Tissues from Non-Small Cell Lung Cancer Patients
Authors: Feng Qinghua , Hawes Stephen E. , Stern Joshua E. , Wiens Linda , Lu Hiep , Dong Zhao Ming , Jordan C. Diana , Kiviat Nancy B. , Vesselle Hubert 
Published: March 2008

Abstract
We used MethyLight assays to analyze DNA methylation status of 27 genes on 49 paired cancerous and noncancerous tissue samples from non-small cell lung cancer (NSCLC) patients who underwent surgical resection. Seven genes (RARB, BVES, CDKN2A, KCNH5, RASSF1, CDH13, and RUNX) were found to be methylated significantly more frequently in tumor tissues than in noncancerous tissues. Only methylation of CCND2 and APC was frequently detected in both cancerous and noncancerous tissues, supporting the hypothesis that the methylation of these two genes is a preneoplastic change and may be associated with tobacco smoking exposure. Methylation of any one of eight genes (RASSF1, DAPK1, BVES, CDH13, MGMT, KCNH5, RARB, or CDH1) was present in 80% of NSCLC tissues but only in 14% of noncancerous tissues. Detection of methylation of these genes in blood might have utility in monitoring and detecting tumor recurrence in early-stage NSCLC after curative surgical resection. (Cancer Epidemiol Biomarkers Prev 2008;17(3):645–54)
Flavonoid Intake and Risk of Pancreatic Cancer in Male Smokers (Finland)
Authors: Bobe Gerd , Weinstein Stephanie J. , Albanes Demetrius , Hirvonen Tero , Ashby Jason , Taylor Phil R. , Virtamo Jarmo , Stolzenberg-Solomon Rachael Z. 
Published: March 2008

Abstract
Extending research on the protective effect of flavonoids in cell culture and animal studies, we examined the association between consumption of flavonoids and flavonoid-rich foods and development of exocrine pancreatic cancer within the α-Tocopherol, β-Carotene Cancer Prevention Study cohort. Of the 27,111 healthy male smokers (50-69 years) who completed a self-administered dietary questionnaire at baseline, 306 developed exocrine pancreatic cancer during follow-up (1985-2004; median, 16.1 years). Intakes of total flavonoids, three flavonoid subgroups, seven individual flavonoids, and flavonoid-rich foods were estimated from a validated food frequency questionnaire. Hazard ratios and 95% confidence intervals were estimated using Cox proportional hazards models. Overall, flavonoid intake was not significantly associated with pancreatic cancer. However, in stratified analysis, greater total flavonoid intake was associated with decreased pancreatic cancer risk in participants randomized during the trial to placebo (fourth versus first quartile: hazard ratio, 0.36; 95% confidence interval, 0.17-0.78; Ptrend = 0.009) and not to supplemental α-tocopherol (50 mg/d) and/or β-carotene (20 mg/d; Pinteraction = 0.002). Similar patterns and significant interactions were observed for flavonols, flavan-3-ols, kaempferol, quercetin, catechin, and epicatechin. Our data suggest that a flavonoid-rich diet may decrease pancreatic cancer risk in male smokers not consuming supplemental α-tocopherol and/or β-carotene. (Cancer Epidemiol Biomarkers Prev 2008;17(3):553–62)
Association between Tortilla Consumption and Human Urinary Fumonisin B1 Levels in a Mexican Population
Authors: Gong Yun Yun , Torres-Sanchez Luisa , Lopez-Carrillo Lizbeth , Peng Jian He , Sutcliffe Anne E. , White Kay L. , Humpf Hans-Ulrich , Turner Paul C. , Wild Christopher P. 
Published: March 2008

Abstract
Fumonisins are mycotoxins produced by Fusarium spp. and commonly contaminate maize and maize products worldwide. Fumonisins are rodent carcinogens and have been associated with human esophageal cancer. However, the lack of a valid exposure biomarker has hindered both the assessment of human exposure and the evaluation of disease risk. A sensitive liquid chromatography-mass spectrometry method to measure urinary fumonisin B1 (FB1) following extraction on Oasis MAX cartridges was established and applied to urine samples from women in a cohort recruited in Morelos County, Mexico. Urinary FB1 was compared with dietary information on tortilla consumption. FB1 recovery in spiked samples averaged 94% as judged by deuterium-labeled FB1 internal standard. Urinary FB1 was determined in 75 samples from women selected based on low, medium, or high consumption of maize-based tortillas. The geometric mean (95% confidence interval) of urinary FB1 was 35.0 (18.8-65.2), 63.1 (36.8-108.2), and 147.4 (87.6-248.0) pg/mL and the frequency of samples above the detection limit (set at 20 pg FB1/mL urine) was 45%, 80%, and 96% for the low, medium, and high groups, respectively. Women with high intake had a 3-fold higher average FB1 levels compared with the “low intake” group (F = 7.3; P = 0.0015). Urinary FB1 was correlated with maize intake (Ptrend = 0.001); the correlation remained significant after adjusting for age, education, and place of residence. This study suggests that measurement of urinary FB1 is sufficiently sensitive for fumonisin exposure assessment in human populations and could be a valuable tool in investigating the associated health effects of exposure. (Cancer Epidemiol Biomarkers Prev 2008;17(3):688–94)
Glycemic Status and Risk of Prostate Cancer
Authors: Darbinian Jeanne A. , Ferrara Assiamira M. , Van Den Eeden Stephen K. , Quesenberry Charles P. , Fireman Bruce , Habel Laurel A. 
Published: March 2008

Abstract
Background: To examine the risk of prostate cancer and glucose tolerance in a large, racially diverse cohort.
Methods: We conducted a cohort study of 47,209 male members of Kaiser Permanente Northern California who had completed at least one Multiphasic Health Checkup (MHC) between 1964 and 1973. The MHC provided information on diabetes, serum glucose 1 h after a 75-g oral glucose challenge test, demographics, and other health conditions. Cox proportional hazards were used to estimate relative risks (RR) while adjusting for confounders.
Results: During a median follow-up of 18.4 years, a total of 2,833 men developed prostate cancer. At baseline, 4.6% (n = 2,159) of the cohort had diabetes and 33% had serum glucose of ≥200 mg/dL. After adjusting for age, race, birth year, and body mass index, RR (95% confidence interval) of prostate cancer associated with 1-h serum glucose ≥200 mg/dL and diabetes were 0.90 (0.81-1.01) and 0.71 (0.62-0.79), respectively, when compared with those with serum glucose &lt;140 mg/dL. During the first 10 years of follow-up, risk was increased among those with serum glucose ≥200 mg/dL or diabetes [RR (95% confidence interval), 1.42 (0.95-2.13) and 1.56 (0.91-2.67), respectively]. In contrast, inverse associations between serum glucose ≥200 mg/dL and diabetes and prostate cancer risk were observed [0.87 (0.77-0.97) and 0.68 (0.52-0.88), respectively] when follow-up began 10 years after MHC.
Conclusion: Our findings are consistent with the hypothesis that prostate cancer risk differs by time since diabetes diagnosis or occurrence of metabolic aberrations associated with impaired glucose tolerance. (Cancer Epidemiol Biomarkers Prev 2008;17(3):628–35)
A Prospective Study of Risk-Reducing Salpingo-oophorectomy and Longitudinal CA-125 Screening among Women at Increased Genetic Risk of Ovarian Cancer: Design and Baseline Characteristics: A Gynecologic Oncology Group Study
Authors: Greene Mark H. , Piedmonte Marion , Alberts Dave , Gail Mitchell , Hensley Martee , Miner Zoe , Mai Phuong L. , Loud Jennifer , Rodriguez Gustavo , Basil Jack , Boggess John , Schwartz Peter E. , Kelley Joseph L. , Wakeley Katie E. , Minasian Lori , Skates Stephen 
Published: March 2008

Abstract
Background: Women who are genetically predisposed to ovarian cancer are at very high risk of developing this disease. Although risk-reducing salpingo-oophorectomy (RRSO) and various screening regimens are currently recommended to reduce ovarian cancer risk, the optimal management strategy has not been established nor have multiple additional issues been adequately addressed. We developed a collaboration among the Clinical Genetics Branch (National Cancer Institute's Intramural Research Program), the Gynecologic Oncology Group (GOG), and the Cancer Genetics Network to address these issues.
Methods: This is a prospective, international, two-cohort, nonrandomized study of women at genetic risk of ovarian cancer, who chose either to undergo RRSO or screening, at study enrollment. Primary study objectives include quantifying and comparing ovarian and breast cancer incidence in the two study groups, assessing feasibility and selected performance characteristics of a novel ovarian cancer screening strategy (the Risk of Ovarian Cancer Algorithm), evaluating various aspects of quality of life and nononcologic morbidity related to various interventions in at-risk women, and creating a biospecimen repository for subsequent translational research.
Results: Study accrual is complete as of November 2006; 2,605 participants enrolled: 1,030 (40%) into the surgical cohort and 1,575 (60%) into the screening cohort. Five years of prospective follow-up ends in November 2011. Verification of BRCA mutation carrier status is under way, either through patient-provided reports from clinical genetic testing done before enrollment or through research-based genetic testing being conducted as part of the protocol. Patient eligibility is currently under evaluation and baseline, surgical, pathology, and outcome data are still being collected. The study design and selected baseline characteristics of cohort members are summarized.
Conclusion: This National Cancer Institute intramural/extramural collaboration will provide invaluable prospectively collected observational data on women at high familial ovarian cancer risk, including substantial numbers of women carrying BRCA1/2 mutations. These data will aid in elucidating the effect of RRSO on breast/ovarian cancer risk and the effects of two management strategies, on quality of life and other issues that may influence patient care, as well as providing preliminary estimates of test specificity and positive predictive value of a novel ovarian cancer screening strategy. (Cancer Epidemiol Biomarkers Prev 2008;17(3):594–604)