bluuebunny/crossref_metadata_2025_split huggingface dataset:
Genetic Variation in XPD, Sun Exposure, and Risk of Skin Cancer
Authors: Han Jiali , Colditz Graham A. , Liu Jun S. , Hunter David J. 
Published: September 2005

Abstract
The XPD gene is involved in the nucleotide excision repair pathway removing DNA photoproducts induced by UV radiation. Genetic variation in XPD may exert a subtle effect on DNA repair capacity. We assessed the associations between two common nonsynonymous polymorphisms (Asp312Asn and Lys751Gln) with skin cancer risk in a nested case-control study within the Nurses' Health Study (219 melanoma, 286 squamous cell carcinoma, 300 basal cell carcinoma, and 874 controls) along with exploratory analysis on the haplotype structure of the XPD gene. There were inverse associations between the Lys751Gln and Asp312Asn polymorphisms and the risks of melanoma and squamous cell carcinoma. No association was observed between these two polymorphisms and basal cell carcinoma risk. We also observed that the association of the 751Gln allele with melanoma risk was modified by lifetime severe sunburns, cumulative sun exposure with a bathing suit, and constitutional susceptibility score (P for interaction = 0.03, 0.04, and 0.02 respectively). Similar interactions were also observed for the Asp312Asn. Our data suggest these two XPD nonsynonymous polymorphisms may be associated with skin cancer risk, especially for melanoma.
Association of an Exon 1 Polymorphism in theIGFBP3Gene with Circulating IGFBP-3 Levels and Colorectal Cancer Risk: The Multiethnic Cohort Study
Authors: Le Marchand Loïc , Kolonel Laurence N. , Henderson Brian E. , Wilkens Lynne R. 
Published: September 2005

AbstractLaboratory and seroepidemiologic studies have suggested that insulin-like growth factor binding protein-3 (IGFBP-3), the main binding protein for IGF-I, may be protective against colorectal cancer. We investigated the association of two polymorphisms (A-202C and G2133C) in the IGFBP3 gene with plasma IGF hormone levels among 887 randomly selected participants in the Multiethnic Cohort study. We found that these two genetic variants were in strong linkage disequilibrium and were both inversely associated with plasma IGFBP-3. However, the effect on plasma IGFBP-3 levels was stronger for the G2133C variant than the A-202C variant. Thus, we assessed the colorectal cancer risk associated with the G2133C in a case-control study of 817 cases and 1,995 controls nested within the Multiethnic Cohort study. Under the assumption of dominant genetic model, carriers of the 1233C allele were at 32% increased risk of colorectal cancer [95 % confidence interval (95% CI) for the odds ratio (OR), 1.07-1.62] and that this effect seemed stronger for the rectum (OR for the C allele, 1.95; 95% CI, 1.35-2.83) than the colon (OR, 1.16; 95% CI, 0.92-1.45). These data suggest that the exon 1 G2133C missense variant in IGFBP3 may be a susceptibility factor for colorectal cancer.
Age-Specific Incidence Rates of In situ Breast Carcinomas by Histologic Type, 1980 to 2001
Authors: Li Christopher I. , Daling Janet R. , Malone Kathleen E. 
Published: September 2005

Abstract
Incidence rates of ductal carcinoma in situ (DCIS) and lobular carcinoma in situ (LCIS) have increased rapidly over the past several decades largely due to the increased use of mammography. However, recent data from 1987 to 1999 indicate that invasive ductal carcinoma incidence rates have remained essentially constant, whereas rates of invasive lobular carcinoma have increased 65%, with greater increases observed among postmenopausal women. Data on recent trends in DCIS and LCIS incidence rates, particularly age-specific trends, are lacking. We evaluated trends in the incidence rates of DCIS overall, noncomedo DCIS, comedo DCIS, and LCIS using data from nine Surveillance, Epidemiology, and End Results cancer registries. DCIS incidence rates increased 7.2-fold [95% confidence interval (95% CI), 6.8-7.7] from 1980 to 2001, 1.8-fold (95% CI, 1.7-1.9) over the past 10 years (1992-2001), and 1.1-fold (95% CI, 1.0-1.2) over the past 5 years (1997-2001). The magnitudes of these increases were highest among women ages ≥50 years. Furthermore, over the past 10- and 5-year periods, rates of noncomedo DCIS have generally increased across all age groups, whereas rates of comedo DCIS held constant or decreased. LCIS incidence rates increased 2.6-fold (95% CI, 2.3-2.9) from 1980 to 2001, 1.3-fold (95% CI, 1.2-1.5) over the past 10 years, and 1.1-fold (95% CI, 1.0-1.3) over the past 5 years. Similar to invasive lobular carcinoma, but unlike invasive ductal carcinoma, incidence rates of both DCIS and LCIS continue to increase in the United States primarily among older women. These trends present important public health and clinical challenges.
Dietary Benzo[a]Pyrene Intake and Risk of Colorectal Adenoma
Authors: Sinha Rashmi , Kulldorff Martin , Gunter Marc J. , Strickland Paul , Rothman Nathaniel 
Published: September 2005

Abstract
We carried out a clinic-based case-control study specifically designed to address the hypothesis that dietary intake of polycyclic aromatic hydrocarbons (PAH) is associated with colorectal adenoma risk. We developed a food frequency questionnaire with detailed questions on meat-cooking methods and doneness levels and a benzo[a]pyrene (BaP) database (as a surrogate for total carcinogenic PAHs) based on the collection and analysis of a wide range of food samples. We estimated BaP intake derived from meat and from all foods to test its relationship with risk of colorectal adenomas. The median (10th and 90th percentiles) BaP intake in controls was 5 ng/d (0.2 and 66 ng/d) estimated from meat and 73 ng/d (35 and 140 ng/d) from all foods. In cases, median BaP intake was 17 ng/d (0.5 and 101 ng/d) from meat and 76 ng/d (44 and 163 ng/d) from all foods. Multivariate analysis was carried out on 146 cases and 228 controls. The odds ratios (95% confidence interval) for dietary BaP from meat with the first quintile as the reference group were 1.19 (0.51-2.80) for the second quintile, 1.71 (0.76-3.83) for the third quintile, 2.16 (0.96-4.86) for the fourth quintile, and 2.82 (1.24-6.43) for the fifth quintile (Ptrend = 0.01). Increased risk of colorectal adenomas was more strongly associated with BaP intake estimated from all foods: 2.61 (1.08-6.29) for the second quintile, 4.21 (1.79-9.91) for the third quintile, 2.45 (0.98-6.12) for the fourth quintile, and 5.60 (2.20-14.20) for the fifth quintile (Ptrend = 0.002). This study provides evidence that dietary BaP plays a role in colorectal adenoma etiology.
Pregnancy Hormone Concentrations Across Ethnic Groups: Implications for Later Cancer Risk
Authors: Potischman Nancy , Troisi Rebecca , Thadhani Ravi , Hoover Robert N. , Dodd Kevin , Davis William W. , Sluss Patrick M. , Hsieh Chung-Cheng , Ballard-Barbash Rachel 
Published: September 2005

Abstract
A variety of in utero factors have been associated with risk of adult cancers, particularly birth weight, toxemia, and gestational age. These factors are thought to reflect hormonal exposures during pregnancy. We hypothesized that the prenatal hormonal milieu may explain part of the variation in cancer rates across ethnic groups, for example, the higher incidence of breast cancer in the Caucasian compared with Hispanic women and the higher incidence of prostate and lower incidence of testicular cancers among African-Americans compared with Caucasians. We measured hormones in early pregnancy blood samples from three ethnic groups in a health care plan in Boston, MA. Mean levels of androstenedione, testosterone, estrone, and prolactin were significantly lower in Caucasian women compared with Hispanic women. Although not statistically significant, estradiol levels were lower in Caucasian compared with Hispanic or African-American women. Concentrations of androstenedione, testosterone, and progesterone were notably higher in African-American compared with Caucasian or Hispanic women. These data are consistent with hypotheses that in utero hormonal exposures may explain some of the ethnic group differences in cancer risk.
Endometrial Cancer Incidence Trends in Europe: Underlying Determinants and Prospects for Prevention
Authors: Bray Freddie , dos Santos Silva Isabel , Moller Henrik , Weiderpass Elisabete 
Published: September 2005

Abstract
More than one in 20 female cancers in Europe are of the endometrium. Surveillance of incidence rates is imperative given the rapidly changing profile in the prevalence and distribution of the underlying determinants. This study presents an analysis of observed and age-period-cohort–modeled trends in 13 European countries. There were increasing trends among postmenopausal women in many Northern and Western countries. Denmark and possibly France and Switzerland were exceptions, with decreasing trends in postmenopausal women. In premenopausal and perimenopausal women, declines were observed in Northern and Western Europe, most evidently in Denmark, Sweden, and the United Kingdom, affecting consecutive generations born after 1925. These contrast with the increasing trends regardless of menopausal age in some Southern and Eastern European countries, particularly Slovakia and Slovenia. These observations provide evidence of changes in several established risk factors over time and have implications for possible primary prevention strategies. In postmenopausal women, changes in reproductive behavior and prevalence of overweight and obesity may partially account for the observed increases, as well as hormone replacement therapy use in certain countries. Combined oral contraceptive use may be responsible for the declines observed among women aged &lt;55 years. Whereas there are some prospects for chemoprevention in premenopausal women as oral contraceptive use becomes more widespread in Europe, increases in obesity and decreases in fertility imply that endometrial cancer in postmenopausal women will become a more substantial public health problem in the future.
The Role of Cytokine Gene Polymorphisms in Colorectal Cancer and Their Interaction with Aspirin Use in the Northeast of Scotland
Authors: Macarthur Mairi , Sharp Linda , Hold Georgina L. , Little Julian , El-Omar Emad M. 
Published: September 2005

AbstractThe reduced risk of colorectal cancer associated with cyclooxygenase enzyme inhibitors, such as aspirin and other nonsteroidal anti-inflammatory drugs, strongly suggests that chronic inflammation is a key mediator in the development of colorectal cancer. This complements recent molecular evidence demonstrating an association between a number of proinflammatory genetic polymorphisms and risk of colorectal cancer. We assessed polymorphisms in the IL-1, IL-10, TNF-A, and TGF-B genes in a population-based case-control study of colorectal cancer cases (n = 264) and frequency-matched controls (n = 408) in the Northeast of Scotland and analyzed their interaction with regular aspirin use. There was no evidence of a relation between any of the individual polymorphisms, or pairs of polymorphisms, and risk of colorectal cancer. There was a significant interaction between the IL-10-592 C/A polymorphism and aspirin use (Pinteraction = 0.03). Carriers of the variant IL-10-592 (A) allele, who produce less of the anti-inflammatory cytokine interleukin-10, had a statistically significant 50% reduced risk of colorectal cancer when taking regular aspirin (odds ratio, 0.5; 95% confidence interval, 0.25-0.97), whereas risk was not reduced in carriers of the A allele who did not use aspirin, or among aspirin users with the CC genotype. It is possible that carriers of the mutant IL-10-592 allele are more likely to derive anti-inflammatory and chemopreventive benefits from aspirin in the presence of a lower production of their own endogenous anti-inflammatory interleukin-10. These results suggest that host genetics may play a role in predicting response to chemopreventive strategies. Confirmation of these findings in other populations is required.
Role of Cytokine Polymorphisms in the Risk of Distal Gastric Cancer Development
Authors: Perez-Perez Guillermo I. , Garza-Gonzalez Elvira , Portal Cynthia , Olivares Asalia Z. 
Published: September 2005

Abstract
We review the current information concerning the role of cytokine polymorphisms and the risk of develop distal gastric cancer in different populations. We have included populations colonized with Helicobacter pylori as well as populations without colonization. We found that the study of polymorphisms alone seems insufficient to assess gastric cancer risk and it is necessary to examine environmental factors in different ethnic groups and geographic areas along with the study of H. pylori strains to define better the risk factors associated with distal gastric cancer.
5,10-Methylenetetrahydrofolate Reductase Polymorphisms and the Risk of Pancreatic Cancer
Authors: Li Donghui , Ahmed Maha , Li Yanan , Jiao Li , Chou Ta-Hsu , Wolff Robert A. , Lenzi Renato , Evans Douglas B. , Bondy Melissa L. , Pisters Peter W. , Abbruzzese James L. , Hassan Manal M. 
Published: September 2005

Abstract
To test the hypothesis that 5,10-methylenetetrahydrofolate reductase (MTHFR) polymorphisms modify the risk of pancreatic cancer, we conducted a hospital-based, case-control study involving 347 patients with newly diagnosed pancreatic adenocarcinoma and 348 healthy controls, frequency matched by age, sex, and race. MTHFR polymorphisms were determined using the PCR-RFLP method. Association of these polymorphisms with the risk of pancreatic cancer was estimated by unconditional logistic regression analysis. We found that the C667T (but not the A1298C) polymorphism had a significant main effect on the risk of pancreatic cancer. The frequencies of the MTHFR 667CC, 667CT, and 667TT genotypes were 49.5%, 38.6%, and 11.9%, respectively, among cases compared with 48.5%, 45.0%, and 6.5%, respectively, among controls. Individuals with the 667TT genotype displayed a 2-fold increased risk for pancreatic cancer compared with those with the CC/CT genotypes [adjusted odds ratio (OR), 2.14; 95% confidence interval (95% CI), 1.14-4.01]. Multivariate analyses found that the effect of the 677TT genotype on the risk of pancreatic cancer was present among ever smokers (OR, 5.53; 95% CI, 2.0-15.3) and ever alcohol drinkers (OR, 3.16; 95% CI, 1.30-7.69) but not in never smokers (OR, 0.82; 95% CI, 0.33-2.06) and never drinkers (OR, 1.42; 95% CI, 0.56-3.62). Furthermore, a positive interaction between the MTHFR TT genotype and heavy smoking or heavy alcohol consumption was detected. The OR (95% CI) of pancreatic cancer was 6.83 (1.91-24.38) for heavy smokers among the TT carriers compared with never smokers with the CC/CT genotypes and 4.23 (0.88-20.3) for heavy drinkers with the TT genotype compared with nondrinkers with the CC/CT genotypes. These observations support a role for folate metabolism in pancreatic cancer, especially among smokers and heavy drinkers.
Polymorphisms in Ghrelin and Neuropeptide Y Genes Are Associated with Non-Hodgkin Lymphoma
Authors: Skibola Danica R. , Smith Martyn T. , Bracci Paige M. , Hubbard Alan E. , Agana Luz , Chi Shawn , Holly Elizabeth A. 
Published: September 2005

Abstract
We previously reported a positive association among body mass index, single nucleotide polymorphisms (SNP) in the leptin and leptin receptor genes that are involved in body weight regulation, and non-Hodgkin lymphoma (NHL). Polymorphisms in the ghrelin (GHRL) and neuropeptide Y (NPY) genes were examined in the same population-based case-control study of NHL to further explore the role of genes involved in energy homeostasis and obesity in susceptibility to NHL. Ghrelin is an orexigenic hormone that induces NPY release and inhibits proinflammatory cytokines via its antagonistic relationship with leptin. NPY is a potent appetite stimulator controlled by ghrelin and leptin and also acts as a mediator of immune function. DNA from 458 cases and 812 controls was genotyped. Among genotyped GHRL SNPs, the variant allele for GHRL −4427G&gt;A was inversely associated with all NHL [odds ratios (OR), 0.78; 95% confidence interval (95% CI), 0.59-1.0] and more specifically with diffuse large cell lymphoma (DLCL; homozygous variant: OR, 0.31; 95% CI, 0.13-0.74). Another SNP, GHRL 5179A&gt;G, decreased the risk of DLCL (homozygous variant: OR, 0.35; 95% CI, 0.10-1.2). NPY −485T&gt;C, 1258G&gt;A, and 5671C&gt;T were in total linkage disequilibrium (D′ = 0.99) and the homozygous variants were associated with an increased risk of NHL in NPY SNPs −485T&gt;C (OR, 1.7; 95% CI, 1.1-2.5), 1258G&gt;A (OR, 1.7; 95% CI, 1.1-2.5), and 5671C&gt;T (OR, 1.9; 95% CI, 1.3-2.8). When stratified by subtype, the variant allele for NPY 1128T&gt;C was positively associated with follicular lymphoma (OR, 2.3; 95% CI, 1.1-4.9) as were homozygous variants for NPY SNPs −485T&gt;C (OR, 2.4; 95% CI, 1.3-4.4), 1258G&gt;A (OR, 2.0; 95% CI, 1.1-3.5), and 5671C&gt;T (OR, 1.8; 95% CI, 1.1-3.0). These results add further support for the hypothesis that SNPs in energy-regulating genes affect risk of NHL.
Prenatal and Postnatal Milk Supplementation and Adult Insulin-like Growth Factor I: Long-term Follow-up of a Randomized Controlled Trial
Authors: Ben-Shlomo Yoav , Holly Jeff , McCarthy Anne , Savage Paul , Davies David , Davey Smith George 
Published: September 2005

Abstract
Objective: Insulin-like growth factors (IGF) are increasingly recognized as important determinants of adult health, in particular risk of certain cancers. However, little is known about the determinants of adult IGFs and to what degree they may be programmed by early life influences.
Design: Randomized controlled trial of prenatal and postnatal milk supplementation among 951 subjects born in 1972 to 1974 in South Wales.
Main outcome measure: Measures of IGF-I, IGF binding protein 3, and the molar ratio.
Results: Data on adult IGFs were available from 663 subjects at a mean age of 25 years. Subjects in the intervention arm had lower IGF-I (−8.5 ng/mL; 95% confidence interval, −15.1 to −1.8, P = 0.01) and ratio (−1.20; 95% confidence interval, −2.33 to −0.04, P = 0.04). These differences could not be explained by follow-up bias or confounding factors.
Conclusions: These results provide experimental data on the role of early life programming either in the intrauterine or postnatal period that may have long-term influences on the IGF axis, with potential implications for disease risk.
Behavioral Consequences of Testing for Obesity Risk
Authors: Frosch Dominick L. , Mello Paul , Lerman Caryn 
Published: September 2005

Abstract
Objective: There is considerable hope that genetic susceptibility testing will motivate behavior that can prevent or reduce the risk of complex conditions such as obesity. This study examined potential behavioral consequences of such testing.
Methods: Participants (n = 249) were randomly assigned to review one of four vignettes that asked them to imagine that they had been tested for their risk of becoming overweight or obese. The experimental factors were test type (genetic versus hormone test) and risk level (increased versus average risk for obesity). Study measures included behavioral intentions and perceived behavioral control related to eating a healthy diet, as well as weight locus of control.
Results: Participants assigned to the increased risk conditions indicated greater intentions to eat a healthy diet compared with participants assigned to the average risk conditions (P &lt; 0.02). There were significant interaction effects of risk × perceived behavioral control (P &lt; 0.02) and risk × weight locus of control (P &lt; 0.003) on dietary intentions. Individuals with low perceived behavioral control or an external weight locus of control who were told to imagine they were at average risk expressed significantly lower intentions to eat a healthy diet. A three-way interaction of body mass index, family history of overweight/obesity, and assigned risk level found the greatest effects of risk feedback among those who either had a family history or a higher body mass index (P &lt; 0.007).
Conclusion: This study provides preliminary evidence that testing for susceptibility to obesity may motivate healthier behavior. However, some individuals may be susceptible to a false reassurance effect after receiving test results indicating a lack of increased risk.
Leptin, Insulin-Like Growth Factor-1, and Insulin-Like Growth Factor-2 Are Mitogens in ApcMin/+ but not Apc+/+ Colonic Epithelial Cell Lines
Authors: Fenton Jenifer I. , Hord Norman G. , Lavigne Jackie A. , Perkins Susan N. , Hursting Stephen D. 
Published: September 2005

Abstract
The obese state is associated with elevated circulating levels of insulin, insulin-like growth factors (IGF), and leptin. Research is contradictory regarding the role of these elevated growth factors in colon cancer risk. We hypothesized that colonic epithelial cells that were Apc deficient (ApcMin/+) but not those expressing wild-type Apc (Apc+/+) would experience a hyperproliferative and antiapoptotic phenotype when exposed to these growth factors. This hypothesis was addressed using two nontumorigenic murine colonic epithelial cell lines with distinct Apc genotypes: Apc+/+ YAMC cells and ApcMin/+ IMCE cells. Cells were treated for 48 hours with various concentrations of leptin (0.001-50 ng/mL), IGF-1 (0.1-200 ng/mL), or IGF-2 (0.1-600 ng/mL). In YAMC cells, leptin caused a significant decrease in cell proliferation (P &lt; 0.01) compared with controls due to induction of caspase activity and apoptosis. In contrast, in the IMCE cells, leptin induced a 75% increase in cell proliferation compared with controls (P &lt; 0.0001). IGF-1 and IGF-2 also induced 50% greater proliferation in the IMCE cells (P &lt; 0.001) compared with controls. Cotreatment of IMCE cells with leptin and either IGF-1 or IGF-2 induced greater proliferation than either growth factor alone (P &lt; 0.0001). IMCE cell proliferation caused by leptin only treatment was associated with activation of p42/44 mitogen-activated protein kinase (MAPK), p38 MAPK, and nuclear factor-κB nuclear translocation but not with MAPK kinase or Janus-activated kinase/signal transducers and activators of transcription activation. These data provide the first evidence that leptin may interact with IGFs to promote survival and expansion of colonic epithelial cells that were Apc deficient (ApcMin/+) but not those expressing wild-type Apc (Apc+/+).