bluuebunny/crossref_metadata_2025_split huggingface dataset:
Smoking Rates and Topography Predict Adolescent Smoking Cessation Following Treatment with Nicotine Replacement Therapy
Authors: Franken Frederick H. , Pickworth Wallace B. , Epstein David H. , Moolchan Eric T. 
Published: March 2006

Abstract
Establishing measurement invariance of tobacco addiction among adolescents remains challenging. In adult smoking cessation trials, poor outcome is predicted by high cigarette consumption and large puff volume at baseline. We examined the predictive value of pretreatment smoking rates and topography variables for abstinence outcomes among 66 adolescents enrolled in a 3-month smoking cessation trial using nicotine replacement and cognitive behavioral therapy. Pretreatment variables included cigarettes per day (CPD), puff volume, puff duration, and several youth-adapted Fagerström-derived questionnaire scores. Outcome measures included prolonged abstinence at end of treatment and point-prevalent abstinence 3 months after the end of the trial. Logistic regression controlling for treatment group showed that increases in baseline CPD (odds ratio, 1.438; 95% confidence interval, 1.051-1.967) and average puff volume (odds ratio, 1.168; 95% confidence interval, 1.030-1.326) predicted continued smoking at the end of treatment. Puff volume (P = 0.013), but not CPD, predicted abstinence at the 3-month follow-up. None of the youth-adapted Fagerström questionnaires predicted outcome on either abstinence measure. If confirmed in a larger sample, our findings suggest that puff topography, and possibly CPD, might predict cessation outcome better than Fagerström scores in adolescent smokers. (Cancer Epidemiol Biomarkers Prev 2006;(15)1:154–7)
Risk Factors Associated with the Development of Intestinal Metaplasia in First-Degree Relatives of Gastric Cancer Patients
Authors: Leung Wai K. , Ng Enders K.W. , Chan Wing Y. , Auyeung Alex C.M. , Chan Kui-fat , Lam Candice C.H. , Chan Francis K.L. , Lau James Y.W. , Sung Joseph J.Y. 
Published: March 2006

Abstract
Family relatives of gastric cancer patients have a higher risk of gastric cancer and premalignant gastric lesions. We sought to determine the risk factors associated with the presence of intestinal metaplasia in a large cohort of gastric cancer relatives. First-degree relatives of gastric cancer patients were invited for screening gastroscopy. Endoscopic gastric biopsies were obtained from the antrum and corpus. Gastric biopsies were analyzed for Helicobacter pylori infection, severity of inflammation, and presence of intestinal metaplasia. Stepwise logistic regressions were used to identify for risk factors associated with presence of intestinal metaplasia in cancer relatives. Two hundred seventy cancer relatives underwent screening endoscopy (median age, 42; 47% male and 48% siblings). Among them, 161 (59.6%) were H. pylori positive and 81 (30%) had confirmed intestinal metaplasia. The following factors were found to be associated with the presence of intestinal metaplasia: age, male sex, H. pylori infection, birth order, alcohol use, siblings with stomach cancer, childhood living conditions, and water supply. Individuals with intestinal metaplasia had more severe acute and chronic inflammation in the antrum and corpus (P &lt; 0.003). With multiple logistic regression, H. pylori infection [odds ratio (OR), 3.23], male gender (OR, 2.09), age (OR, 1.07), and a history of gastric cancer in siblings (OR, 1.91) were independent factors associated with the development of intestinal metaplasia in cancer relatives. In conclusion, we have identified risk factors associated with gastric intestinal metaplasia in stomach cancer relatives, which may be useful in the understanding of gastric carcinogenesis in these high-risk individuals. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2982–6)
Polymorphisms in DNA Repair Genes, Medical Exposure to Ionizing Radiation, and Breast Cancer Risk
Authors: Millikan Robert C. , Player Jon S. , deCotret Allan Rene , Tse Chiu-Kit , Keku Temitope 
Published: March 2006

AbstractAn epidemiologic study was conducted to determine whether polymorphisms in DNA repair genes modify the association between breast cancer risk and exposure to ionizing radiation. Self-reported exposure to ionizing radiation from medical sources was evaluated as part of a population-based, case-control study of breast cancer in African-American (894 cases and 788 controls) and White (1,417 cases and 1,234 controls) women. Genotyping was conducted for polymorphisms in four genes involved in repair of radiation-induced DNA damage, the double-strand break repair pathway: X-ray cross-complementing group 3 (XRCC3) codon 241 Thr/Met, Nijmegen breakage syndrome 1 (NBS1) codon 185 Glu/Gln, X-ray cross-complementing group 2 (XRCC2) codon 188 Arg/His, and breast cancer susceptibility gene 2 (BRCH2) codon 372 Asn/His. Allele and genotype frequencies were not significantly different in cases compared with controls for all four genetic polymorphisms, and odds ratios for breast cancer were close to the null. Combining women with two, three, and four variant genotypes, a positive association was observed between breast cancer and number of lifetime mammograms (Ptrend &lt; 0.0001). No association was observed among women with zero or one variant genotype (P = 0.86). Odds ratios for radiation treatments to the chest and number of lifetime chest X-rays were slightly elevated but not statistically significant among women with two to four variant genotypes. The study has several limitations, including inability to distinguish between diagnostic and screening mammograms or reliably classify prediagnostic mammograms and chest X-rays in cases. Prospective studies are needed to address whether common polymorphisms in DNA repair genes modify the effects of low-dose radiation exposure from medical sources.
Variation of the Killer Cell Immunoglobulin-Like Receptors andHLA-CGenes in Nasopharyngeal Carcinoma
Authors: Butsch Kovacic Melinda , Martin Maureen , Gao Xiaojiang , Fuksenko Tatyana , Chen Chien-Jen , Cheng Yu-Juen , Chen Jen-Yang , Apple Raymond , Hildesheim Allan , Carrington Mary 
Published: March 2006

AbstractNasopharyngeal carcinoma (NPC) is an Epstein-Barrvirus (EBV)-associated malignancy. Previous studies have shown that NPC is associated with specific human leukocyte antigen (HLA) alleles which function in adaptive immunity to present viral and other antigens to the immune system. The role of innate immunity in NPC development is unknown. To determine whether innate immunity is associated with NPC, a case-control study was conducted among 295 Taiwanese NPC cases (99% EBV seropositive) and 252 community controls (29% EBV seropositive). Using high-resolution genotyping, we evaluated the variation of HLA class I alleles and killer cell immunoglobulin-like receptor (KIR) alleles. Located on the surface of natural killer (NK) cells and a subset of T cells, inhibitory KIRs diminish NK cytolysis of target cells upon binding to their HLA class I ligands and activating KIRs are thought to stimulate NK destruction of target cells. Our results suggest that an increasing number of activating KIRs may be associated with increasing NPC risk, particularly in individuals seropositive for anti-EBV antibodies known to be linked to NPC susceptibility (Ptrend = 0.07). Among EBV-seropositive individuals, carriers of ≥5 activating KIRs had a 3.4-fold increased risk of disease (95% confidence interval, 0.74-15.7) compared with individuals with no functional activating KIRs. In contrast, there was no clear evidence of risk associated with increasing numbers of inhibitory KIRs. When evaluating HLA-Cw alleles, we observed that carriers of HLA-Cw*0401 alleles were at a significantly reduced NPC risk (odds ratio, 0.46; 95% confidence intervals, 0.23-0.92), an effect that could not be explained by linkage disequilibrium with other NPC-associated HLA alleles. Our results suggest that KIR-mediated activation may be associated with NPC risk. As this finding is consistent with a recent report examining cervical cancer, a malignancy caused by human papillomavirus, the data raises the possibility that KIRs, and more generally innate immunity, may be involved in the pathogenesis of viral-associated cancers.
Variation of theN-Acetyltransferase 2Gene in a Romanian and a Kyrgyz Population
Authors: Rabstein Sylvia , Unfried Klaus , Ranft Ulrich , Illig Thomas , Kolz Melanie , Rihs Hans-Peter , Mambetova Chinara , Vlad Mariana , Brüning Thomas , Pesch Beate 
Published: March 2006

AbstractAs part of a project on environmental disasters in minority populations, this study aimed to evaluate differences in the sequence of N-acetyltransferase 2 (NAT2) as a metabolic susceptibility gene in yet unexplored ethnicities. Eight single nucleotide polymorphisms (SNP) in the NAT2 coding region and a variant in the 3′ flanking region were analyzed in 290 unrelated Kyrgyz and 140 unrelated Romanians by SNP-specific PCR analysis. The variants 341C, 481T, and 803G were less and 857A more prevalent in Kyrgyz (P &lt; 0.0001). The variant at site 857 indicates Asian descent. 282C&gt;T and 590G&gt;A showed no significant variation by ethnicity. 364G&gt;A and 411A&gt;T turned out to be monomorphic. Database comparisons of the NAT2 minor allele frequencies support that Romanians belong to Caucasians and Kyrgyz are in between Caucasians and East Asians. The distributions of predicted haplotypes differed significantly between the two ethnicities where the Kyrgyz showed a higher genetic diversity. The haplotype without mutations was more common in Kyrgyz (40.1% in Kyrgyz, 29.3% in Romanians). Accordingly, the imputed slow acetylator phenotype was less prevalent in Kyrgyz (35.2% versus 51.4% in Romanians). We found pronounced ethnic differences in NAT2 genotypes with yet unknown effect on the health risks for environmental or occupational exposures in minority populations. (Cancer Epidemiol Biomarkers Prev 2006;(15)1:138–41)
Expression of Vitamin D Receptor and 25-Hydroxyvitamin D3-1α-Hydroxylase in Normal and Malignant Human Colon
Authors: Matusiak Damien , Murillo Genoveva , Carroll Robert E. , Mehta Rajendra G. , Benya Richard V. 
Published: March 2006

Abstract
Considerable evidence exists to support the use of vitamin D to prevent and/or treat colorectal cancer. However, the routine use of bioactive vitamin D, 1,25-dihydroxyvitamin D3, is limited by the side effect of toxic hypercalcemia. Recent studies, however, suggest that colonic epithelial cells express 25-hydroxyvitamin D3-1α-hydroxylase, an enzyme that converts nontoxic pro-vitamin D, 25-hydroxycholecalciferol [25(OH)D3], to its bioactive form. Yet, nothing is known as to the cellular expression of 1α-hydroxylase and the vitamin D receptor (VDR) in the earliest histopathologic structures associated with malignant transformation such as aberrant crypt foci (ACF) and polyps [addressing the possibility of using nontoxic 25(OH)D3 for chemoprevention], nor is anything known as to the expression of these proteins in colorectal cancer as a function of tumor cell differentiation or metastasis [relevant to using 25(OH)D3 for chemotherapy]. In this study, we show that 1α-hydroxylase is present at equal high levels in normal colonic epithelium as in ACFs, polyps, and colorectal cancer irrespective of tumor cell differentiation. In contrast, VDR levels were low in normal colonic epithelial cells; were increased in ACFs, polyps, and well-differentiated tumor cells; and then declined as a function of tumor cell de-differentiation. Both 1α-hydroxylase and VDR levels were negligible in tumor cells metastasizing to regional lymph nodes. Overall, these data support using 25(OH)D3 for colorectal cancer chemoprevention but suggest that pro-vitamin D is less likely to be useful for colorectal cancer chemotherapy.
Reliability and Validity of a Telephone Questionnaire for Estimating Lifetime Personal Sun Exposure in Epidemiologic Studies
Authors: Kricker Anne , Vajdic Claire M. , Armstrong Bruce K. 
Published: March 2006

AbstractOur Australia-wide case-control study of ocular melanoma diagnosed in 1996 to 1997 needed a short telephone interview on sun exposure. We constructed one by examining data from 700 controls ages 40 to 64 years in the Geraldton Skin Cancer Survey in 1988; they had answered a “whole-of-life” questionnaire in a face-to-face interview. Sun exposure in their first 4 decade years of age best predicted their lifetime annual average sun exposure, so the shortened questionnaire asked about sun exposure in these 4 decade years only. Retesting 60 participants 1 year later with the whole-of-life questionnaire gave an intraclass correlation coefficient of 0.65 (95% confidence interval, 0.48-0.78) for ranked total sun exposure between the two interviews; the intraclass correlation coefficient was higher in men (0.73) than in women (0.54). Correlations were also high between parallel measurements of sun exposure on working days in the decade years and in outdoor occupations throughout life in the telephone interview of the ocular melanoma study (Spearman's R = 0.75) and in another study of non-Hodgkin's lymphoma (R = 0.71). Agreement between simultaneous parallel measures of total exposure (nonworking + working day and recreational + occupational exposure) was slightly weaker and of nonworking day and recreational exposure much weaker. Occupational exposure in women was much less strongly correlated with total exposure than it was in men possibly because of their frequently combined work and family roles, which the questionnaires did not try to separate. Research is needed into how this might be done to improve sun exposure measurement in women.
Interest in Testing for Genetic Susceptibility to Lung Cancer among Black College Students “At Risk” of Becoming Cigarette Smokers
Authors: McBride Colleen M. , Lipkus Isaac M. , Jolly David , Lyna Pauline 
Published: March 2006

AbstractReceptivity to genetic testing for lung cancer susceptibility was assessed among African American college freshmen, who held attitudes favorable towards or had experimented with cigarette smoking. Students (n = 95) completed a telephone survey that assessed beliefs about genetics and lung cancer risk, interest in genetic testing, and expectations about the test outcome. Interest in being tested was moderately high (mean, 5; SD, 2.2; scale of 1-7) and highest among those who believed lung cancer was influenced by genetics (r = 0.22, P &lt; 0.05) and those who expected to be at high risk (r = 0.27, P &lt; 0.05). Overall, 34% thought if tested, the result would show high risk for lung cancer. In multivariate analyses, students' test result expectation was the only significant predictor of interest in testing. Those who believed the test would show them to be at higher risk were thrice more likely to be interested in testing than those who thought the test would show that they were at lower risk (odds ratio, 2.99; confidence interval, 1.03-8.64; P = 0.04). Future research is needed to understand how young adults will respond to genetic susceptibility feedback that confirms or contradicts their expectations about personal risks of smoking. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2978–81)
Uptake of the Tobacco-Specific Lung Carcinogen 4-(Methylnitrosamino)-1-(3-pyridyl)-1-Butanone by Moldovan Children
Authors: Stepanov Irina , Hecht Stephen S. , Duca Gheorghe , Mardari Igor 
Published: March 2006

Abstract
The evidence of an association between childhood exposure to environmental tobacco smoke (ETS) and an increased risk of lung cancer is inconsistent. However, taking into account the existing association between lung cancer and adulthood ETS exposure, it is plausible that children exposed to ETS also would be at risk of developing lung cancer later in life. In this study, we investigated the uptake by Moldovan children of the tobacco-specific lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) by measuring total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), the sum of the NNK metabolites, NNAL, and its O-glucuronide and N-glucuronide (NNAL-Glucs) in urine. We also measured urinary cotinine and its glucuronide (total cotinine). Total NNAL was detected in 69 of 80 samples, including those that were low in cotinine (&lt;5 ng/mL). The mean ± SD level of total NNAL (0.09 ± 0.077 pmol/mL) was comparable with those observed in previous studies of children and adults exposed to ETS. Total NNAL correlated with total cotinine (r = 0.8, P &lt; 0.0001). The mean ± SD levels of total NNAL and total cotinine were higher in children who were exposed to ETS (0.1 ± 0.08 and 109 ± 126 pmol/mL, respectively) than in those who were classified as unexposed to ETS based on questionnaire data (0.049 ± 0.016 pmol/mL and 0.043 ± 0.040 nmol/mL). The results of this study for the first time show widespread and considerable uptake of nicotine and the tobacco-specific lung carcinogen NNK in Moldovan children. These results should be useful in heightening the awareness of the dangers of smoking and ETS exposure in this eastern European country. (Cancer Epidemiol Biomarkers Prev 2006;15(1):7–11)
Evaluating Bias due to Population Stratification in Epidemiologic Studies of Gene-Gene or Gene-Environment Interactions
Authors: Wang Yiting , Localio Russell , Rebbeck Timothy R. 
Published: March 2006

Abstract
Confounding by ethnicity (i.e. population stratification) can result in bias and incorrect inferences in genotype-disease association studies, but the effect of population stratification in gene-gene or gene-environment interaction studies has not been addressed. We used logistic regression models to fit multiplicative interactions between two dichotomous variables that represented genetic and/or environmental factors for a binary disease outcome in a hypothetical cohort of multiple ethnicities. Biases in main effects and interactions due to population stratification were evaluated by comparing regression coefficients in mis-specified models that ignored ethnicities with their counterparts in models that accounted for ethnicities. We showed that biases in main effects and interactions were constrained by the differences in disease risks across the ethnicities. Therefore, large biases due to population stratification are not possible when baseline disease risk differences among ethnicities are small or moderate. Numerical examples of biases in genotype-genotype and/or genotype-environment interactions suggested that biases due to population stratification for main effects were generally small but could become large for studies of interactions, particularly when strong linkage disequilibrium between genes or large correlations between genetic and environmental factors existed. However, when linkage disequilibrium among genes or correlations among genes and environments were small, biases to main effects or interaction odds ratios were small to nonexistent. (Cancer Epidemiol Biomarkers Prev 2006;15(1):124–32)
Androgen Receptor and Prostate-Specific Antigen Gene Polymorphisms and Breast Cancer in African-American Women
Authors: Wang Wei , John Esther M. , Ingles Sue Ann 
Published: March 2006

AbstractSeveral previous studies have found the CAG repeat polymorphism in exon 1 of the androgen receptor (AR) gene to be associated with breast cancer risk among some groups of Caucasian and Asian women. In a population-based case-control study of 488 African-American women (239 cases and 249 controls), we examined this polymorphism along with a polymorphism (−158 G/A) in an androgen-regulated gene (PSA) whose expression has been correlated with breast cancer prognosis. Overall, we did not observe any significant association between the CAG repeat polymorphism and breast cancer risk. However, among women with a first-degree family history of breast cancer, longer CAG repeats were associated with a significantly increased risk. Women carrying at least one longer allele [(CAG)n ≥ 22] had a 3-fold increased risk compared to those with two shorter alleles (odds ratio, 3.18; 95% confidence interval, 1.08-9.36). There was no significant association between the PSA gene polymorphism and breast cancer risk, nor was there significant gene-gene interaction. In summary, our results further support that shorter CAG repeats (stronger AR transactivation activity) may reduce the risk of breast cancer, at least among some groups of women. Our data, however, are unable to provide evidence that PSA is the pathway through which the protective effect of androgens operates. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2990–4)
A Randomized Controlled Trial of Financial Incentives for Smoking Cessation
Authors: Volpp Kevin G. , Gurmankin Levy Andrea , Asch David A. , Berlin Jesse A. , Murphy John J. , Gomez Angela , Sox Harold , Zhu Jingsan , Lerman Caryn 
Published: March 2006

Abstract
Background: Although 435,000 Americans die each year of tobacco-related illness, only ∼3% of smokers quit each year. Financial incentives have been shown to be effective in modifying behavior within highly structured settings, such as drug treatment programs, but this has not been shown in treating chronic disease in less structured settings. The objective of this study was to determine whether modest financial incentives increase the rate of smoking cessation program enrollment, completion, and quit rates in a outpatient clinical setting.
Methods: 179 smokers at the Philadelphia Veterans Affairs Medical Center who reported smoking at least 10 cigarettes per day were randomized into incentive and nonincentive groups. Both groups were offered a free five-class smoking cessation program at the Philadelphia Veterans Affairs Medical Center. The incentive group was also offered $20 for each class attended and $100 if they quit smoking 30 days post program completion. Self-reported smoking cessation was confirmed with urine cotinine tests.
Results: The incentive group had higher rates of program enrollment (43.3% versus 20.2%; P &lt; 0.001) and completion (25.8% versus 12.2%; P = 0.02). Quit rates at 75 days were 16.3% in the incentive group versus 4.6% in the control group (P = 0.01). At 6 months, quit rates in the incentive group were not significantly higher (6.5%) than in the control group (4.6%; P &gt; 0.20).
Conclusion: Modest financial incentives are associated with significantly higher rates of smoking cessation program enrollment and completion and short-term quit rates. Future studies should consider including an incentive for longer-term cessation. (Cancer Epidemiol Biomarkers Prev 2006;15(1):12–8)