bluuebunny/crossref_metadata_2025_split huggingface dataset:
Serum β-Glucuronidase Activity in Response to Fruit and Vegetable Supplementation: A Controlled Feeding Study
Authors: Maruti Sonia S. , Chang Jyh-Lurn , Prunty Jo Ann , Bigler Jeannette , Schwarz Yvonne , Li Shuying S. , Li Lin , King Irena B. , Potter John D. , Lampe Johanna W. 
Published: July 2008

AbstractBackground: Fruit and vegetable (F&V) intake may lower the risk of some cancers. One hypothesized, but understudied, chemopreventive mechanism is that plant food constituents inhibit β-glucuronidase, an acid hydrolase that deconjugates glucuronides.Methods: We conducted a crossover feeding trial in 63 healthy women and men ages 20 to 40 years to examine the effect of diet on serum β-glucuronidase activity. Participants were randomized to two 2-week experimental diets with an intervening washout period: a diet high in selected citrus fruit, crucifers, and soy (F&V) and a diet devoid of fruits, vegetables, and soy (basal). Serum β-glucuronidase activity was measured during the preintervention, F&V, and basal periods. Linear mixed models were used to obtain effect estimates and 95% confidence intervals (95% CI).Results: We observed statistically significantly higher β-glucuronidase activity during the F&V than the basal diet (ratio, F&V versus basal diet, 1.09; 95% CI, 1.05-1.13; P &lt; 0.01). These results were probably due to decreased β-glucuronidase activity during the basal diet (ratio, basal period versus preintervention, 0.93; 95% CI, 0.87-0.98; P = 0.01) rather than increased enzyme activity during the F&V diet (ratio, F&V period versus preintervention, 1.01; 95% CI, 0.96-1.06; P = 0.64). Response to the experimental diet did not differ by sex (Pinteraction = 0.30), but there was a suggestion of a short-term diet effect at 8 versus 15 days (Pinteraction = 0.06).Conclusion: This intervention of selected F&V did not lower β-glucuronidase activity. Further investigation is needed regarding what other foods and phytochemicals may influence β-glucuronidase activity and effect modifiers of this relation. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1808–12)
Racial/Ethnic Disparities in the Use of Nicotine Replacement Therapy and Quit Ratios in Lifetime Smokers Ages 25 to 44 Years
Authors: Fu Steven S. , Kodl Molly M. , Joseph Anne M. , Hatsukami Dorothy K. , Johnson Eric O. , Breslau Naomi , Wu Baolin , Bierut Laura 
Published: July 2008

Abstract
We examined racial/ethnic variations in the use of nicotine replacement therapy (NRT) and quit ratios among Caucasian, African American, Asian, and Latino lifetime smokers ages 25 to 44 years. We conducted cross-sectional analyses using data from individuals (n = 27,031) screened for enrollment in the Collaborative Study of the Genetics of Nicotine Dependence. Participants were randomly sampled from three Midwestern metropolitan areas using Health Maintenance Organization membership lists in Detroit, MI and Minneapolis, MN and a driver’s license registry in St. Louis, MO from March 2003 to August 2005. A telephone survey collected information on smoking history, previous quit attempts, and sociodemographic characteristics. Among lifetime smokers (n = 9,216), univariate analysis indicated that African Americans (22%) and Latinos (22%) were significantly less likely to report having ever used NRT for smoking cessation than Caucasians (31%). Asians (22%) also reported lower rates of using NRT than Caucasians, but this difference was marginally significant (P = 0.06). These disparities persisted in multivariate analysis for African Americans [adjusted odds ratio (OR), 0.76; 95% confidence interval (95% CI), 0.63-0.91; P &lt; 0.01] but not for Latinos (adjusted OR, 0.76; 95% CI, 0.54-1.06; P = 0.11) or Asians (adjusted OR, 0.98; 95% CI, 0.60-1.60; P = 0.95). As measured by the quit ratio, African Americans (35%) were less likely to have quit smoking than Caucasians (52%). This disparity persisted in multivariate logistic regression (adjusted OR, 0.66; 95% CI, 0.56-0.78; P &lt; 0.001). Asian and Latino smokers were as likely as Caucasians to report smoking cessation. Future prospective studies are needed to assess whether lower utilization of cessation treatments such as NRT contribute to the observed disparity in quit ratios for African Americans. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1640–7)
Community-Based Mass Ultrasonographic Screening of Hepatocellular Carcinoma among Thrombocytopenic Adults
Authors: Lu Sheng-Nan , Wang Jing-Houng , Chen Pao-Fei , Tung Hung-Da , Tseng Po-Lin , Hung Chao-Hung , Kee Kwong-Ming , Chen Chien-Hung , Chang Kuo-Chin , Lee Chuan-Mo , Changchien Chi-Sin , Chen Yao-Der , Tsai Lin-San , Chen Tony Hsiu-Hsi 
Published: July 2008

Abstract
Thrombocytopenia has been reported as a valid surrogate for liver cirrhosis and could be used to identify groups at high risk of hepatocellular carcinoma (HCC) for ultrasonographic (US) screening. We designed this two-stage community-based screening for HCC. In 2004, subjects (ages ≥40 years) were invited to undergo comprehensive health examinations, with 17,551 men (ages 63.0 ± 11.5 years) and 39,151 women (ages 59.9 ± 11.7 years) participating. Subjects with platelet counts &lt;150 × 109/L or α-fetoprotein (AFP) &gt;20 ng/mL were enrolled for the second-stage US screening; 3,242 subjects (5.7%; male/female, 1,415/1,827; age 66 ± 10 years) were candidates for US screening and 2,983 (92.2%) responded. Of 137 suspected cases, 124 (90.5%) complied with referral for confirmation and 72 (58.1%) were confirmed to be HCC cases (male/female, 41/31; age 68.1 ± 8.8 years). Screening with AFP, thrombocytopenia, or both could identify 0.64% (n = 364), 5.33% (n = 3,205), and 5.7% (n = 3,242) of the high-risk subjects from the population, estimated to include 50.5%, 54.5%, and 71.3% of all HCC cases. Among confirmed patients, tumor diameters were &lt;3 cm for the 27 (37.5%) patients and 3 to 5 cm for the 23 (31.9%) patients. Only 5 (6.9%) patients' conditions were too advanced to be actively treated. This study enrolled only 5.7% of the participants for US, which cover 64.7% to 71.3% of the HCC cases. Most (93%) of the detected cases were caught early enough to undergo effective treatment modalities. This HCC screening protocol should be feasible, economical, and effective. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1813–21)
Effect of Raloxifene on Mammographic Density and Breast Magnetic Resonance Imaging in Premenopausal Women at Increased Risk for Breast Cancer
Authors: Eng-Wong Jennifer , Orzano-Birgani Jennifer , Chow Catherine K. , Venzon David , Yao Jianhua , Galbo Claudia E. , Zujewski Jo Anne , Prindiville Sheila 
Published: July 2008

Abstract
Background: Mammographic density is a risk factor for breast cancer. Mammographic density and breast magnetic resonance imaging (MRI) volume (MRIV) assess the amount of fibroglandular tissue in the breast. Mammographic density and MRIV can be modulated with hormonal interventions, suggesting that these imaging modalities may be useful as surrogate endpoint biomarkers for breast cancer chemoprevention trials. We evaluated the effect of raloxifene on mammographic density and MRIV in premenopausal women at increased risk for breast cancer.
Methods: Mammograms and MRI were obtained at baseline and after 1 and 2 years of 60 mg raloxifene by mouth daily for 27 premenopausal women. Mammographic percent dense area was calculated using a semiquantitative thresholding technique. T1-weighted spoiled gradient-echo MRI with fat suppression was used to determine breast MRIV using a semiautomatic method. Mean change in mammographic density and median change in MRIV were assessed by the Wilcoxon signed-rank test.
Results: No significant change in mammographic density was seen after treatment with raloxifene. Mean change after 1 year was 1% [95% confidence interval (95% CI), −3 to +5] and after 2 years was 1% (95% CI, −2 to +5). MRIV decreased on raloxifene. Median relative change in MRIV after 1 year was -17% (95% CI, -28 to -9; P = 0.0017) and after 2 years was -16% (95% CI, -31 to -4; P = 0.0004).
Conclusions: In high-risk premenopausal women, mammographic density did not change on raloxifene, whereas MRIV significantly declined. Our findings suggest that MRIV is a promising surrogate biomarker in premenopausal women at increased risk for breast cancer and should be investigated further in breast cancer prevention trials. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1696–701)
Cervical and Vulvar Cancer Risk in Relation to the Joint Effects of Cigarette Smoking and Genetic Variation in Interleukin 2
Authors: Hussain Shehnaz K. , Madeleine Margaret M. , Johnson Lisa G. , Du Qin , Malkki Mari , Wilkerson Hui-Wen , Farin Federico M. , Carter Joseph J. , Galloway Denise A. , Daling Janet R. , Petersdorf Effie W. , Schwartz Stephen M. 
Published: July 2008

Abstract
Cigarette smoking is an established cofactor to human papillomavirus (HPV) in the development of cervical and vulvar squamous cell carcinoma (SCC), and may influence risk through an immunosuppressive pathway. Genetic variation in interleukin 2 (IL2), associated in some studies with the inhibition of HPV-targeted immunity, may modify the effect of smoking on the risk of HPV-related anogenital cancers. We conducted a population-based case-only study to measure the departure from a multiplicative joint effect of cigarette smoking and IL2 variation on cervical and vulvar SCC. Genotyping of the four IL2 tagSNPs (rs2069762, rs2069763, rs2069777, and rs2069778) was done in 399 cervical and 486 vulvar SCC cases who had been interviewed regarding their smoking history. Compared with cases carrying the rs2069762 TT genotype, we observed significant departures from multiplicativity for smoking and carriership of the TG or GG genotypes in vulvar SCC risk [interaction odds ratio (IOR), 1.67; 95% confidence interval (CI), 1.16-2.41]. Carriership of one of three diplotypes, together with cigarette smoking, was associated with either a supramultiplicative (TGCT/GGCC; IOR, 2.09; 95% CI, 0.98-4.46) or submultiplicative (TTCC/TGTC; IOR, 0.37; 95% CI, 0.16-0.85 or TGCT/TGCC; IOR, 0.37; 95% CI, 0.15-0.87) joint effect in vulvar cancer risk. For cervical SCC, departure from multiplicativity was observed for smokers homozygous for the rs2069763 variant allele (TT versus GG or GT genotypes; IOR, 1.87; 95% CI, 1.00-3.48), and for carriership of the TTCC/TTCC diplotype (IOR, 2.08; 95% CI, 1.01-4.30). These results suggest that cervical and vulvar SCC risk among cigarette smokers is modified by genetic variation in IL2. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1790–9)
Sp1, a New Biomarker That Identifies a Subset of Aggressive Pancreatic Ductal Adenocarcinoma
Authors: Jiang Naomi Y. , Woda Bruce A. , Banner Barbara F. , Whalen Giles F. , Dresser Karen A. , Lu Di 
Published: July 2008

AbstractPancreatic adenocarcinoma is one of the leading causes of cancer-related deaths in the United States. Sp1 is a sequence-specific DNA binding protein that is important in the transcription of a number of regulatory genes involved in cancer cell growth, differentiation, and metastasis. In this study, we investigated Sp1 expression in pancreatic ductal adenocarcinoma and its association with clinical outcome. We studied 42 patients with primary pancreatic adenocarcinoma. The expression of Sp1 in pancreatic adenocarcinoma was evaluated by immunohistochemical staining. All 42 patients had clinical follow-up information and were evaluated for survival. Sp1 protein was aberrantly overexpressed in a subset of primary pancreatic adenocarcinoma. These tumors all developed metastasis, whereas none of the primary tumors without lymph node metastasis showed Sp1 overexpression. Statistically, Sp1 overexpression was associated with higher stage, higher grade, and lymph node metastasis (P &lt; 0.001, P = 0.036, and P &lt; 0.0001, respectively). Additionally, patients of this subset had a much shorter overall survival than patients without Sp1 overexpression, as evidenced by Kaplan-Meier plots and the log-rank test (P = 0.002). The 5-year overall survival rate was 19% in patients with Sp1 overexpression, compared with 55% in patients without Sp1 overexpression. The median survival was only 13 months for patients with Sp1 overexpression, compared with 65 months for patients without Sp1 overexpression. In conclusion, Sp1 is a new biomarker that identifies a subset of pancreatic ductal adenocarcinoma with aggressive clinical behavior. It can be used at initial diagnosis of pancreatic adenocarcinoma to identify patients with an increased probability of cancer metastasis and much shortened overall survival. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1648–52)
Human Papillomavirus Infection in Ulaanbaatar, Mongolia: A Population-Based Study
Authors: Dondog Bolormaa , Clifford Gary M. , Vaccarella Salvatore , Waterboer Tim , Unurjargal Davaajav , Avirmed Damdin , Enkhtuya Sharkhuu , Kommoss Friedrich , Wentzensen Nicolas , Snijders Peter J.F. , Meijer Chris J.L.M. , Franceschi Silvia , Pawlita Michael 
Published: July 2008

Abstract
Data on human papillomavirus (HPV) and cervical cancer burden in Central Asia are scarce. To investigate HPV infection in Ulaanbaatar, the capital of Mongolia, we obtained cervical cell specimens from a population of 969 women ages 15 to 59 years. DNA of 44 HPV types was detected using a GP5+/6+ PCR-based assay. Seropositivity for L1 proteins of HPV 16, 18, 31, 33, 45, 52, and 58 was assessed using multiplex HPV serology. Cytologic abnormalities were detected in 127 women (13.1%), among whom 6 cervical intraepithelial neoplasia grade 3 and 2 invasive cervical cancers were diagnosed. Overall HPV DNA prevalence was 35.0%, being highest (48.5%) in women ages &lt;25 years. High-risk types were detected in 24.5% of women. HPV DNA prevalence declined with age but remained &gt;25% in all age groups. HPV seroprevalence was also very high (38.0%) and increased steadily from 33.2% to 48.9% in women ages &lt;25 and 50 to 59 years, respectively. However, the proportion of women positive for both HPV markers of any individual HPV type was low. HPV16 was the most frequently detected type by PCR (6.1%), serology (23.0%), or both (2.1%). Lifetime number of sexual partners and induced abortions were shown to be directly associated with HPV DNA and/or seroprevalence. HPV prevalence in Ulaanbaatar was higher than that detected by similar HPV testing protocols in other populations in Asia or elsewhere and would suggest an important, yet unquantified, cervical cancer burden. Improving cervical cancer prevention, through screening and HPV vaccination, is an important public health issue for Mongolia. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1731–8)
Association of Aryl Hydrocarbon Receptor Gene Polymorphisms and Urinary 1-Hydroxypyrene in Polycyclic Aromatic Hydrocarbon–Exposed Workers
Authors: Bin Ping , Leng Shuguang , Cheng Juan , Dai Yufei , Huang Chuanfeng , Pan Zufei , Niu Yong , Duan Huawei , Li Haishan , Liu Qingjun , Chen Wen , Zheng Yuxin 
Published: July 2008

AbstractPolycyclic aromatic hydrocarbons (PAH) in coke oven emissions could cause lung cancer in human. Individual's genotype of the metabolic enzymes and early biological changes were known to be associated with the susceptibility of cancer development. Knowledge of metabolic gene polymorphisms, which affect on the urinary 1-hydroxypyrene (1-OHP), could benefit us in understanding the interindividual difference in the mechanism of PAH-induced carcinogenesis. In this study, we investigated the association of aryl hydrocarbon receptor (AhR) gene polymorphisms and urinary 1-OHP. One hundred forty-seven workers exposed to PAH and 69 nonexposure workers were recruited. Seven tagging single nucleotide polymorphisms in AhR gene were selected by pariwise r2 method and minor allele frequency cutoff of 0.05 from Chinese genotype data in HapMap project. These seven tagging single nucleotide polymorphisms were genotyped by PCR-based methods. Multivariate analysis of covariance revealed that the levels of 1-OHP in PAH-exposed workers carrying genotype CT were lower than workers carrying wild genotype TT at loci rs10250822 and rs2282885 of AhR gene (P = 0.032 and 0.044, respectively). In PAH-exposed workers, the urinary 1-OHP levels showed a linear correlation (Ptrend = 0.041) with the genotypes at locus rs2282885, especially in low and moderate exposure groups. In contrast, no significant association was found between urinary 1-OHP level and AhR genotypes among nonexposed workers. Our findings indicated that polymorphisms of AhR gene were associated with the level of 1-OHP among PAH-exposed workers, suggesting that AhR-mediated signaling might contribute to individual susceptibility to PAH exposure. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1702–8)
Breast Cancer Risk and Hormone Receptor Status in Older Women by Parity, Age of First Birth, and Breastfeeding: A Case-Control Study
Authors: Lord Sarah J. , Bernstein Leslie , Johnson Karen A. , Malone Kathleen E. , McDonald Jill A. , Marchbanks Polly A. , Simon Michael S. , Strom Brian L. , Press Michael F. , Folger Suzanne G. , Burkman Ronald T. , Deapen Dennis , Spirtas Robert , Ursin Giske 
Published: July 2008

Abstract
Background: Early age at first birth and multiparity reduce the risk of estrogen receptor-progesterone receptor (ERPR)–positive breast cancer, whereas breastfeeding reduces the risk of both ERPR-positive and ERPR-negative cancers.
Methods: We used multivariable logistic regression analysis to investigate whether age at first birth (&lt;25 or ≥25 years) and breastfeeding (ever/never) modify the long-term effect of parity on risk of ERPR-positive and ERPR-negative cancer using 1,457 incident breast cancer cases and 1,455 controls ages ≥55 years who participated in the Women's Contraceptive and Reproductive Experiences Study.
Results: Women who gave birth before age 25 years had a 36% reduced risk of breast cancer compared with nulligravida that was not observed for women who started their families at an older age (Pheterogeneity = 0.0007). This protective effect was restricted to ERPR-positive breast cancer (Pheterogeneity = 0.004). Late age at first birth increased the risk of ERPR-negative cancers.
Additional births reduced the risk of ERPR-positive cancers among women with an early first birth (Ptrend = 0.0001) and among women who breastfed (Ptrend = 0.004) but not among older mothers or those who never breastfed. In women with a late first birth who never breastfed, multiparity was associated with increased risk of breast cancer.
Conclusions: These findings suggest that the effect of parity on a woman's long-term risk of breast cancer is modified by age at first full-term pregnancy and possibly by breastfeeding. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1723–30)
Use of Common Medications and Breast Cancer Risk
Authors: Moysich Kirsten B. , Beehler Gregory P. , Zirpoli Gary , Choi Ji-Yeob , Baker Julie A. 
Published: July 2008

AbstractPrescription and over-the-counter medications are widely used in the United States and many western countries. More than two-thirds of women ages &gt;45 years, who are at greatest risk for breast cancer, take prescription medication. In light of the ubiquitous nature of medication use and the fact that breast cancer remains the most common cancer in women, research on the role of medication use in breast cancer etiology is warranted. We summarize the epidemiologic evidence on the association between breast cancer risk and use of common medications, including antibiotics, antidepressants, statins, antihypertensives, and nonsteroidal anti-inflammatory drugs. Overall, there is little evidence that would implicate the use of antibiotics, antidepressants, statins, and antihypertensives in the etiology of breast cancer. Although several prospective studies and a randomized low-dose aspirin chemoprevention trial have not shown lower risk of breast cancer among aspirin users, most studies that have examined the potential chemoprotective effect of nonsteroidal anti-inflammatory drugs have shown significant risk reductions for regular and prolonged use of these drugs. The existing literature on the role of medication use in breast carcinogenesis is complicated. Interpretation of the evidence is hampered due to major methodologic differences across studies, including exposure assessment, exposure classification, and adjustment for potential confounding variables. These differences largely stem from the fact that the majority of articles on this topic represent secondary data analyses from studies with inadequate information on exposure or confounders. Thus, future epidemiologic studies specifically designed to study these ubiquitous and biologically plausible exposures are warranted. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1564–95)
Colorectal Cancer Test Use from the 2005 National Health Interview Survey
Authors: Shapiro Jean A. , Seeff Laura C. , Thompson Trevor D. , Nadel Marion R. , Klabunde Carrie N. , Vernon Sally W. 
Published: July 2008

Abstract
Background: Screening is effective in reducing colorectal cancer mortality. Recommended colorectal cancer screening options include a home fecal occult blood test (FOBT) or colorectal endoscopy (sigmoidoscopy or colonoscopy). Past surveys have indicated that colorectal cancer screening prevalence in the United States is low. The purpose of this analysis was to determine the prevalence of colorectal cancer test use in the United States by various factors and to examine reasons for not having a colorectal cancer test.
Methods: Data on respondents ages ≥50 years from the 2005 National Health Interview Survey (n = 13,269) were analyzed. The proportion of the U.S. population that had home FOBT within the past year or endoscopy within the past 10 years was examined by sociodemographic, health-care access, and other health-related factors. Reported reasons for not having FOBT or endoscopy were also analyzed.
Results: The age-standardized proportion of respondents who reported FOBT within the past year and/or endoscopy within the past 10 years was 50.0% [95% confidence interval (95% CI), 48.8-51.2]. Colorectal cancer testing rates were particularly low among people without health-care coverage (24.1%; 95% CI, 19.2-29.7) or without a usual source of health care (24.7%; 95% CI, 20.8-29.0). The most commonly reported reason for not having a colorectal cancer test was “never thought about it.”
Conclusions: In 2005, about half of Americans ages ≥50 years did not have appropriate colorectal cancer testing. Increased efforts to expand health-care coverage or to provide colorectal cancer tests to people without health-care coverage are needed to increase colorectal cancer screening. (Cancer Epidemiol Biomarkers Prev 2008;17(7):1623–30)