bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Novel Approach to Exploring Potential Interactions among Single-Nucleotide Polymorphisms of Inflammation Genes in Gliomagenesis: An Exploratory Case-Only Study
Authors: Amirian E. Susan , Scheurer Michael E. , Liu Yanhong , D'Amelio Anthony M. , Houlston Richard S. , Etzel Carol J. , Shete Sanjay , Swerdlow Anthony J. , Schoemaker Minouk J. , McKinney Patricia A. , Fleming Sarah J. , Muir Kenneth R. , Lophatananon Artitaya , Bondy Melissa L. 
Published: August 2011

Abstract
Background: Despite extensive research on the topic, glioma etiology remains largely unknown. Exploration of potential interactions between single-nucleotide polymorphisms (SNP) of immune genes is a promising new area of glioma research. The case-only study design is a powerful and efficient design for exploring possible multiplicative interactions between factors that are independent of one another. The purpose of our study was to use this exploratory design to identify potential pair wise SNP–SNP interactions from genes involved in several different immune-related pathways for investigation in future studies.
Methods: The study population consisted of two case groups: 1,224 histologic confirmed, non-Hispanic white glioma cases from the United States and a validation population of 634 glioma cases from the United Kingdom. Polytomous logistic regression, in which one SNP was coded as the outcome and the other SNP was included as the exposure, was utilized to calculate the ORs of the likelihood of cases simultaneously having the variant alleles of two different SNPs. Potential interactions were examined only between SNPs located in different genes or chromosomes.
Results: Using this data mining strategy, we found 396 significant SNP–SNP interactions among polymorphisms of immune-related genes that were present in both the U.S. and U.K. study populations.
Conclusion: This exploratory study was conducted for the purpose of hypothesis generation, and thus has provided several new hypotheses that can be tested using traditional case–control study designs to obtain estimates of risk.
Impact: This is the first study, to our knowledge, to take this novel approach to identifying SNP–SNP interactions relevant to glioma etiology. Cancer Epidemiol Biomarkers Prev; 20(8); 1683–9. ©2011 AACR.
ABO Genotype and the Risk of Gastric Cancer, Atrophic Gastritis, and Helicobacter pylori Infection
Authors: Nakao Makoto , Matsuo Keitaro , Ito Hidemi , Shitara Kohei , Hosono Satoyo , Watanabe Miki , Ito Seiji , Sawaki Akira , Iida Shinsuke , Sato Shigeki , Yatabe Yasushi , Yamao Kenji , Ueda Ryuzo , Tajima Kazuo , Hamajima Nobuyuki , Tanaka Hideo 
Published: August 2011

Abstract
Background: Although several studies have investigated the association between ABO blood type and risk of gastric cancer (GC), atrophic gastritis (AG), and Helicobacter pylori (HP) infection, no study has investigated these associations by using ABO genotype.
Methods: We conducted a case–control study in 703 patients with GC and 1,465 noncancer patients. We also conducted a cross-sectional study by using 1,406 of these 1,465 controls, who were examined for pepsinogens and anti-HP IgG antibody levels in serum. ABO genotype was determined from single nucleotide polymorphisms in ABO gene. We used rs8176719 to mark the O allele, and rs8176746 and rs8176747 to mark the B allele. ORs and 95% CIs were calculated by a multivariate logistic model.
Results: We observed significant associations between ABO genotype and GC, AG, and HP infection. ORs (95% CIs) of GC were 0.70 (0.50–0.99) for OO and 0.53 (0.36–0.77) for BO relative to AA genotype. An increased risk of GC was observed with addition of the A allele (Ptrend &lt; 0.001), and a decreased risk with that of the B allele (Ptrend = 0.023). An OR of AG was 0.73 (95% CI, 0.53–0.99) for blood type B relative to blood type A, and an OR of HP infection was 0.39 (95% CI, 0.17–0.87) for BB relative to AA genotype.
Conclusion: This study identified a statistically significant association between ABO genotype and GC risk. In addition, ABO gene locus may influence AG prevalence and HP infection.
Impact: Further studies are necessary to confirm these findings. Cancer Epidemiol Biomarkers Prev; 20(8); 1665–72. ©2011 AACR.
Trends in Colorectal Cancer Test Use among Vulnerable Populations in the United States
Authors: Klabunde Carrie N. , Cronin Kathleen A. , Breen Nancy , Waldron William R. , Ambs Anita H. , Nadel Marion R. 
Published: August 2011

Abstract
Background: Evaluating trends in colorectal cancer (CRC) screening use is critical for understanding screening implementation, and whether population groups targeted for screening are receiving it, consistent with guidelines. This study examines recent national trends in CRC test use, including among vulnerable populations.
Methods: We used the 2000, 2003, 2005, and 2008 National Health Interview Survey to examine national trends in CRC screening use overall and for fecal occult blood test (FOBT), sigmoidoscopy, and colonoscopy. We also assessed trends by race/ethnicity, educational attainment, income, time in the United States, and access to health care.
Results: During 2000 to 2008, significant declines in FOBT and sigmoidoscopy use and significant increases in colonoscopy use and in the percentages of adults up-to-date with CRC screening occurred overall and for most population subgroups. Subgroups with consistently lower rates of colonoscopy use and being up-to-date included Hispanics; people with minimal education, low income, or no health insurance; recent immigrants; and those with no usual source of care or physician visits in the past year. Among up-to-date adults, there were few subgroup differences in the type of test by which they were up-to-date (i.e., FOBT, sigmoidoscopy, or colonoscopy).
Conclusions: Although use of CRC screening and colonoscopy increased among U.S. adults, including those from vulnerable populations, 45% of adults aged 50 to 75—or nearly 35 million people—were not up-to-date with screening in 2008.
Impact: Continued monitoring of CRC screening rates among population subgroups with consistently low utilization is imperative. Improvement in CRC screening rates among all population groups in the United States is still needed. Cancer Epidemiol Biomarkers Prev; 20(8); 1611–21. ©2011 AACR.
Sunlight Exposure–Mediated DNA Damage in Young Adults
Authors: Kato Masashi , Iida Machiko , Goto Yuji , Kondo Takaaki , Yajima Ichiro 
Published: August 2011

Abstract
Background: Previous experimental studies showed that single ultraviolet B (UVB) light irradiation increased levels of 8-hydroxy-2′-deoxyguanosine (8-OHdG), a well-established biomarker of carcinogenesis and oxidative DNA damage, in epithelial cells in animals and humans. We conducted for the first time an epidemiologic study to investigate the correlations among levels of oxidative DNA damage, skin pigmentation, and sunlight exposure in human daily life.
Methods: Digitalized skin pigmentation levels and creatinine-adjusted urinary 8-OHdG levels were examined in 127 healthy young adults aged 20 to 24 years and in hairless mice with normal pigmented skin (HL-mice; n = 20) and hyperpigmented skin (HL-HPS-mice; n = 20). Data obtained by a questionnaire were also analyzed for the 127 subjects.
Results: Binary logistic regression analysis showed that increased sunlight intensity, but not sunlight-exposed time or sunlight-exposed skin area, was correlated with elevation in creatinine-adjusted urinary 8-OHdG levels. In contrast, increased skin pigmentation level, but not the use of sunscreen, was correlated with reduction in urinary 8-OHdG level in humans. UVB irradiation corresponding to several minutes of sunlight exposure significantly increased urinary 8-OHdG levels in HL-mice but not in HL-HPS-mice.
Conclusions: We showed that increase in intensity of sunlight in human daily life increased levels of DNA damage. We also showed a protective effect of skin pigmentation on sunlight exposure–mediated DNA damage.
Impact: We have provided more reliable evidence of routine sunlight exposure–mediated DNA damage in humans through the combination of epidemiologic and experimental studies. Cancer Epidemiol Biomarkers Prev; 20(8); 1622–8. ©2011 AACR.
Aberrant Methylation ofRARβ2andAPCGenes in Voided Urine as Molecular Markers for Early Detection of Bilharzial and Nonbilharzial Bladder Cancer
Authors: Eissa Sanaa , Swellam Menha , El-Khouly Inas M. , Kassim Samar K. , Shehata Hanan , Mansour Amal , Esmat Mohamed , Nossier Ahmed Ibrahim , Hamdy Mohamed A. , Awad Nahla M. , El-Ahmady Omar 
Published: August 2011

AbstractBackground: Bladder cancer cells illustrate major disruptions in their DNA methylation patterns as compared with normal ones. Authors aimed to identify epigenetic molecular markers in urine for early detection of bladder cancer.Materials and Methods: We retrospectively analyzed the methylation status of RARβ2 and APC genes in urine samples from 210 bladder cancer patients, 61 patients with benign urological diseases, and 49 healthy volunteers by using methylation-specific PCR.Results: Methylated RARβ2 and APC were significantly higher in bladder cancer patients (62.8%, 59.5%) than benign (16.4%, 5%) but not detected in healthy volunteers (0%) at (P &lt; 0.0001). Both methylated genes showed no significant difference among clinicopathologic factors; however, they were detected in all grades and stages. Among the 128 patients with bilharzial bladder cancer, 94 (73.4%) showed methylated RARβ2 and 86 (67.2%) showed methylated APC. Homoplasmic methylation pattern of both genes were only detected in bilharzial bladder cancer cases. Both sensitivities and specificities of the methylated genes for bladder cancer detection were superior to urine cytology and when altogether combined, the sensitivities improved to (91.8%), (93.5%), (91.9%), and (80.9%) in detection of: bladder cancer, non-muscle invasive bladder cancer, low-grade tumors, and bilharzial associated bladder cancer, respectively.Conclusion: Thus, methylated RARβ2 and APC genes might be valuable urinary molecular markers for early detection of bilharzial and nonbilharzial bladder cancer. Cancer Epidemiol Biomarkers Prev; 20(8); 1657–64. ©2011 AACR.
A Systematic Review of Replication Studies of Prostate Cancer Susceptibility Genetic Variants in High-Risk Men Originally Identified from Genome-Wide Association Studies
Authors: Ishak Miriam B. , Giri Veda N. 
Published: August 2011

Abstract
Background: Several prostate cancer genome-wide association studies (GWAS) have identified risk-associated genetic variants primarily in populations of European descent. Less is known about the association of these variants in high-risk populations, including men of African descent and men with a family history of prostate cancer. This article provides a detailed review of published studies of prostate cancer–associated genetic variants originally identified in GWAS and replicated in high-risk populations.
Methods: Articles replicating GWAS findings (National Human Genome Research Institute GWAS database) were identified by searching PubMed and relevant data were extracted.
Results: Eleven replication studies were eligible for inclusion in this review. Of more than 30 single-nucleotide polymorphisms (SNP) identified in prostate cancer GWAS, 19 SNPs (63%) were replicated in men of African descent and 10 SNPs (33%) were replicated in men with familial and/or hereditary prostate cancer (FPC/HPC). The majority of SNPs were located at the 8q24 region with modest effect sizes (OR 1.11–2.63 in African American men and OR 1.3–2.51 in men with FPC). All replicated SNPs at 8q24 among men of African descent were within or near regions 2 and 3.
Conclusions: This systematic review revealed several GWAS markers with replicated associations with prostate cancer in men of African descent and men with FPC/HPC. The 8q24 region continues to be the most implicated in prostate cancer risk. These replication data support ongoing study of clinical utility and potential function of these prostate cancer–associated variants in high-risk men.
Impact: The replicated SNPs presented in this review hold promise for personalizing risk assessment for prostate cancer for high-risk men upon further study. Cancer Epidemiol Biomarkers Prev; 20(8); 1599–610. ©2011 AACR.
Hormonal Factors and the Risk of Papillary Thyroid Cancer in the California Teachers Study Cohort
Authors: Horn-Ross Pamela L. , Canchola Alison J. , Ma Huiyan , Reynolds Peggy , Bernstein Leslie 
Published: August 2011

Abstract
Background: Despite the increasing incidence of thyroid cancer, there is limited information on its etiology. The strikingly higher rates in young women, compared with men, suggest that sex steroid hormones may be involved in the development of this disease.
Methods: We investigated the effects of menstrual, reproductive, and other hormonal factors on papillary thyroid cancer risk in the prospective California Teachers Study cohort. Among 117,646 women, 233 were diagnosed with invasive histologically confirmed papillary thyroid cancer after cohort enrollment and before January 1, 2008. Relative risks (RR) and 95% CIs were estimated by using Cox proportional hazards regression models.
Results: Among younger women (age &lt;45 years at baseline; approximately one-third of the cohort), but not older women, later age at menarche (age ≥14 years) was associated with increased risk (RR = 1.88, 95% CI: 1.13–3.13; pinteraction by age = 0.06). Risk was also increased among young women who had longer (&gt;30 days) adolescent menstrual cycles (RR = 1.78, 95% CI: 1.01–3.14) and whose last pregnancy had ended within five years of cohort enrollment (RR = 2.21, 95% CI: 1.13–4.34). Among older women (age ≥45 years at baseline), ever use of estrogen-only therapy was associated with a statistically nonsignificant increase in risk (RR = 1.69, 95% CI: 0.95–2.98).
Conclusions: The findings from this prospective analysis suggest that several factors related to delayed pubertal development and the transient effects of pregnancy may be particularly important in influencing risk in young women.
Impact: These results suggest the importance of future research into the role of progesterone and the estrogen-to-progesterone ratio. Cancer Epidemiol Biomarkers Prev; 20(8); 1751–9. ©2011 AACR.
MicroRNA Processing and Binding Site Polymorphisms Are Not Replicated in the Ovarian Cancer Association Consortium
Authors: Permuth-Wey Jennifer , Chen Zhihua , Tsai Ya-Yu , Lin Hui-Yi , Chen Y. Ann , Barnholtz-Sloan Jill , Birrer Michael J. , Chanock Stephen J. , Cramer Daniel W. , Cunningham Julie M. , Fenstermacher David , Fridley Brooke L. , Garcia-Closas Montserrat , Gayther Simon A. , Gentry-Maharaj Aleksandra , Gonzalez-Bosquet Jesus , Iversen Edwin , Jim Heather , McLaughlin John , Menon Usha , Narod Steven A. , Phelan Catherine M. , Ramus Susan J. , Risch Harvey , Song Honglin , Sutphen Rebecca , Terry Kathryn L. , Tyrer Jonathan , Vierkant Robert A. , Wentzensen Nicolas , Lancaster Johnathan M. , Cheng Jin Q. , Berchuck Andrew , Pharoah Paul D.P. , Schildkraut Joellen M. , Goode Ellen L. , Sellers Thomas A. 
Published: August 2011

Abstract
Background: Single nucleotide polymorphisms (SNP) in microRNA-related genes have been associated with epithelial ovarian cancer (EOC) risk in two reports, yet associated alleles may be inconsistent across studies.
Methods: We conducted a pooled analysis of previously identified SNPs by combining genotype data from 3,973 invasive EOC cases and 3,276 controls from the Ovarian Cancer Association Consortium. We also conducted imputation to obtain dense coverage of genes and comparable genotype data for all studies. In total, 226 SNPs within 15 kb of 4 miRNA biogenesis genes (DDX20, DROSHA, GEMIN4, and XPO5) and 23 SNPs located within putative miRNA binding sites of 6 genes (CAV1, COL18A1, E2F2, IL1R1, KRAS, and UGT2A3) were genotyped or imputed and analyzed in the entire dataset.
Results: After adjustment for European ancestry, no overall association was observed between any of the analyzed SNPs and EOC risk.
Conclusions: Common variants in these evaluated genes do not seem to be strongly associated with EOC risk.
Impact: This analysis suggests earlier associations between EOC risk and SNPs in these genes may have been chance findings, possibly confounded by population admixture. To more adequately evaluate the relationship between genetic variants and cancer risk, large sample sizes are needed, adjustment for population stratification should be carried out, and use of imputed SNP data should be considered. Cancer Epidemiol Biomarkers Prev; 20(8); 1793–7. ©2011 AACR.
Nonsteroidal Anti-inflammatory Drug and Acetaminophen Use and Risk of Adult Myeloid Leukemia
Authors: Ross Julie A. , Blair Cindy K. , Cerhan James R. , Soler John T. , Hirsch Betsy A. , Roesler Michelle A. , Higgins Rodney R. , Nguyen Phuong L. 
Published: August 2011

Abstract
Background: Little is known about the causes of adult leukemia. A few small studies have reported a reduced risk associated with regular use of nonsteroidal anti-inflammatory drugs (NSAID).
Methods: In a population-based case–control study, we evaluated analgesic use among 670 newly diagnosed myeloid leukemia cases [including 420 acute myeloid leukemias (AML) and 186 chronic myeloid leukemias (CML)] and 701 controls aged 20 to 79 years. Prior use of aspirin, ibuprofen, acetaminophen, other NSAIDs, and COX-2 inhibitors was assessed and included frequency, duration, and quantity. ORs and 95% CIs were calculated using unconditional logistic regression adjusting for potential confounders.
Results: Regular/extra strength aspirin use was inversely associated with myeloid leukemia in women (OR = 0.59, 95% CI = 0.37–0.93) but not in men (OR = 0.85, 95% CI = 0.58–1.24). In contrast, acetaminophen use was associated with an increased risk of myeloid leukemia in women only (OR = 1.60, 95% CI = 1.04–2.47). These relationships were stronger with increasing dose and duration. When stratified by leukemia type, aspirin use was inversely associated with AML and CML in women. No significant overall associations were found with ibuprofen or COX-2 inhibitors for either sex; however, a decreased risk was observed with other anti-inflammatory analgesic use for women with AML or CML (OR = 0.47, 95% CI = 0.22–0.99; OR = 0.31, 95% CI = 0.10–0.92, respectively).
Conclusions: Our results provide additional support for the chemopreventive benefits of NSAIDs, at least in women. Because leukemia ranks fifth in person-years of life lost due to malignancy, further investigation is warranted.
Impact: NSAIDs may reduce, whereas acetaminophen may increase, myeloid leukemia risk in women. Cancer Epidemiol Biomarkers Prev; 20(8); 1741–50. ©2011 AACR.
Differentials in Survival for Childhood Cancer in Australia by Remoteness of Residence and Area Disadvantage
Authors: Youlden Danny R. , Baade Peter D. , Valery Patricia C. , Ward Leisa J. , Green Adele C. , Aitken Joanne F. 
Published: August 2011

Abstract
Background: It is not known whether improvements in cancer survival over recent decades have benefited children from different geographic locations equally. This is the first study to produce national survival estimates for childhood cancer in Australia by remoteness of residence and area-based socioeconomic status.
Methods: The study utilized population-based data from the Australian Paediatric Cancer Registry for children diagnosed with cancer from 1996 onward who were at risk of mortality between January 2001 and December 2006 (n = 6,289). Remoteness was specified according to the Australian Standard Geographical Classification Remoteness Areas, whereas an index of area disadvantage was obtained from census information. Five-year relative survival estimates were produced by the period method for all cancers and the most common diagnostic groups, with corresponding age–sex adjusted mortality hazard ratios calculated using Poisson regression.
Results: Overall, children with cancer from remote/very remote areas had a significantly lower survival rate than their counterparts in major cities (HR = 1.55, 95% CI = 1.08–2.23). Survival was also lower for children with leukemia living in inner regional (HR = 1.52, 95% CI = 1.11–2.08) or outer regional areas (HR = 1.53, 95% CI = 1.03–2.28). There was weak evidence (Pgrad = 0.051) of a trend toward poorer survival by greater area disadvantage for all childhood cancers.
Conclusions: Some variation in prognosis by place of residence was present for children with cancer in Australia, particularly among leukemia patients.
Impact: Treatment, clinical or area-related factors that contribute to these survival differentials need to be identified. Cancer Epidemiol Biomarkers Prev; 20(8); 1649–56. ©2011 AACR.
Circulating Insulin-like Growth Factor-I in Pregnancy and Maternal Risk of Breast Cancer
Authors: Toriola Adetunji T. , Lundin Eva , Schock Helena , Grankvist Kjell , Pukkala Eero , Chen Tianhui , Zeleniuch-Jacquotte Anne , Toniolo Paolo , Lehtinen Matti , Surcel Helja-Marja , Lukanova Annekatrin 
Published: August 2011

Abstract
Background: Elevated serum concentrations of insulin-like growth factor (IGF)-I have been associated with increased risk of developing breast cancer. Previously, we reported a similar association in samples obtained during pregnancy. This study was conducted to further characterize the association of IGF-I during pregnancy with maternal breast cancer risk.
Methods: A case–control study was nested within the Finnish Maternity Cohort. The study was limited to primiparous women younger than 40 years, who donated blood samples during early (median, 12 weeks) pregnancy and delivered a single child at term. Seven hundred nineteen women with invasive breast cancer were eligible. Two controls (n = 1,434) were matched with each case on age and date at blood donation. Serum IGF-I concentration was measured using an Immulite 2000 analyzer. Conditional logistic regression was used to estimate ORs and 95% CIs.
Results: No significant associations were observed between serum IGF-I concentrations and breast cancer risk in both the overall analysis (OR, 1.08; 95% CI, 0.80–1.47) and in analyses stratified by histologic subtype, lag time to cancer diagnosis, age at pregnancy, or age at diagnosis.
Conclusion: There was no association between IGF-I and maternal breast cancer risk during early pregnancy in this large nested case–control study.
Impact: Serum IGF-I concentrations during early pregnancy may not be related to maternal risk of developing breast cancer. Cancer Epidemiol Biomarkers Prev; 20(8); 1798–801. ©2011 AACR.
Public Opinion Discourses on Democratization in the Arab Middle East
Authors: Al-Sumait Fahed 
Published: August 2011

AbstractIn contemporary political discussions, the Middle East is often lamented as democratically deficient. During the last decade, processes of democratization in the region have gained considerable momentum as accepted goals of the international community—a condition noticeably accelerated following the events of 11 September 2001 and recent revolutions in North Africa. With democratization promoted as an explicit foreign policy objective, new discourses have emerged examining democracy's efficacy when translated into these contexts. Such discourses are heavily influenced by strategic political rhetoric rather than empirical assessments; a condition with significant consequences for public perceptions and policy decisions. Public opinion polls are starting to play an important role in these emerging discourses, yet polling research in the Middle East is still in its infancy. Major reports from three large-scale polls are used to highlight existing gaps between theoretical assessments of democratic attitudes and their empirical measures. Applying a four-part definition of democratization, this article assesses the relative ability of these polls to communicate the diversity of transnational perspectives concerning democracy's tenets. It is concluded that many Arab populations are not given adequate voice since polls often over-generalize attitudes based on interests in regional measures of central tendency rather than reflecting on the diversity among individual nation states.