bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect Modification by Catalase Genotype Suggests a Role for Oxidative Stress in the Association of Hormone Replacement Therapy with Postmenopausal Breast Cancer Risk
Authors: Quick Sylvia K. , Shields Peter G. , Nie Jing , Platek Mary E. , McCann Susan E. , Hutson Alan D. , Trevisan Maurizio , Vito Dominica , Modali Ramakrishna , Lehman Teresa A. , Seddon Mike , Edge Stephen B. , Marian Catalin , Muti Paola , Freudenheim Jo L. 
Published: May 2008

AbstractCatalase, a ubiquitous heme enzyme, catalyzes conversion of hydrogen peroxide to water and molecular oxygen, protecting cells from oxidative stress. A C/T polymorphism in the promoter region of the CAT gene (rs1001179) affects transcriptional activity and RBC catalase levels. Oxidative stress may explain the observed increased postmenopausal breast cancer risk associated with hormone replacement therapy (HRT). We examined CAT genotype, HRT, and postmenopausal breast cancer risk in the Western New York Exposures and Breast Cancer case-control study. Cases (n = 616) were women with primary, incident, pathologically confirmed breast cancer. Randomly selected controls (n = 1,082) were frequency matched to cases on age and race. Genotype was assayed by matrix-assisted laser desorption ionization time-of-flight mass spectrometry. Unconditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI) adjusted for potential confounders. CAT genotype alone was not associated with breast cancer risk. Ever use of HRT was associated with increased risk (OR, 1.39; 95% CI, 1.11-1.75). The increase with ever use was more pronounced among those with variant CT or TT CAT genotype (OR, 1.88; 95% CI, 1.29-2.75) than among those with CC (OR, 1.15; 95% CI, 0.86-1.54). Similarly, risk associated with ≥5 years of HRT use was greater among those with at least one variant T allele (OR, 2.32; 95% CI, 1.50-3.59). Increased risk was limited to estrogen receptor–positive tumors. Our findings suggest that CAT genotype modifies the effect of HRT use on breast cancer risk and that HRT may affect risk by affecting oxidative stress. (Cancer Epidemiol Biomarkers Prev 2008;17(5):1082–7)
Teeth Loss and Risk of Cancer at 14 Common Sites in Japanese
Authors: Hiraki Akio , Matsuo Keitaro , Suzuki Takeshi , Kawase Takakazu , Tajima Kazuo 
Published: May 2008

Abstract
Background: Tooth loss has been associated with a higher risk of several types of cancer. To clarify the significance of tooth loss to the risk of 14 common cancers, we conducted a large-scale, case-control study based on the Hospital-based Epidemiologic Research Program at Aichi Cancer Center.
Methods: A total of 5,240 cancer subjects and 10,480 age- and sex-matched noncancer controls were recruited. Patients with 14 types of cancer newly diagnosed from 2000 to 2005 were eligible as case subjects, and new outpatients without cancer in the same time period were eligible as controls. Tooth loss was categorized into four groups: group 1, number of remaining teeth, ≥21; group 2, 9 to 20; group 3, 1 to 8; and group 4, 0. The effect of tooth loss was assessed as odds ratios (OR) with 95% confidence intervals (95% CI) calculated with conditional logistic regression models, with adjustment for potential confounders.
Results: A decreased number of remaining teeth was associated with increased OR of head and neck (OR, 1.68; 95% CI, 0.88-1.93; Ptrend = 0.055), esophageal (OR, 2.36; 95% CI, 1.17-4.75; Ptrend = 0.002), and lung (OR, 1.54; 95% CI, 1.05-2.27; Ptrend = 0.027) cancers.
Conclusions: We showed a significant positive association between tooth loss and the risk of head and neck, esophageal, and lung cancers after adjustment for potential confounding factors. The findings indicate that preventive efforts aimed at the preservation of teeth may decrease the risk of these cancers. (Cancer Epidemiol Biomarkers Prev 2008;17(5):1222–7)
A 9-Year Follow-up Study of Participants and Nonparticipants in Sigmoidoscopy Screening: Importance of Self-Selection
Authors: Blom Johannes , Yin Li , Lidén Annika , Dolk Anders , Jeppsson Bengt , Påhlman Lars , Holmberg Lars , Nyrén Olof 
Published: May 2008

Abstract
Background: Self-selection may compromise cost-effectiveness of screening programs. We hypothesized that nonparticipants have generally higher morbidity and mortality than participants.
Methods: A Swedish population-based random sample of 1,986 subjects ages 59 to 61 years was invited to sigmoidoscopy screening and followed up for 9 years by means of multiple record linkages to health and population registers. Gender-adjusted cancer incidence rate ratio (IRR) and overall and disease group-specific and mortality rate ratio (MRR) with 95% confidence intervals (95% CI) were estimated for nonparticipants relative to participants. Cancer and mortality rates were also estimated relative to the age-matched, gender-matched, and calendar period-matched Swedish population using standardized incidence ratios and standardized mortality ratios.
Results: Thirty-nine percent participated. The incidence of colorectal cancer (IRR, 2.2; 95% CI, 0.8-5.9), other gastrointestinal cancer (IRR, 2.7; 95% CI, 0.6-12.8), lung cancer (IRR, 2.2; 95% CI, 0.8-5.9), and smoking-related cancer overall (IRR, 1.4; 95% CI, 0.7-2.5) tended to be increased among nonparticipants relative to participants. Standardized incidence ratios for most of the studied cancers tended to be &gt;1.0 among nonparticipants and &lt;1.0 among participants. Mortality from all causes (MRR, 2.4; 95% CI, 1.7-3.4), neoplastic diseases (MRR, 1.9; 95% CI, 1.1-3.5), gastrointestinal cancer (MRR, 4.7; 95% CI, 1.1-20.7), and circulatory diseases (MRR, 2.3; 95% CI, 1.2-4.2) was significantly higher among nonparticipants than among participants. Standardized mortality ratio for the studied outcomes tended to be increased among nonparticipants and was generally decreased among participants.
Conclusion: Individuals who might benefit most from screening are overrepresented among nonparticipants. This self-selection may attenuate the cost-effectiveness of screening programs on a population level. (Cancer Epidemiol Biomarkers Prev 2008;17(5):1163–8)
CYP1A1, GSTM1, and GSTT1 Polymorphisms, Smoking, and Lung Cancer Risk in a Pooled Analysis among Asian Populations
Authors: Lee Kyoung-Mu , Kang Daehee , Clapper Margie L. , Ingelman-Sundberg Magnus , Ono-Kihara Masko , Kiyohara Chikako , Min Shen , Lan Qing , Le Marchand Loic , Lin Pinpin , Lung Maria Li , Pinarbasi Hatice , Pisani Paola , Srivatanakul Petcharin , Seow Adeline , Sugimura Haruhiko , Tokudome Shinkan , Yokota Jun , Taioli Emanuela 
Published: May 2008

Abstract
To evaluate the roles of CYP1A1 polymorphisms [Ile462Val and T6235C (MspI)] and deletion of GSTM1 and GSTT1 in lung cancer development in Asian populations, a pooled analysis was conducted on 13 existing studies included in Genetic Susceptibility to Environmental Carcinogenesis database. This pooled analysis included 1,971 cases and 2,130 controls. Lung cancer risk was estimated as odds ratios (OR) and 95% confidence intervals (95% CI) using unconditional logistic regression model adjusting for age, sex, and pack-year. The CYP1A1 6235C variant was associated with squamous cell lung cancer (TC versus TT: OR, 1.42; 95% CI, 0.96-2.09; CC versus TT: OR, 1.97; 95% CI, 1.26-3.07; Ptrend = 0.003). In haplotype analysis, 462Val-6235T and Ile-C haplotypes were associated with lung cancer risk with reference to the Ile-T haplotype (OR, 3.41; 95% CI, 1.78-6.53 and OR, 1.39; 95% CI, 1.12-1.71, respectively). The GSTM1-null genotype increased squamous cell lung cancer risk (OR, 1.36; 95% CI, 1.05-1.77). When the interaction was evaluated with smoking, increasing trend of lung cancer risk as pack-year increased was stronger among those with the CYP1A1 6235 TC/CC genotype compared with those with TT genotype (Pinteraction = 0.001) and with the GSTM1-null genotype compared with the present type (Pinteraction = 0.08, when no genotype effect with no exposure was assumed). These results suggest that genetic polymorphisms in CYP1A1 and GSTM1 are associated with lung cancer risk in Asian populations. However, further investigation is warranted considering the relatively small sample size when subgroup analyses were done and the lack of environmental exposure data other than smoking. (Cancer Epidemiol Biomarkers Prev 2008;17(5):1120–6)
A 22-year Prospective Study of Fish,n-3 Fatty Acid Intake, and Colorectal Cancer Risk in Men
Authors: Hall Megan N. , Chavarro Jorge E. , Lee I-Min , Willett Walter C. , Ma Jing 
Published: May 2008

AbstractBackground: Fish is the main dietary source of long-chain n-3 fatty acids, which have been suggested to play a protective role in colorectal cancer development in laboratory and animal studies. Human studies have not shown consistent results. We examined the association between intakes of fish and n-3 fatty acids from fish and colorectal cancer risk in men enrolled in the Physicians' Health Study.Methods: The Physicians' Health Study began as a randomized trial to examine the effect of aspirin and β-carotene supplementation on cancer and cardiovascular disease. Fish intake was assessed at the 12-month follow-up with an abbreviated food-frequency questionnaire. Cox proportional hazards models were used to estimate multivariate relative risks for colorectal cancer for the categories of fish intake and quartiles of n-3 fatty acid intake.Results: During 22 years of follow-up, 500 men had a confirmed diagnosis of colorectal cancer. Fish intake was inversely associated with colorectal cancer risk [multivariate relative risk (95% confidence interval) for highest versus lowest category, 0.60 (0.40-0.91); Ptrend = 0.01]. The inverse association was observed for both colon and rectal cancers. Our findings for n-3 fatty acids were similar to those for fish; the multivariate relative risk (95% confidence interval) of total colorectal cancer for the highest versus lowest quartile of n-3 fatty acids was 0.74 (0.57-0.95; Ptrend = 0.01).Conclusions: Our results from this long-term prospective study suggest that intakes of fish and long-chain n-3 fatty acids from fish may decrease the risk for colorectal cancer. (Cancer Epidemiol Biomarkers Prev 2008;17(5):1136–43)
Multiple Independent Genetic Variants in the 8q24 Region Are Associated with Prostate Cancer Risk
Authors: Salinas Claudia A. , Kwon Erika , Carlson Christopher S. , Koopmeiners Joseph S. , Feng Ziding , Karyadi Danielle M. , Ostrander Elaine A. , Stanford Janet L. 
Published: May 2008

Abstract
Recently, the 8q24 region has been identified as a prostate cancer susceptibility locus in a genome-wide scan of prostate cancer families in Iceland and an admixture scan of African Americans. Further investigations of variants at 8q24 have shown the existence of additional single nucleotide polymorphisms (SNPs) that enhance prostate cancer risk, suggesting the possibility of multiple regions harboring variants for the disease. In the present population-based study of Caucasians (1,308 cases and 1,266 controls) and African Americans (149 cases and 85 controls), we tested the association between prostate cancer and 23 SNPs in the 8q24 region. Fourteen SNPs in Caucasians and 5 SNPs in African Americans were significantly associated with risk of prostate cancer after adjusting for multiple comparisons; of these, 5 SNPs in Caucasians and 3 in African Americans were independently associated with risk. The strongest association was for rs6983561 (carriers of any C allele) with an odds ratio of 1.6 (95% confidence interval, 1.1-2.1) in Caucasians; variants in rs979200, rs1016343, rs7837328, and rs10090154 were also independently associated with risk. In African Americans, the strongest association was for rs7000448 (carriers of any T allele) with an odds ratio of 3.4 (95% confidence interval, 1.3-8.7). In addition, two SNPs that extend the boundaries of the 8q24 region were significantly associated with risk: rs979200 at the centromeric boundary and rs3891248, located in the first intron of the c-MYC gene (IVS1-355), which identifies a new telomeric boundary. (Cancer Epidemiol Biomarkers Prev 2008;17(5):1203–13)
Alcohol Consumption and the Risk for Prostate Cancer in the European Prospective Investigation into Cancer and Nutrition
Authors: Rohrmann Sabine , Linseisen Jakob , Key Timothy J. , Jensen Majken K. , Overvad Kim , Johnsen Nina Føns , Tjønneland Anne , Kaaks Rudolf , Bergmann Manuela M. , Weikert Cornelia , Naska Androniki , Trichopoulou Antonia , Trichopoulos Dimitrios , Pala Valeria , Sacerdote Carlotta , Palli Domenico , Tumino Rosario , Bueno-de-Mesquita H. Bas , Vrieling Alina , González Carlos A. , Larrañaga Nerea , Navarro Carmen , Barricarte Aurelio , Quiros J. Ramon , Martínez-García Carmen , Hallmans Göran , Stattin Pär , Manjer Jonas , Wirfält Elisabet , Bingham Sheila , Khaw Key-Tee , Egevad Lars , Ferrari Pietro , Jenab Mazda , Riboli Elio 
Published: May 2008

Abstract
Alcohol is a risk factor for several types of cancer. However, the results for prostate cancer have been inconsistent, with most studies showing no association. Within the European Prospective Investigation into Cancer and Nutrition, detailed information were collected from 142,607 male participants on the intake of alcoholic beverages at recruitment (for 100% of the cohort) and over lifetime (for 76% of the cohort) between 1992 and 2000. During a median follow-up of 8.7 years, 2,655 prostate cancer cases were observed. Multivariate Cox proportional hazard models were used to examine the association of alcohol consumption at recruitment and average lifetime alcohol consumption with prostate cancer adjusted for age, center, smoking, height, weight, physical activity, and nonalcohol energy intake. Overall, neither alcohol consumption at baseline nor average lifetime alcohol consumption was associated with the risk for prostate cancer in this cohort of men. Men who consumed ≥60 g alcohol per day had a relative risk of 0.88 [95% confidence interval (95% CI) 0.72-1.08] compared with men with an intake of 0.1-4.9 g/d; the respective relative risk for average lifetime intake was 1.09 (95% CI, 0.86-1.39). For advanced prostate cancer (n = 537), the relative risks for ≥60 and 0.1-4.9 g alcohol per day at baseline were 0.98 (95% CI, 0.66-1.44) and 1.28 (95% CI, 0.79-2-07), respectively, for average lifetime intake. No statistically significant association was observed for alcohol intake from specific alcoholic beverages. Our results indicate no association between the consumption of alcohol and prostate cancer in this cohort of European men. (Cancer Epidemiol Biomarkers Prev 2008;17(5):1282–7)
A Comparison of Linear Array and Hybrid Capture 2 for Detection of Carcinogenic Human Papillomavirus and Cervical Precancer in ASCUS-LSIL Triage Study
Authors: Gravitt Patti E. , Schiffman Mark , Solomon Diane , Wheeler Cosette M. , Castle Philip E. 
Published: May 2008

Abstract
Background: We were interested in comparing the performance of Linear Array (LA; Roche Molecular Systems) to Hybrid Capture 2 (hc2; Digene) for the detection of carcinogenic human papillomavirus (HPV) and cervical precancer.
Methods: LA and hc2 results were compared on baseline specimens collected from women with an atypical squamous cells of undetermined significance (ASCUS) Pap referred into ASCUS and Low-Grade Squamous Intraepithelial Lesion Triage Study (n = 3,488). hc2 was conducted at the time of the study on liquid cytology specimens. LA was conducted retrospectively on aliquots from a second, stored cervical specimen masked to the hc2 results and clinical data. Paired LA and hc2 results (n = 3,289; 94%) were compared for the detection of carcinogenic HPV (HPV 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68) and 2-year cumulative cervical intraepithelial neoplasia (CIN) grade ≥3 as diagnosed by the quality-control pathology review.
Results: LA was more likely to test positive for carcinogenic HPV than hc2 (55% versus 53%; P = 0.001). For 2-year cumulative ≥CIN3, LA and hc2 had similar sensitivities (93.3% versus 92.6%, respectively; P = 1), and LA was marginally less specific than hc2 (48.1% versus 50.6%, respectively; P = 0.05). LA and hc2 had similar negative predictive values (98.70% versus 98.64% respectively; P = 0.4), and LA had a slightly lower positive predictive value than hc2 (14.6% versus 15.1%, respectively; P &lt; 0.0001).
Conclusion: We observed that LA and hc2 performed similarly in the detection of carcinogenic HPV and identification of CIN3 among women with an ASCUS Pap. (Cancer Epidemiol Biomarkers Prev 2008;17(5):1248–54)
Variation in the Selenoenzyme Genes and Risk of Advanced Distal Colorectal Adenoma
Authors: Peters Ulrike , Chatterjee Nilanjan , Hayes Richard B. , Schoen Robert E. , Wang Yinghui , Chanock Stephen J. , Foster Charles B. 
Published: May 2008

Abstract
Background: Epidemiologic and animal studies provide evidence for a chemopreventive effect of selenium on colorectal cancer, which may be mediated by the antioxidative and anti-inflammatory properties of selenoenzymes. We therefore investigated whether genetic variants in selenoenzymes abundantly expressed in the colon are associated with advanced colorectal adenoma, a cancer precursor.
Methods: Cases with a left-sided advanced adenoma (n = 772) and matched controls (n = 777) screen negative for polyps based on sigmoidoscopy examination were randomly selected from participants in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. The underlying genetic variation was determined by resequencing. We genotyped 44 tagging single nucleotide polymorphisms (SNP) in six genes [glutathione peroxidase 1-4 (GPX1, GPX2, GPX3, and GPX4), selenoprotein P (SEPP1), and thioredoxin reductase 1 (TXNRD1)] to efficiently predict common variation across these genes.
Results: Four variants in SEPP1 were significantly associated with advanced adenoma risk. A rare variant in the 5′ region of SEPP1 (-4166C&gt;G) was present in nine cases but in none of the controls (exact P = 0.002). Three SNPs located in the 3′ region of SEPP1, which is overlapping with the promoter region of an antisense transcript, were significantly associated with adenoma risk: homozygotes at two SEPP1 loci (31,174 bp 3′ of STP A&gt;G and 43,881 bp 3′ of STP G&gt;A) were associated with increased adenoma risk [odds ratio (OR), 1.48; 95% confidence interval (95% CI), 1.00-2.19 and OR, 1.53; 95% CI, 1.05-2.22, respectively] and the variant SEPP1 44,321 bp 3′ of STP C&gt;T was associated with a reduced adenoma risk (CT versus CC OR, 0.85; 95% CI, 0.63-1.15). Furthermore, we observed a significant 80% reduction for advanced colorectal adenoma risk for carriers of the variant allele at TXNRD1 IVS1-181C&gt;G (OR, 0.20; 95% CI, 0.07-0.55; Ptrend = 0.004). Consistent with the individual SNP results, we observed a significant overall association with adenoma risk for SEPP1 and TXNRD1 (global P = 0.02 and 0.008, respectively) but not for the four GPX genes.
Conclusion: Our study suggests that genetic variants at or near the SEPP1 and TXNRD1 loci may be associated with advanced colorectal adenoma. As this is the first study to comprehensively investigate this hypothesis, confirmation in independent study populations is needed. (Cancer Epidemiol Biomarkers Prev 2008;17(5):1144–54)
Low Serum Levels of 25-Hydroxyvitamin D Predict Fatal Cancer in Patients Referred to Coronary Angiography
Authors: Pilz Stefan , Dobnig Harald , Winklhofer-Roob Brigitte , Riedmüller Gunter , Fischer Joachim E. , Seelhorst Ursula , Wellnitz Britta , Boehm Bernhard O. , März Winfried 
Published: May 2008

Abstract
Accumulating evidence suggests that vitamin D may protect against cancer, but results from epidemiologic studies are inconclusive so far, and other studies looking into the prospective association of total cancer mortality and serum 25-hydroxyvitamin D [25(OH)D] levels, which are considered to be the best indicator of vitamin D status, are scarce. We measured 25(OH)D and 1,25-dihydroxyvitamin D in 3,299 patients from the Ludwigshafen Risk and Cardiovascular Health study. The baseline examination was done between July 1997 and January 2000 and included a fasting blood sampling in the morning before coronary angiography. During a median follow-up period of 7.75 years, 95 patients died due to cancer. After adjustment for possible confounders, the Cox proportional hazard ratio (95% confidence interval) of the fourth 25(OH)D quartile was 0.45 (0.22-0.93) when compared with the first quartile and the hazard ratio per increase of 25 nmol/L in serum 25(OH)D concentrations was 0.66 (0.49-0.89). We found no association between serum 1,25-dihydroxyvitamin D levels and fatal cancer. In summary, our data suggest that low levels of 25(OH)D are associated with increased risk of fatal cancer in patients referred to coronary angiography and that the maintenance of a sufficient vitamin D status might therefore be a promising approach for the prevention and/or treatment of cancer. (Cancer Epidemiol Biomarkers Prev 2008;17(5):1228–33)
Phase I Clinical and Pharmacokinetic Study of Plitidepsin as a 1-Hour Weekly Intravenous Infusion in Patients with Advanced Solid Tumors
Authors: Izquierdo Miguel A. , Bowman Angela , García Margarita , Jodrell Duncan , Martinez Marisa , Pardo Beatriz , Gómez Javier , López-Martin José A. , Jimeno José , Germá José R. , Smyth John F. 
Published: May 2008

Abstract
Purpose: Plitidepsin, given as a 1-hour weekly i.v. infusion for 3 consecutive weeks during a 4-week treatment cycle, was investigated in patients with solid tumors to determine the maximum tolerated dose and the recommended dose (RD) using this administration schedule.
Experimental Design: Consecutive cohorts of patients with metastatic solid tumors or non–Hodgkin's lymphomas were to be treated at escalating doses of plitidepsin in a conventional phase I study including pharmacokinetic analyses of plitidepsin in plasma, whole blood, and blood cell pellets.
Results: Forty-nine patients with solid tumors were enrolled, and 48 were treated with plitidepsin (doses from 0.133 to 3.6 mg/m2/week). Dose-limiting toxicities (defining 3.6 mg/m2/week as the maximum tolerated dose) included myalgia, increased creatine phosphokinase levels, and sustained grade 3/4 increases of hepatic enzyme levels. The RD was established at 3.2 mg/m2/week. The most common toxicities were fatigue, vomiting/nausea, anorexia, injection site reaction, and pain, mostly of mild or moderate severity. Muscular toxicity manifested by mild-moderate myalgia, weakness, and/or creatine phosphokinase elevations occurred in ∼25% of patients and seemed to be dose related. Transient transaminase elevations were frequent but achieved grade 3 or 4 in only ∼10% of patients. Plitidepsin lacked significant hematologic toxicity. No complete or partial tumor responses were observed; however, five patients had disease stabilization (including one patient with medullary thyroid carcinoma with an unconfirmed partial response and one patient with renal carcinoma with major tumor shrinkage in lung metastases). Pharmacokinetic results for the RD indicated a long plasma half-life give value (16.8 ± 7.7 hour) and a high volume of distribution value (525.2 ± 219.3 L).
Conclusions: The recommended dose for plitidepsin given as a weekly 1-hour schedule was 3.2 mg/m2/week. Muscular and liver toxicity were dose limiting at 3.6 mg/m2/week. Additional evaluation of this dose dense schedule is warranted.