bluuebunny/crossref_metadata_2025_split huggingface dataset:
APC Asp1822Val and Gly2502Ser Polymorphisms and Risk of Colorectal Cancer and Adenoma
Authors: Tranah Gregory J. , Giovannucci Edward , Ma Jing , Fuchs Charles , Hunter David J. 
Published: September 2005

Abstract
Mutation of the adenomatous polyposis coli (APC) tumor suppressor gene is an important initiating factor in the early stages of the adenoma-carcinoma sequence. The aim of this study was to investigate the two most common APC variants (Asp1822Val and Gly2502Ser) and their association with colorectal cancer and adenoma and whether these relationships are influenced by dietary and lifestyle factors. We analyzed 556 adenoma cases and 557 matched controls and 197 cancer cases and 490 matched controls nested within the Nurses' Health Study cohort, 274 cancer cases and 456 matched controls nested within the Physicians' Health Study cohort, and 375 adenoma cases and 724 matched controls nested within the Health Professionals Follow-up Study cohort. APC Asp1822Val and Gly2502Ser polymorphisms were not associated with risk of colorectal cancer or adenoma. For colorectal cancer, a significant interaction was found between Asp1822Val genotype and postmenopausal hormone (PMH) use among postmenopausal women (Pinteraction = 0.03). Current PMH use was associated with reduced risk overall and a statistically significant lower risk of colorectal cancer among carriers of one or two copies of the APC 1822Val allele (relative risk, 0.46; 95% confidence interval, 0.24-0.88) relative to wild-type never or past PMH users. Our results suggest that cigarette smoking, alcohol intake, and family history of colorectal cancer were positively associated and regular aspirin intake was inversely associated with colorectal adenoma in men and women. No gene-environment interactions were observed with these risk factors or with other dietary risk factors previously hypothesized to interact with the APC Asp1822Val polymorphism.
The Association of XRCC1 Haplotypes and Chromosomal Damage Levels in Peripheral Blood Lymphocyte among Coke-Oven Workers
Authors: Leng Shuguang , Cheng Juan , Zhang Linyuan , Niu Yong , Dai Yufei , Pan Zufei , Li Bin , He Fengsheng , Zheng Yuxin 
Published: September 2005

Abstract
Theoretically, a haplotype has a higher level of heterozygosity than individual single nucleotide polymorphism (SNP) and the association study based on the haplotype may have an increased power for detecting disease associations compared with SNP-based analysis. In this study, we investigated the effects of four haplotype-tagging SNPs (htSNP) and the inferred haplotype pairs of the X-ray cross-complementing group 1 (XRCC1) gene on chromosome damage detected by the cytokinesis-block micronucleus assay. The study included 141 coke-oven workers with exposure to a high level of polycyclic aromatic hydrocarbons and 66 nonexposed controls. The frequencies of total MN and MNed cells were borderline associated with the Arg194Trp polymorphism (P = 0.053 and P = 0.050, respectively) but not associated with the Arg280His, Arg399Gln and Gln632Gln polymorphisms among coke-oven workers. Five haplotypes, including CGGG, TGGG, CAGG, CGAG, and CGGA, were inferred based on the four htSNPs of XRCC1 gene. The haplotype CGGG was associated with the decreased frequencies of total MN and MNed cells, and the haplotypes TGGG and CGAG were associated with the increased frequencies of total MN and MNed cells with adjustment for covariates among coke-oven workers. This study showed that the haplotypes derived from htSNPs in the XRCC1 gene were more likely than single SNPs to correlate with the polycyclic aromatic hydrocarbon–induced chromosome damage among coke-oven workers.
Cigarette Smoking and Risk of Non-Hodgkin Lymphoma: A Pooled Analysis from the International Lymphoma Epidemiology Consortium (InterLymph)
Authors: Morton Lindsay M. , Hartge Patricia , Holford Theodore R. , Holly Elizabeth A. , Chiu Brian C.H. , Vineis Paolo , Stagnaro Emanuele , Willett Eleanor V. , Franceschi Silvia , La Vecchia Carlo , Hughes Ann Maree , Cozen Wendy , Davis Scott , Severson Richard K. , Bernstein Leslie , Mayne Susan T. , Dee Fred R. , Cerhan James R. , Zheng Tongzhang 
Published: September 2005

Abstract
Background: The International Lymphoma Epidemiology Consortium (InterLymph) provides an opportunity to analyze the relationship between cigarette smoking and non-Hodgkin lymphoma with sufficient statistical power to consider non-Hodgkin lymphoma subtype. The results from previous studies of this relationship have been inconsistent, likely due to the small sample sizes that arose from stratification by disease subtype. To clarify the role of cigarette smoking in the etiology of non-Hodgkin lymphoma, we conducted a pooled analysis of original patient data from nine case-control studies of non-Hodgkin lymphoma conducted in the United States, Europe, and Australia.
Methods: Original data were obtained from each study and uniformly coded. Risk estimates from fixed-effects and two-stage random-effects models were compared to determine the impact of interstudy heterogeneity. Odds ratios (OR) and 95% confidence intervals (95% CI) were derived from unconditional logistic regression models, controlling for study center, age, sex, and race.
Results: In our pooled study population of 6,594 cases and 8,892 controls, smoking was associated with slightly increased risk estimates (OR, 1.07; 95% CI, 1.00-1.15). Stratification by non-Hodgkin lymphoma subtype revealed that the most consistent association between cigarette smoking and non-Hodgkin lymphoma was observed among follicular lymphomas (n = 1452). Compared with nonsmokers, current smokers had a higher OR for follicular lymphoma (1.31; 95% CI, 1.12-1.52) than former smokers (1.06; 95% CI, 0.93-1.22). Current heavy smoking (≥36 pack-years) was associated with a 45% increased OR for follicular lymphoma (1.45; 95% CI, 1.15-1.82) compared with nonsmokers.
Conclusions: Cigarette smoking may increase the risk of developing follicular lymphoma but does not seem to affect risk of the other non-Hodgkin lymphoma subtypes we examined. Future research is needed to determine the biological mechanism responsible for our subtype-specific results.
Variation in Plasma Insulin-Like Growth Factor-1 and Insulin-Like Growth Factor Binding Protein-3: Genetic Factors
Authors: Morimoto Libby M. , Newcomb Polly A. , White Emily , Bigler Jeannette , Potter John D. 
Published: September 2005

Abstract
Insulin-like growth factors (IGFs) play key roles in cell proliferation and apoptosis. Whereas relatively stable within individuals, IGFs vary substantially between individuals, and a large component of this variation may be determined by genetic factors. Several polymorphisms in IGF genes have been identified, although their functional significance is not clear. We evaluated the association of polymorphisms in IGF-1 and IGFBP-3 and circulating levels of IGF-1 and IGFBP-3 in 323 population-based control subjects enrolled in a case-control study of colorectal cancer from September 1999 through February 2002. Total IGF-1 and IGFBP-3 levels were measured using ELISA assays, and all subjects were genotyped for a microsatellite polymorphism in IGF-1 and a single nucleotide polymorphism in IGFBP-3. Multiple linear regression was used to assess the association of genotype with circulating IGFs. IGF-1 levels were unrelated to either polymorphism. IGFBP-3 was significantly associated with IGFBP-3 genotype, with IGFBP-3 levels increasing from CC (1,895 ng/mL) → GC (2,029 ng/mL) → GG (2,182 ng/mL), (p-trend &lt; 0.001). Having an IGF-1 genotype other than homozygous for the 19-repeat allele was associated with higher IGFBP-3 levels (1,945 versus 2,052 ng/mL). Furthermore, both IGF-1 and IGFBP-3 genotypes modified the relationship between postmenopausal hormone use and IGFs. This analysis provides evidence that common variation in IGF genes may contribute to the variation in circulating levels observed between individuals.
Mortality From Lung Cancer and Tobacco Smoking in Ohio (U.S.): Will Increasing Smoking Prevalence Reverse Current Decreases in Mortality?
Authors: Tyczynski Jerzy E. , Berkel Hans J. 
Published: September 2005

Abstract
Background: Despite significant changes in smoking patterns within the past few decades, lung cancer remains a major cause of cancer deaths in many developed countries in people of each sex, and one of the most important public health issues. The study aims to analyze the possible impact of changes in tobacco smoking practices in the state of Ohio (U.S.) on current and future trends and patterns of lung cancer mortality.
Materials and Methods: Mortality rates from lung cancer were calculated for the period 1970 to 2001 on the basis of data from the National Center for Health Statistics. The Joinpoint regression approach was used to evaluate changes in time trends by sex, age, and race. Data on smoking prevalence in Ohio were retrieved from the Centers for Disease Control and Prevention website.
Results: Lung cancer mortality rates in Ohio have declined among men of all ages as well as in specific age groups in the 1990s, and the rate of increase among middle-aged and elderly women has dropped over time. The mortality rate among young women (ages 20-44) began to increase during the early 1990s. The prevalence of smoking in Ohio has increased since the early 1990s, especially among young persons.
Conclusions: Recent trends in tobacco smoking in Ohio indicate that the declining trends in lung cancer mortality might be reversed in the future. An early indicator of possible change is the recent increase in mortality among young women. Implementation of the Ohio Comprehensive Tobacco Use Prevention Strategic Plan might help to disseminate proven prevention strategies among the inhabitants of Ohio and might thus prevent future increases in lung cancer mortality rates in the state.
Insulin-Like Growth Factor-I, IGF-Binding Protein-3, and Mammographic Breast Density
Authors: Diorio Caroline , Pollak Michael , Byrne Celia , Mâsse Benoît , Hébert-Croteau Nicole , Yaffe Martin , Coté Gary , Bérubé Sylvie , Morin Carol , Brisson Jacques 
Published: September 2005

AbstractSome studies have suggested that insulin-like growth factor (IGF) pathway is related to premenopausal breast density, one of the strongest known breast cancer risk factors. This study was designed specifically to test the hypothesis that higher levels of IGF-I and lower levels of IGF-binding protein (IGFBP)-3 are associated with high mammographic breast density among premenopausal but not among postmenopausal women. A total of 783 premenopausal and 791 postmenopausal healthy women were recruited during screening mammography examinations. Blood samples were collected at the time of mammography, and plasma IGF-I and IGFBP-3 levels were measured by ELISA. Mammographic breast density was estimated using a computer-assisted method. Spearman's partial correlation coefficients (rs) were used to evaluate the associations. Adjusted mean breast density was assessed by joint levels of IGF-I and IGFBP-3 using generalized linear models. Among premenopausal women, high levels of IGF-I and low levels of IGFBP-3 were independently correlated with high breast density (rs = 0.083; P = 0.021 and rs = −0.124; P = 0.0005, respectively). Correlation of IGF-I with breast density was stronger among women in the lowest tertile of IGFBP-3 than among those in the highest tertile of IGFBP-3 (rs = 0.138; P = 0.027 and rs = −0.039; P = 0.530, respectively). In contrast, the correlation of IGFBP-3 with breast density was stronger among women in the highest tertile of IGF-I than among those in the lowest tertile of IGF-I (rs = −0.150; P = 0.016 and rs = −0.008; P = 0.904, respectively). Women in the combined top tertile of IGF-I and bottom tertile of IGFBP-3 had higher mean breast density than those in the combined bottom tertile of IGF-I and top tertile of IGFBP-3 (53.8% versus 40.9%; P = 0.014). No significant association was observed among postmenopausal women. Our findings confirm that IGF-I and IGFBP-3 are associated with breast density among premenopausal women. They provide additional support for the idea that, among premenopausal women, these growth factors may affect breast cancer risk, at least in part, through their influence on breast tissue morphology as reflected on mammogram.
Response Rates to a Mailed Survey Targeting Childhood Cancer Survivors: A Comparison of Conditional versus Unconditional Incentives
Authors: Rosoff Philip M. , Werner Cary , Clipp Elizabeth C. , Guill Ann Bebe , Bonner Melanie , Demark-Wahnefried Wendy 
Published: September 2005

Abstract
Objective: Mailed surveys are widely used to collect epidemiologic and health service data. Given that nonresponse can threaten the validity of surveys, modest incentives are often used to increase response rates. A study was undertaken among childhood cancer survivors and their parents to determine if response rate to a mailed survey differed with provision of immediate versus delayed incentives.
Design: A self-administered survey designed to ascertain health behaviors was mailed to 397 childhood cancer survivors (and their parents if the survivor was &lt;18 years of age). Subjects were randomized into two groups based on gender, age, race, and cancer type. One group received a $10 incentive with their blank survey (unconditional incentive), whereas the other group received the incentive upon receipt of their completed survey (conditional incentive). If children were minors, both the parent and the child received incentives.
Results: No significant differences in response rates were observed with respect to gender, age, race, or cancer type. However, significant differences in response rates were observed between incentive groups, with unconditional incentives yielding significantly higher response rates than conditional incentives for child survivors who were ≥18 years (64.4% versus 49.0%), as well as younger child survivors (62.5% versus 43.6%) and their parents (64.8% versus 41.5%; all P &lt; 0.05).
Conclusions: The provision of an immediate incentive generated significantly higher response rates to this mailed health survey among childhood cancer survivors and their parents. Given that survey studies are commonly conducted across various pediatric populations, these findings may help inform the design of future pediatric survey research.
Mammographic Features and Subsequent Risk of Breast Cancer: A Comparison of Qualitative and Quantitative Evaluations in the Guernsey Prospective Studies
Authors: Torres-Mejía Gabriela , De Stavola Bianca , Allen Diane S. , Pérez-Gavilán Juan J. , Ferreira Jorge M. , Fentiman Ian S. , dos Santos Silva Isabel 
Published: September 2005

Abstract
Mammographic features are known to be associated with breast cancer but the magnitude of the effect differs markedly from study to study. Methods to assess mammographic features range from subjective qualitative classifications to computer-automated quantitative measures. We used data from the UK Guernsey prospective studies to examine the relative value of these methods in predicting breast cancer risk. In all, 3,211 women ages ≥35 years who had a mammogram taken in 1986 to 1989 were followed-up to the end of October 2003, with 111 developing breast cancer during this period. Mammograms were classified using the subjective qualitative Wolfe classification and several quantitative mammographic features measured using computer-based techniques. Breast cancer risk was positively associated with high-grade Wolfe classification, percent breast density and area of dense tissue, and negatively associated with area of lucent tissue, fractal dimension, and lacunarity. Inclusion of the quantitative measures in the same model identified area of dense tissue and lacunarity as the best predictors of breast cancer, with risk increasing by 59% [95% confidence interval (95% CI), 29-94%] per SD increase in total area of dense tissue but declining by 39% (95% CI, 53-22%) per SD increase in lacunarity, after adjusting for each other and for other confounders. Comparison of models that included both the qualitative Wolfe classification and these two quantitative measures to models that included either the qualitative or the two quantitative variables showed that they all made significant contributions to prediction of breast cancer risk. These findings indicate that breast cancer risk is affected not only by the amount of mammographic density but also by the degree of heterogeneity of the parenchymal pattern and, presumably, by other features captured by the Wolfe classification.
Association of Breast Cancer Risk with a Common Functional Polymorphism (Asp327Asn) in the Sex Hormone–Binding Globulin Gene
Authors: Cui Yong , Shu Xiao-Ou , Cai Qiuyin , Jin Fan , Cheng Jia-Rong , Cai Hui , Gao Yu-Tang , Zheng Wei 
Published: September 2005

Abstract
Sex hormones play a central role in the development of breast cancer. Sex hormone–binding globulin (SHBG) modulates the bioavailability of circulating sex hormones and regulates their signaling system in the breast tissue. We evaluated the association of a common functional polymorphism (Asp327Asn) in the SHBG gene with breast cancer risk in a population-based case-control study (1,106 cases and 1,180 controls) conducted in Shanghai, China. The variant Asn allele was associated with a reduced breast cancer risk in postmenopausal women [odds ratio (OR), 0.73; 95% confidence interval (95% CI), 0.53-0.99], but not in premenopausal women (OR, 1.03; 95% CI, 0.82-1.27). The protective association was much stronger in postmenopausal women with a low body mass index (BMI; OR, 0.46; 95% CI, 0.29-0.75) or waist-to-hip ratio (OR, 0.51; 95% CI, 0.32-0.83) than those with a high BMI or waist-to-hip ratio (P for interaction &lt; 0.05). Furthermore, the association was stronger for estrogen receptor–positive (OR, 0.64; 95% CI, 0.42-0.98) than for estrogen receptor–negative breast cancer (OR, 0.85; 95% CI, 0.50-1.45). Among postmenopausal controls, blood SHBG levels were 10% higher in carriers of the variant Asn allele than noncarriers (P = 0.06). Postmenopausal control women with the Asn allele and low BMI or waist-to-hip ratio had 20% higher SHBG levels (P &lt; 0.05). This study suggests that the Asn allele in the SHBG gene may be related to a reduced risk of breast cancer among postmenopausal women by increasing their blood SHBG levels.
Childhood and Adult Cancer in Twins: Evidence from the Utah Genealogy
Authors: Neale Rachel E. , Mineau Geraldine , Whiteman David C. , Brownbill Pat A. , Murphy Michael F.G. 
Published: September 2005

AbstractObjective: Evidence suggests that the in utero environment may contribute to subsequent development of cancers in childhood and adulthood. Raised levels of estrogen during pregnancy may be the primary in utero etiologic factor. Mothers of twins have higher estrogen levels during pregnancy than mothers of singletons, therefore, assessment of cancer risk in twins may be informative.Method: We conducted a retrospective cohort study of cancer among twin and singleton newborns selected from the Utah Population Database, matched on birth year and sex. Cancer diagnoses were determined by linkage with the Utah state cancer register. Relative rates of all cancers in childhood and in adulthood in twins compared with singletons, and for specific cancers including testicular, breast and melanoma, were calculated using Poisson regression.Results: Twin (35,271) and singleton (74,199) births were identified, among whom there were 336 and 691 cancer diagnoses, respectively. The relative risk (RR) of childhood cancer in twins compared with singletons was 0.82 [95% confidence interval (CI) 0.55-1.24] and of adult cancer was 1.06 (0.92-1.22). We found nonsignificant increases in risk among adult twins for cancers of the breast, prostate, testis, lymphatic system, thyroid, and large bowel. The largest departures from unity were for testicular cancer (RR 1.47; 95% CI, 0.73-2.95) and melanoma (RR 0.67; 95% CI, 0.42-1.06).Conclusions: These results are consistent with the body of evidence suggesting that twins have a reduced risk of cancer in childhood. Although there is no overall differential in adult cancer risk, these data support the hypothesis that the in utero environment may play an important role in specific cancers.
Association of Genetic Polymorphisms with Serum Estrogens Measured Multiple Times During a 2-Year Period in Premenopausal Women
Authors: Lurie Galina , Maskarinec Gertraud , Kaaks Rudolf , Stanczyk Frank Z. , Le Marchand Loïc 
Published: September 2005

Abstract
There is evidence that circulating estrogens are associated with breast cancer risk. In this study of premenopausal women, we explored the association of polymorphisms in genes in the estrogen synthesis and metabolism pathways with serum and urinary levels of estrone (E1) and estradiol (E2) and with the urinary ratio of 2-hydroxyestrone (2-OHE1)/16α-hydroxyestrone (16α-OHE1). This analysis included 220 women, who were participants in a 2-year randomized soy intervention. Blood specimens were collected in the luteal phase of the menstrual cycle an average of 4.4 times over 2 years. Overnight urinary specimens were collected on the same cycle day, only at baseline. Levels of E1, E2, 2-OHE1, and 16α-OHE1 were measured by enzyme immunoassays. The DNA samples were analyzed by PCR/RFLP for the COMT Val158Met, CYP1A1*2A, CYP1A1*2B, CYP1A2*1F, CYP1B1 Val432Leu, and CYP17 T27C polymorphisms. We applied mixed models to investigate the relations between genotypes and repeated serum hormone measurements and generalized linear models to assess associations between genotypes and urinary estrogen metabolites. The CYP1A2 C allele was significantly associated with lower serum E2 levels; in CC genotype carriers, serum E2 levels were 26.3% lower than in homo- and heterozygous common allele carriers combined (P = 0.01). CYP1A2*1F also affected the urinary 2-OHE1/16α-OHE1 ratio; carriers of the variant C allele had a markedly lower ratio than individuals with the AA genotype (1.37 versus 1.76; P = 0.002). These data suggest that CYP1A2*1F is associated with lower circulating levels of E2, and that it may be a susceptibility locus for breast cancer.