bluuebunny/crossref_metadata_2025_split huggingface dataset:
TP53 Mutation Spectrum in Lung Cancer Is Not Different in Women and Men
Authors: Marrogi Aizen J. , Mechanic Leah E. , Welsh Judith A. , Bowman Elise D. , Khan Mohammed A. , Enewold Lindsey , Shields Peter G. , Harris Curtis C. 
Published: September 2005

Abstract
Whether women are more susceptible to lung cancer than men has been controversial. Several case-control studies suggested that women have greater risk of lung cancer compared with men at similar levels of cigarette smoking, whereas some large cohort studies failed to observe this association. Other studies indicated that lung cancer may have biological characteristics and mechanisms of carcinogenesis that are gender specific. Therefore, we hypothesized that women are more susceptible to the carcinogenic effects of tobacco smoke exposure, as evidenced by a higher frequency of G:C-to-T:A somatic mutations in tumors from women in comparison with men at similar levels of tobacco smoke exposure. To investigate our hypothesis, we examined the TP53 mutational spectrum in a case-only (102 women and 201 men) series study where complete smoking information was available. A similar frequency and type of somatic TP53 mutations were observed in women and men. In conclusion, our study indicates that the TP53 mutation spectrum is similar in women and men. Our results are consistent with a recent large cohort study and summary of previous cohort studies, suggesting that women likely have equivalent susceptibility to lung cancer as men.
Genetic Variants in the Vitamin D Receptor Gene and Prostate Cancer Risk
Authors: Hayes Vanessa M. , Severi Gianluca , Padilla Emma J.D. , Eggleton Sarah A. , Southey Melissa C. , Sutherland Robert L. , Hopper John L. , Giles Graham G. 
Published: September 2005

Abstract
Vitamin D receptor (VDR), a member of the steroid/thyroid hormone nuclear receptor family, is bound by the steroid hormone 1,25-dihydroxyvitamin D3, which is thought to play a role in the etiology and progression of prostate cancer. Polymorphisms in the VDR gene have been associated with prostate cancer risk, although findings are inconclusive. The purpose of this study was to determine if VDR polymorphisms were associated with prostate cancer risk using a large, Australian population–based study of 812 cases and 713 controls frequency-matched by age. As the 3′ region polymorphisms are in strong linkage disequilibrium, for joint effects, we only evaluated the common g.60890G &gt; A polymorphism with the unlinked g.27823C &gt; T (5′ region) polymorphism. Allele frequencies were similar in cases and controls (g.27823C &gt; T, 36% versus 36%; g.60890 G&gt;A, 41% versus 43%). No genotypes were individually associated with prostate cancer risk (all P &gt; 0.3). All nine possible genotype combinations were evident, and although the g.27823CT/g.60890GA combination was nominally more prevalent in controls (24%) than in cases (19%, P = 0.03), there was no difference in the combined genotype distribution between cases and controls (P = 0.2). The associations of risk with genotype were between 0.91 and 1.03, all with 95% confidence intervals within 0.81 to 1.15. In conclusion, VDR polymorphisms either alone or in combination do not seem to contribute appreciably to prostate cancer risk.
Dietary Feeding of Silibinin Prevents Early Biomarkers of UVB Radiation–Induced Carcinogenesis in SKH-1 Hairless Mouse Epidermis
Authors: Gu Mallikarjuna , Dhanalakshmi Sivanandhan , Singh Rana P. , Agarwal Rajesh 
Published: September 2005

Abstract
Solar radiation is the causal etiologic factor in the development of nonmelanoma skin cancer (NMSC). Depletion of the stratospheric ozone layer leads to an increase in ambient UV radiation loads, which are expected to further raise skin cancer incidence in many temperate parts of the world, including the United States, suggesting that skin cancer chemopreventive approaches via biomarker efficacy studies or vice versa are highly warranted. Based on our recent study reporting strong efficacy of silibinin against photocarcinogenesis, we assessed here the protective effects of its dietary feeding on UVB-induced biomarkers involved in NMSC providing a mechanistic rationale for an early-on silibinin efficacy in skin cancer prevention. Dietary feeding of silibinin at 1% dose (w/w) to SKH-1 hairless mice for 2 weeks before a single UVB irradiation at 180 mJ/cm2 dose resulted in a strong and significant (P &lt; 0.001) decrease in UVB-induced thymine dimer–positive cells and proliferating cell nuclear antigen, terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling, and apoptotic sunburn cells together with an increase (P &lt; 0.001) in p53 and p21/cip1-positive cell population in epidermis. These findings suggest that dietary feeding of silibinin affords strong protection against UVB-induced damages in skin epidermis by (a) either preventing DNA damage or enhancing repair, (b) reducing UVB-induced hyperproliferative response, and (c) inhibiting UVB-caused apoptosis and sunburn cell formation, possibly via silibinin-caused up-regulation of p53 and p21/cip1 as major UVB-damage control sensors.
Fatty Acid Composition of Red Blood Cell Membranes and Risk of Squamous Cell Carcinoma of the Skin
Authors: Harris Robin B. , Foote Janet A. , Hakim Iman A. , Bronson Dan L. , Alberts David S. 
Published: September 2005

Abstract
Differential effects of fatty acids on carcinogenesis suggest that fatty acid composition is important in tumor development. Arachidonic acid and its metabolites elicit inflammation and promote tumor formation in mouse skin. Inhibitors of the arachidonic cascade inhibit tumor incidence. A population-based case control study in Southeastern Arizona tested the hypothesis that lower levels of arachidonic acid in RBC membranes were associated with decreased risk of skin squamous cell carcinoma (SCC; n = 335 SCC cases and 321 controls). Extracted and esterified RBC fatty acids were analyzed using capillary gas chromatography. Individual peaks for 14 fatty acids were measured as a percentage of total fatty acids. Logistic regression was used to estimate odds ratios (OR), adjusting for SCC risk factors (age, gender, actinic keratosis history, freckling, and tanning ability). Increased levels of arachidonic acid in RBC membranes were associated with increased risk of SCC [odds ratio (OR), 1.08 per mg/100 mL change; 95% confidence interval (95% CI), 1.02-1.15] and this association remained when controls with actinic keratosis precursor lesions were excluded. SCC risk was highest among the upper quartile of arachidonic acid (OR, 2.38; 95% CI, 1.37-4.12). In contrast, increasing proportions of palmitic acid (OR, 0.94; 95% CI, 0.89-1.00) and palmitoleicacid (OR, 0.49; 95% CI, 0.30-0.81) were associated with reduced SCC risk. More studies are needed to elucidate the function of RBC fatty acids so that recommendations can be made to alter the human diet for cancer prevention.
Evidence for an Association between Compound Heterozygosity for Germ Line Mutations in the Hemochromatosis (HFE) Gene and Increased Risk of Colorectal Cancer
Authors: Robinson James P. , Johnson Victoria L. , Rogers Pauline A. , Houlston Richard S. , Maher Earmonn R. , Bishop D.Timothy , Evans D.Gareth R. , Thomas Huw J.W. , Tomlinson Ian P.M. , Silver Andrew R.J. ,   Colorectal Cancer Gene Identification (CORGI) consortium
Published: September 2005

Abstract
Whereas a recent study reported an increased risk of colorectal cancer associated with any HFE germ line mutation (C282Y or H63D), other investigators have concluded there is no increased risk, or that any increase is dependent on polymorphisms in HFE-interacting genes such as the transferrin receptor (TFR). We have established the frequency of HFE mutations in colorectal cancer patients (n = 327) with a family history of the disease and randomly selected controls (n = 322); this design increases greatly the study's power. Genotyping for the TRF S142G polymorphism was also conducted on a large proportion of the study group. Using PCR, restriction enzyme mapping, sequencing followed by data analysis with Fisher's exact test and logistic regression, we show that the presence of any HFE mutation (Y282 or D63) was not associated with colorectal cancer risk (P = 0.57). In contrast, individuals compound heterozygous for both mutations (15 cases versus 5 controls) had thrice the odds of developing colorectal cancer (odds ratio, 3.03; 95% confidence interval, 1.06-8.61) compared with those with a single mutation. This finding did not quite reach statistical significance after allowing for multiple post hoc testing (Pobserved = 0.038 versus P = 0.025, with Bonferonni correction). Overall, our data indicate that individuals with a single HFE mutation, C282Y or H63D, are unlikely predisposed to develop colorectal cancer. However, risk of colorectal cancer might be increased by compound heterozygosity for the HFE mutations in the small number of subjects studied. TFR gene polymorphism was not an independent risk factor and did not modify the disease risk associated with HFE mutation.
Markers of Past Infection with Simian Virus 40 (SV40) and Risk of Incident Non-Hodgkin Lymphoma in a Maryland Cohort
Authors: Rollison Dana E. , Helzlsouer Kathy J. , Halsey Neal A. , Shah Keerti V. , Viscidi Raphael P. 
Published: September 2005

Abstract
Simian virus 40 (SV40) genome sequences have been detected in human non-Hodgkin lymphoma (NHL) tissues, and past infection with SV40 may be a risk factor for NHL. We conducted a population-based nested case-control study to investigate the association between serum antibodies to SV40 and incident NHL. Two research serum banks were established in Washington County, MD, with &gt;45,000 volunteers contributing blood samples collected in 1974 and 1989. Incident cases of NHL diagnosed through 2002 (n = 170) were identified among participants by linkage to population-based cancer registries. Two controls were matched to each case (n = 340) on age, sex, and date of blood draw. Circulating immunoglobulin G antibodies to SV40 were measured using virus-like particle (VLP) ELISA. Positive samples were tested for cross-reactivity with JC virus (JCV) and BK virus (BKV) through competitive inhibition assays. Associations between SV40 antibody seropositivity and NHL were estimated using conditional logistic regression. Whereas SV40 antibodies were detected by VLP ELISA in 15% of cases and 10% of controls [matched odds ratio (OR), 1.97; 95% confidence interval (95% CI), 1.03-3.76], the SV40 reactivity of 85% of the SV40 antibody-positive sera was decreased by adsorption with BKV and/or JCV VLPs. Antibodies specific for SV40 (not cross-reactive) were identified in only 1.8% of cases and 1.6% of controls (OR, 1.51; 95% CI, 0.41-5.52). Our findings suggest that past infection with SV40 is not associated with an increased risk of developing NHL.
Joint Effects between UDP-Glucuronosyltransferase 1A7 Genotype and Dietary Carcinogen Exposure on Risk of Colon Cancer
Authors: Butler Lesley M. , Duguay Yannick , Millikan Robert C. , Sinha Rashmi , Gagné Jean-François , Sandler Robert S. , Guillemette Chantal 
Published: September 2005

Abstract
The UDP-glucuronosyltransferase 1A7 (UGT1A7) gene is polymorphic and encodes an enzyme involved in the detoxification of heterocyclic amines (HCA) and polycyclic aromatic hydrocarbons (PAH). Consumption of pan-fried and well-done meat are surrogates for HCA and PAH exposure and are possibly associated with colon cancer. We have evaluated whether UGT1A7 allelic variations are associated with colon cancer and whether UGT1A7 genotype modified associations among meat intake, exposure to HCAs and PAHs, and colon cancer in a population-based case-control study of African Americans (197 cases and 202 controls) and whites (203 cases and 210 controls). As part of a 150-item food frequency questionnaire, meat intake was assessed by cooking method and doneness and used to estimate individual HCA and PAH exposure. UGT1A7 alleles (UGT1A7*1, UGT1A7*2, UGT1A7*3, and UGT1A7*4) were measured and genotypes were categorized into predicted activity groups (high: *1/*1, *1/*2, *2/*2; intermediate: *1/*3, *1/*4, *2/*3; low: *3/*3, *3/*4, *4/*4). There was no association with UGT1A7 low versus high/intermediate genotype [odds ratio (OR), 1.1; 95% confidence interval (95% CI), 0.7-1.8], regardless of race. Greater than additive joint effects were observed for UGT1A7 low genotype and HCA-related factors. For example, equal to or greater than the median daily intake of the HCA, 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx) and having UGT1A7 low genotype was positively associated with colon cancer (OR, 2.4; 95% CI, 1.2-4.8), compared with less than the median daily intake and UGT1A7 high/intermediate genotypes. These data suggest that the associations among cooked meat–derived compound exposure, and colon cancer are modified by the UGT1A7 genotype.
Dietary and Plasma Lycopene and the Risk of Breast Cancer
Authors: Sesso Howard D. , Buring Julie E. , Zhang Shumin M. , Norkus Edward P. , Gaziano J. Michael 
Published: September 2005

Abstract
Lycopene is potentially effective in the prevention of breast cancer from laboratory and observational studies. Among 39,876 women initially free of cardiovascular disease and cancer, we first conducted a prospective cohort study of dietary lycopene and its food sources. Participants completed a baseline food frequency questionnaire and provided self-reports of breast cancer risk factors. Dietary lycopene levels were divided into quintiles, and lycopene food sources were categorized. During 9.9 years of follow-up, 1,076 breast cancer cases were confirmed by medical record review. In a nested case-control study, we then identified 508 breast cancer cases and 508 controls matched by age, smoking, and follow-up time. Plasma lycopene and other carotenoids were measured. In the prospective cohort study, women with increasing quintiles of dietary lycopene had multivariate relative risks (RR) of breast cancer of 1.00 (ref), 0.95, 1.00, 1.10, and 1.00 (P, linear trend = 0.71). Women consuming &lt;1.5, 1.5 to &lt;4, 4 to &lt;7, 7 to &lt;10, and ≥10 servings/week of tomato-based products had RRs of 1.00 (ref), 1.00, 1.20, 1.18, and 1.16 (P, linear trend = 0.11). No individual lycopene food sources were associated with breast cancer. In the nested case-control study, women in increasing quartiles of plasma lycopene had multivariate RRs of breast cancer of 1.00 (ref), 0.95, 1.15, and 0.93 (P, linear trend = 0.86). The stepwise addition of individual plasma carotenoids did not impact the RRs for plasma lycopene, nor were other carotenoids associated with breast cancer. In conclusion, neither higher dietary nor plasma lycopene levels were associated with a reduced risk of breast cancer in middle-aged and older women.
Genetic Polymorphisms of SULT1A1 and SULT1E1 and the Risk and Survival of Breast Cancer
Authors: Choi Ji-Yeob , Lee Kyoung-Mu , Park Sue Kyung , Noh Dong-Young , Ahn Sei-Hyun , Chung Hye-Won , Han Wonshik , Kim Jeong Soo , Shin Sang Goo , Jang In-Jin , Yoo Keun-Young , Hirvonen Ari , Kang Daehee 
Published: September 2005

Abstract
We examined whether common single nucleotide polymorphisms (SNP) in SULT1A1 (c.779G&gt;A, *14A&gt;G, and *85C&gt;T) and SULT1E1 (IVS1-447C&gt;A, IVS4-1653T&gt;C, and *959G&gt;A) genes influenced the risk and survival of breast cancer. Our study population consisted of 989 histologically confirmed sporadic breast cancer patients and 1,054 controls without history of cancer recruited from three teaching hospitals in Seoul. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated by logistic regression model. In the survival analysis for 529 breast cancer patients with completed treatments, the hazard ratios (HR) were calculated with Cox proportional hazard model. Women with the SULT1E1 *959 GA/AA genotype had a moderately decreased breast cancer risk compared with those with the GG genotypes (OR, 0.8; 95% CI, 0.70-1.00). When the haplotypes were considered, the homozygous *959 AA genotype together with the IVS4-1653 T&gt;C base change (CTA-CCA haplotype) was associated with halved breast cancer risk (OR, 0.5; 95% CI, 0.24-0.88) compared with the wild type CTG-CTG haplotype. No other significant overall association was observed between the SULT1A1 and SULT1E1 SNPs nor haplotypes and breast cancer risk. When stratified by survival, patients with the SULT1E1 IVS4-1653 TC/CC genotypes showed a &gt;3-fold risk of recurrence (HR, 3.2; 95% CI, 1.39-7.48) compared with those with the TT genotype. Moreover, when the haplotypes were considered, the SULT1E1 *959 G&gt;A base change together with the IVS4-1653 T&gt;C base change (CTG-CCA haplotype) was associated with a &gt;4-fold risk of breast cancer (OR, 4.2; 95% CI, 1.15-15.15). These findings suggest that genetic polymorphisms of SULT1E1 are associated with increased risk and a disease free survival of breast cancer in Korean women.
Lifestyle Determinants and Mortality in German Vegetarians and Health-Conscious Persons: Results of a 21-Year Follow-up
Authors: Chang-Claude Jenny , Hermann Silke , Eilber Ursula , Steindorf Karen 
Published: September 2005

Abstract
Background: The long-term observation of vegetarians in affluent countries can provide insight into the relative effects of a vegetarian diet and lifestyle factors on mortality.
Methods: A cohort study of vegetarians and health-conscious persons in Germany was followed-up prospectively for 21 years, including 1,225 vegetarians and 679 health-conscious nonvegetarians. Standardized mortality ratios compared with the German general population were calculated for all causes and specific causes. Within the cohort, Poisson regression modeling was used to investigate the joint effects of several risk factors on overall and cause-specific mortality.
Results: Standardized mortality ratios for all-cause mortality was significantly below 100: 59 [95% confidence interval (95% CI), 54-64], predominantly due to a deficit of deaths from circulatory diseases. Within the cohort, vegetarian compared with nonvegetarian diet had no effect on overall mortality [rate ratio (RR), 1.10; 95% CI, 0.89-1.36], whereas moderate and high physical activity significantly reduced risk of death (RR, 0.62, 0.64), adjusted for age, sex, smoking, alcohol intake, body mass index, and educational level. Vegetarian diet was however associated with a reduced RR of 0.70 (95% CI, 0.41-1.18) for ischemic heart disease, which could partly be related to avoidance of meat.
Conclusions: Both vegetarians and nonvegetarian health-conscious persons in this study have reduced mortality compared with the general population. Within the study, low prevalence of smoking and moderate or high level of physical activity but not strictly vegetarian diet was associated with reduced overall mortality. The nonsignificant reduction in mortality from ischemic heart diseases in vegetarians compared with health-conscious persons could be explained in part by avoidance of meat intake.
Controlled Physical Activity Trials in Cancer Survivors: A Systematic Review and Meta-analysis
Authors: Schmitz Kathryn H. , Holtzman Jeremy , Courneya Kerry S. , Mâsse Louise C. , Duval Sue , Kane Robert 
Published: September 2005

Abstract
Background: Approximately 9.8 million cancer survivors are alive in the United States today. Enthusiasm for prescribing physical activity for cancer survivors depends on evidence regarding whether physical activity during or after completion of treatment results in improved outcomes such as cardiorespiratory fitness, fatigue, symptoms, quality of life, mental health, or change in body size.
Methods: A systematic qualitative and quantitative review of the English language scientific literature identified controlled trials of physical activity interventions in cancer survivors during and after treatment. Data from 32 studies were abstracted, weighted mean effect sizes (WMES) were calculated from the 22 high-quality studies, and a systematic level of evidence criteria was applied to evaluate 25 outcomes.
Results: There was qualitative and quantitative evidence of a small to moderate effect of physical activity interventions on cardiorespiratory fitness (WMES = 0.51 and 0.65 during and after treatment respectively, P &lt; 0.01), physiologic outcomes and symptoms during treatment (WMES = 0.28, P &lt; 0.01 and 0.39, P &lt; 0.01, respectively), and vigor posttreatment (WMES = 0.83, P = 0.04). Physical activity was well tolerated in cancer survivors during and after treatment, but the available literature does not allow conclusions to be drawn regarding adverse events from participation.
Conclusions: Physical activity improves cardiorespiratory fitness during and after cancer treatment, symptoms and physiologic effects during treatment, and vigor posttreatment. Additional physical activity intervention studies are needed to more firmly establish the range and magnitude of positive effects of physical activity among cancer survivors.
Comparative Gene Expression Analysis of Ovarian Carcinoma and Normal Ovarian Epithelium by Serial Analysis of Gene Expression
Authors: Peters David G. , Kudla Donna M. , DeLoia Julie A. , Chu Tian Jiao , Fairfull Liane , Edwards Robert P. , Ferrell Robert E. 
Published: September 2005

Abstract
Despite the poor prognosis of ovarian cancer and the importance of early diagnosis, there are no reliable noninvasive biomarkers for detection in the early stages of disease. Therefore, to identify novel ovarian cancer markers with potential utility in early-stage screening protocols, we have undertaken an unbiased and comprehensive analysis of gene expression in primary ovarian tumors and normal human ovarian surface epithelium (HOSE) using Serial Analysis of Gene Expression (SAGE). Specifically, we have generated SAGE libraries from three serous adenocarcinomas of the ovary and, using novel statistical tools, have compared these to SAGE data derived from two pools of normal HOSE. Significantly, in contrast to previous SAGE-based studies, our normal SAGE libraries are not derived from cultured cell lines. We have also compared our data with publicly available SAGE data obtained from primary tumors and “normal” HOSE-derived cell lines. We have thus identified several known and novel genes whose expressions are elevated in ovarian cancer. These include but are not limited to CLDN3, WFDC2, FOLR1, COL18A1, CCND1, and FLJ12988. Furthermore, we found marked differences in gene expression patterns in primary HOSE tissue compared with cultured HOSE. The use of HOSE tissue as a control for these experiments, along with hierarchical clustering analysis, identified several potentially novel biomarkers of ovarian cancer, including TACC3, CD9, GNAI2, AHCY, CCT3, and HMGA1. In summary, these data identify several genes whose elevated expressions have not been observed previously in ovarian cancer, confirm the validity of several existing markers, and provide a foundation for future studies in the understanding and management of this disease.