bluuebunny/crossref_metadata_2025_split huggingface dataset:
Macrophage Scavenger Receptor 1 999C&gt;T (R293X) Mutation and Risk of Prostate Cancer
Authors: Hope Questa , Bullock Sarah , Evans Christopher , Meitz Julia , Hamel Nancy , Edwards Stephen M. , Severi Gianluca , Dearnaley David , Jhavar Sameer , Southgate Christine , Falconer Alison , Dowe Anna , Muir Kenneth , Houlston Richard S. , Engert James C. , Roquis David , Sinnett Daniel , Simard Jacques , Heimdal Ketil , Møller Pål , Maehle Lovise , Badzioch Michael , Eeles Rosalind A. , Easton Douglas F. , English Dallas R. , Southey Melissa C. , Hopper John L. , Foulkes William D. , Giles Graham G. ,   The Cancer Research UK/British Association of Urological Surgeons' Section of Oncology Collaborators
Published: September 2005

Abstract
Background: Variants in the gene encoding the macrophage scavenger receptor 1 (MSR14) protein have been identified in men with prostate cancer, and several small studies have suggested that the 999C&gt;T (R293X) protein-truncating mutation may be associated with an increased risk for this disease.
Methods: Using large case-control, cohort, and prostate cancer family studies conducted in several Western countries, we tested for the 999C&gt;T mutation in 2,943 men with invasive prostate carcinoma, including 401 males from multiple-case families, 1,982 cases unselected for age, and 575 men diagnosed before the age of 56 years, and in 2,870 male controls. Risk ratios were estimated by unconditional logistic regression adjusting for country and by a modified segregation analysis. A meta-analysis was conducted pooling our data with published data.
Results: The prevalence of MSR1*999C&gt;T mutation carriers was 0.027 (SE, 0.003) in cases and 0.022 (SE, 0.002) in controls, and did not differ by country, ethnicity, or source. The adjusted risk ratio for prostate cancer associated with being a 999C&gt;T carrier was 1.31 [95% confidence interval (CI), 0.93-1.84; P = 0.16]. The modified segregation analysis estimated the risk ratio to be 1.20 (95% CI, 0.87-1.66; P = 0.16). The risk ratio estimated from the meta-analysis was 1.34 (95% CI, 0.94-1.89; P = 0.10).
Conclusion: Our large-scale analysis of case and controls from several countries found no evidence that the 999C&gt;T mutation is associated with increased risk of prostate cancer. The meta-analysis suggests it is unlikely that this mutation confers more than a 2-fold increased risk.
Polymorphisms in XPD Exons 10 and 23 and Bladder Cancer Risk
Authors: Schabath Matthew B. , Delclos George L. , Grossman H. Barton , Wang Yunfei , Lerner Seth P. , Chamberlain Robert M. , Spitz Margaret R. , Wu Xifeng 
Published: September 2005

Abstract
Introduction: The nucleotide excision repair gene, xeroderma pigmentosum complementation group D (XPD), has been hypothesized to have a role in cancer risk, but results from prior molecular epidemiologic studies and genotype-phenotype analyses are conflicting.
Materials and Methods: We examined the frequency of the XPD Asp312Asn polymorphism in exon 10 and the XPD Lys751Gln polymorphism in exon 23 in 505 incident bladder cancer cases and 486 healthy controls.
Results: Overall, the XPD exon 10 and 23 genotypes were not associated with bladder cancer risk, after adjusting for age, sex, ethnicity, and smoking status. A gender-specific role was evident that showed an increased risk for women, but not for men, associated with the variant genotypes for both exons. For example, when the exon 23 variant allele genotypes were combined (Lys/Gln + Gln/Gln), there was an increased bladder cancer risk in women [odds ratio (OR), 1.69; 95% confidence interval (95% CI), 1.12-2.58] but not in men (OR, 0.99; 95% CI, 0.79-1.24; Pinteraction = 0.041; OR, 1.62; 95% CI, 1.02-2.58). There was also a gene-smoking interaction that showed the variant alleles for either exon or the combination of both increase the risk of bladder cancer for light and heavy smokers. For exon 23 (Pinteraction = 0.057; OR, 1.21; 95% CI, 0.99-1.47), heavy smokers (≥20 pack-years) who carried the exon 23 variant allele genotypes had an OR of 4.13 (95% CI, 2.53-6.73), whereas heavy smokers with the wild-type genotypes were at lower risk (OR, 3.55; 95% CI, 2.19-5.75). Moderate smokers (1-19 pack-years) with the variant allele genotypes had an OR of 1.54 (95% CI, 0.94-2.53), whereas moderate smokers with the wild-type genotypes had an OR of 1.12 (95% CI, 0.63-1.98).
Conclusions: Although we did not observe main effects associated with the XPD genotypes, these results do suggest the variant allele genotypes were associated with increased bladder cancer risk in women and smokers with statistically significant interactions in the exon 23 polymorphism. Although there is biological plausibility, these novel findings for gender and smoking should be interpreted with caution upon confirmation in larger studies.
Intraindividual Variability in Arsenic Methylation in a U.S. Population
Authors: Steinmaus Craig , Yuan Yan , Kalman Dave , Atallah Raja , Smith Allan H. 
Published: September 2005

Abstract
Several recent investigations have reported associations between a reduced capacity to fully methylate inorganic arsenic and increased susceptibility to arsenic-caused cancer. In these studies, methylation patterns were based on a single assessment of urinary arsenic metabolites collected at the time of cancer diagnosis. However, the latency of arsenic-caused cancer may be several decades, and the extent to which a recent measurement can be used to estimate a person's past methylation pattern is unknown. In this investigation, the distribution of urinary inorganic arsenic, monomethylarsonate, and dimethylarsinate was used to assess intraindividual variation in methylation capacity in 81 subjects with low to moderate arsenic exposures. Multiple urine samples were collected from each subject over a 1-year period. Duplicate analyses done on 27 samples were used to assess laboratory measurement imprecision. The intraclass correlation coefficients (ICC) for the proportion of urinary arsenic as inorganic arsenic, monomethylarsonate, and dimethylarsinate in samples taken an average of 258 days apart, were 0.45 [95% confidence interval (95% CI), 0.23-0.63] 0.46 (95% CI, 0.24-0.64), and 0.49 (95% CI, 0.28-0.66). In analyses of duplicate samples, ICCs for the concentration of arsenic species ranged from 0.87 to 0.93, whereas ICCs for species proportions ranged from 0.63 to 0.76. These data suggest that individual methylation patterns remain fairly stable over time, although variability due to measurement imprecision or intraindividual changes over time does occur. This variability could lead to misclassification of methylation patterns and could bias relative risk estimates in studies of methylation and cancer towards the null.
Double-Strand Break Repair Gene Polymorphisms and Risk of Breast or Ovarian Cancer
Authors: Webb Penelope M. , Hopper John L. , Newman Beth , Chen Xiaoqing , Kelemen Livia , Giles Graham G. , Southey Melissa C. , Chenevix-Trench Georgia , Spurdle Amanda B. 
Published: September 2005

AbstractDeficiencies in DNA repair have been hypothesized to increase cancer risk and excess cancer incidence is a feature of inherited diseases caused by defects in DNA damage recognition and repair. We investigated, using a case-control design, whether the double-strand break repair gene polymorphisms RAD51 5′ untranslated region −135 G &gt; C, XRCC2 R188H G &gt; A, and XRCC3 T241M C &gt; T were associated with risk of breast or ovarian cancer in Australian women. Sample sets included 1,456 breast cancer cases and 793 age-matched controls ages under 60 years of age, 549 incident ovarian cancer cases, and 335 controls of similar age distribution. For the total sample and the subsample of Caucasian women, there were no significant differences in genotype distribution between breast cancer cases and controls or between ovarian cancer cases and combined control groups. The crude odds ratios (OR) and 95% confidence intervals (95% CI) associated with the RAD51 GC/CC genotype frequency was OR, 1.10; 95% CI, 0.80-1.41 for breast cancer and OR, 1.22; 95% CI, 0.92-1.62 for ovarian cancer. Similarly, there were no increased risks associated with the XRCC2 GA/AA genotype (OR, 0.98; 95% CI, 0.76-1.26 for breast cancer and OR, 0.93; 95% CI, 0.69-1.25 for ovarian cancer) or the XRCC3 CT/TT genotype (OR, 0.92; 95% CI, 0.77-1.10 for breast cancer and OR, 0.87; 95% CI, 0.71-1.08 for ovarian cancer). Results were little changed after adjustment for age and other measured risk factors. Although there was little statistical power to detect modest increases in risk for the homozygote variant genotypes, particularly for the rare RAD51 and XRCC2 variants, the data suggest that none of these variants play a major role in the etiology of breast or ovarian cancer.
A Correlation Study of Organochlorine Levels in Serum, Breast Adipose Tissue, and Gluteal Adipose Tissue among Breast Cancer Cases in India
Authors: Rusiecki Jennifer A. , Matthews Aleyama , Sturgeon Susan , Sinha Rashmi , Pellizzari Edo , Zheng Tongzhang , Baris Dalsu 
Published: September 2005

AbstractWe used data from a breast cancer pilot study carried out in Kerala, India in 1997, for which organochlorine levels were measured in three biological media, blood serum, breast adipose tissue, and gluteal adipose tissue, of 37 fasting breast cancer cases (pretreatment). Our objective was to investigate the relationships between organochlorine concentrations in different biological media. Gas-liquid chromatography determined serum, breast adipose, and gluteal adipose tissue levels of dichlorodiphenyltricholorethane, dichlorodiphenyldichloroethane, β-benzene hexachloride, and polychlorinated biphenyl (PCB) congeners, PCB-153 and PCB-180. Correlation plots were made and Spearman correlation coefficients (r) calculated for breast adipose tissue versus serum, gluteal adipose tissue versus serum, and breast adipose versus gluteal adipose tissue. We also examined paired ratios of all summary statistics. There were strong correlations among serum, breast adipose tissue, and gluteal adipose tissue concentrations for most organochlorines analyzed, one exception being gluteal versus serum for PCB-153. The correlations for all other comparisons ranged from r = 0.65 to 0.94. Serum (ng/g) versus adipose ratios approached 1:1 for most of the organochlorine pesticide comparisons and did not vary by summary statistic. To our knowledge, this is the first study to use three different media from fasting subjects and to comprehensively investigate the relationship between organochlorines measured across the three media for both organochlorine pesticides and PCBs. These data indicate that blood serum reflects the present body burden of a range of organochlorines to the same extent as adipose tissue, and they support the view that serum may be collected in lieu of adipose tissue to obtain similar information. However, such measurements are a combination of both recent exposures and past exposures, which have metabolized slowly and may still persist. Therefore, investigators should use caution when assigning a level as lifetime body burden.
Genotyping of Patients with Sporadic and Radiation-Associated Meningiomas
Authors: Sadetzki Siegal , Flint-Richter Pazit , Starinsky Sigal , Novikov Ilya , Lerman Yehuda , Goldman Boleslaw , Friedman Eitan 
Published: September 2005

Abstract
Ionizing radiation is the most established risk factor for meningioma formation. Our aim was to evaluate the main effect of selected candidate genes on the development of meningioma and their possible interaction with ionizing radiation in the causation of this tumor. The total study population included 440 cases and controls: 150 meningioma patients who were irradiated for tinea capitis in childhood, 129 individuals who were similarly irradiated but did not develop meningioma, 69 meningioma patients with no previous history of irradiation, and 92 asymptomatic population controls. DNA from peripheral blood samples was genotyped for single nucleotide polymorphisms (SNP) in 12 genes: NF2, XRCC1, XRCC3, XRCC5, ERCC2, Ki-ras, p16, cyclin D1, PTEN, E-cadherin, TGFB1, and TGFBR2. SNP analysis was done using the MassArray system (Sequenom, San Diego, CA) and computerized analysis by SpectroTYPER. Logistic regressions were applied to evaluate main effect of each gene on meningioma formation and interaction between gene and radiation. Intragenic SNPs in the Ki-ras and ERCC2 genes were associated with meningioma risk (odds ratio, 1.76; 95% confidence interval, 1.07-2.92 and odds ratio, 1.68; 95% confidence interval, 1.00-2.84, respectively). A significant interaction was found between radiation and cyclin D1 and p16 SNPs (P for interaction = 0.005 and 0.057, respectively). Our findings suggest that Ki-ras and ERCC2 SNPs are possible markers for meningioma formation, whereas cyclin D1 and p16 SNPs may be markers of genes that have an inverse effect on the risk to develop meningioma in irradiated and nonirradiated populations.
Sex Hormones, Risk Factors, and Risk of Estrogen Receptor–Positive Breast Cancer in Older Women: A Long-term Prospective Study
Authors: Cummings Steven R. , Lee Jennifer S. , Lui Li-Yung , Stone Katie , Ljung Britt Marie , Cauleys Jane A. ,   for the Study of Osteoporotic Fractures Research Group
Published: September 2005

Abstract
Objective: Antiestrogens reduce the risk of estrogen receptor–positive (ER+) but not ER-negative (ER−) breast cancer. Women at high risk of ER+ cancer would be the most likely to benefit from these treatments, but the best approach to predicting ER+ cancer is uncertain.
Methods: We prospectively assessed putative risk factors for breast cancer and archived serum at −190°C from a community-based cohort of 7,676 women ages ≥65 years who had no history of breast cancer. Follow-up for breast cancer over 10.5 years was 99% complete. Using a case-cohort design, we measured baseline levels of estradiol and testosterone in 196 cases of invasive ER+ cancer and 378 randomly selected controls.
Results: Women whose testosterone level in highest two quintiles had a 4-fold increased risk of ER+ breast cancer (P &lt; 0.0001). High estradiol concentration also indicated an increased risk but was not a significant predictor after adjustment for testosterone. Women with &gt;16 years of education had a 2.1 times increased risk (P = 0.03) of ER+ cancer, but no other risk factors were significantly related to an increased risk of ER+ cancer. Women with a family history of breast cancer had a 2.9-fold increased risk of ER− cancer (P = 0.002) but no increased risk of ER+ cancer (relative hazard = 1.2, 0.8-1.8).
Conclusions: High serum testosterone and advanced education predicted ER+ breast cancer. If confirmed, high testosterone level may be more accurate than family history of breast cancer and other conventional risk factors for identifying older women who are most likely to benefit from antiestrogen chemoprevention.
Hepatitis B 1762T/1764A Mutations, Hepatitis C Infection, and Codon 249 p53 Mutations in Hepatocellular Carcinomas from Thailand
Authors: Kuang Shuang-Yuan , Lekawanvijit Suree , Maneekarn Niwat , Thongsawat Satawat , Brodovicz Kimberly , Nelson Kenrad , Groopman John D. 
Published: September 2005

Abstract
Hepatocellular carcinoma is one of the leading causes of cancer death worldwide. The etiology of liver cancer is multifactorial, and infection with hepatitis B virus (HBV), whose pathogenesis is exacerbated by the acquisition of mutations that accelerate carcinogenesis, or hepatitis C virus (HCV) and dietary exposure to aflatoxin B1 all contribute to elevating one's risk for this disease. In this study, we sought to determine the contributions of these agents by measuring the occurrence of an HBV 1762T/1764A double mutation, an aflatoxin-specific 249G→T mutation of the p53 gene, and HCV in plasma of 34 HCC cases and 68 age- and gender-matched controls, and in 25 liver tumors from northern Thailand. In total, 14 cases, 5 controls, and 19 tumors had detectable levels of HBV DNA. All 14 cases, 2 controls (2.9%), and 17 tumors (89.5%) were positive for the HBV double mutation. Nine cases (26.5%), 10 controls (14.7%), and 6 tumors (24%) were positive for the p53 mutation. Five cases (14.7%), no controls, and 4 tumors (16%) had both mutations. The median age of HCC diagnosis in these 5 cases was 34 years versus 51 years for other cases. Five cases (14.7%) and 1 control (1.5%) were HCV enzyme immunoassay positive. Thus, specific HBV, HCV, and aflatoxin biomarkers reveal the complexity of risks contributing to HCC in northern Thailand and suggest further application of these biomarkers as intermediate end points in prevention, intervention trials, and etiologic investigations.
Cytochrome P450 1B1 and Catechol-O-Methyltransferase Genetic Polymorphisms and Breast Cancer Risk in Chinese Women: Results from the Shanghai Breast Cancer Study and a Meta-analysis
Authors: Wen Wanqing , Cai Qiuyin , Shu Xiao-Ou , Cheng Jia-Rong , Parl Fritz , Pierce Larry , Gao Yu-Tang , Zheng Wei 
Published: September 2005

Abstract
Cytochrome P450 1B1 (CYP1B1) and catechol-O-methyltransferase (COMT) are important estrogen-metabolizing enzymes and, thus, genetic polymorphisms of these enzymes may affect breast cancer risk. A population-based case-control study was conducted to assess the association of breast cancer risk with CYP1B1 and COMT polymorphisms. A meta-analysis was done to summarize the findings from this and previous studies. Included in this study were 1,135 incident breast cancer cases diagnosed from August 1996 through March 1998 among female residents of Shanghai and 1,235 randomly selected, age frequency-matched controls from the same general population. The common alleles of the CYP1B1 gene were Arg (79.97%) in codon 48, Ala (80.53%) in codon 119, and Leu (86.57%) in codon 432. The Val allele accounted for 72.46% of the total alleles identified in codon 108/158 of the COMT gene. No overall associations of breast cancer risk were found with any of the single nucleotide polymorphisms described above. This finding was supported by a meta-analysis of all previous published studies. No gene-gene interactions were observed between CYP1B1 and COMT genotypes. The associations of breast cancer risk with factors related to endogenous estrogen exposure, such as years of menstruation and body mass index, were not significantly modified by the CYP1B1 and COMT genotypes. We observed, however, that women who carried one copy of the variant allele in CYP1B1 codons 48 or 119 were less likely to have estrogen receptor–positive breast cancer than those who carried two copies of the corresponding wild-type alleles. The results from this study were consistent with those from most previous studies, indicating no major associations of breast cancer risk with CYP1B1 and COMT polymorphisms.
A Basal Epithelial Phenotype Is More Frequent in Interval Breast Cancers Compared with Screen Detected Tumors
Authors: Collett Karin , Stefansson Ingunn M. , Eide Johan , Braaten Audun , Wang Hege , Eide Geir Egil , Thoresen Steinar Ø. , Foulkes William D. , Akslen Lars A. 
Published: September 2005

Abstract
Interval breast cancer reduce the effectiveness of mammography screening programs. We studied 95 interval cancers, diagnosed during 1996 to 2001 as part of the population-based Norwegian Breast Cancer Screening Program. These cases were matched on size (±2.0 mm) to 95 screen-detected breast cancers, and the tumors were compared by immunohistochemical methods using tissue microarrays. Patients with interval cancers were more likely to be younger [odds ratio (OR), 4.7; P = 0.0001], to have dense breasts (OR, 3.4; P = 0.004), and to have estrogen receptor–negative tumors (OR, 2.6, P = 0.01), and p53 expression was more frequent (OR, 4.0; P = 0.001). Notably, interval cancers were more likely to have a basal epithelial phenotype, in that expression of cytokeratin 5/6 (OR, 2.3; P = 0.04) and P-cadherin (OR, 2.5; P = 0.04) was more frequent in interval cases than in size-matched, screen-detected tumors. In a logistic regression model, p53 expression, age, and breast density were independent predictors of interval cancers. Our data suggest that breast cancers with a basal epithelial phenotype are more likely than nonbasal breast cancers to present between regular mammograms.
Resveratrol-Induced Gene Expression Profiles in Human Prostate Cancer Cells
Authors: Jones Sunita B. , DePrimo Samuel E. , Whitfield Michael L. , Brooks James D. 
Published: September 2005

Abstract
Objective: The transhydroxystilbene resveratrol is found at high levels in red wine and grapes, and red wine consumption may be inversely associated with prostate cancer risk. To gain insights into the possible mechanisms of action of resveratrol in human prostate cancer, we did DNA microarray analysis of the temporal transcriptional program induced by treatment of the human prostate cancer cell line LNCaP with resveratrol.
Methods: Spotted DNA microarrays containing over 42,000 elements were used to obtain a global view of the effects of resveratrol on gene expression. Prostate-specific antigen (PSA) and androgen receptor (AR) expression were determined by Northern blot and immunoblot analyses. Cell proliferation was determined by the 3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide assay and cell cycle analysis by flow cytometry.
Results: We observed time-dependent expression changes in &gt;1,600 transcripts as early as 6 hours after treatment with resveratrol. Most striking was the modulation of a number of important genes in the androgen pathway including PSA and AR. Resveratrol also down-regulated expression of cell cycle and proliferation-specific genes involved in all phases of the cell cycle, induced negative regulators of proliferation, caused accumulation of cells at the sub-G1 and S phases of the cell cycle, and inhibited cell proliferation in a time- and dose-dependent manner.
Conclusion: Resveratrol produces gene expression changes in the androgen axis and cell cycle regulators that may underlie its putative anticancer activities in prostate cancer.
Dietary Intake of Folate and Riboflavin, MTHFR C677T Genotype, and Colorectal Adenoma Risk: A Dutch Case-Control Study
Authors: van den Donk Maureen , Buijsse Brian , van den Berg Saskia W. , Ocké Marga C. , Harryvan Jan L. , Nagengast Fokko M. , Kok Frans J. , Kampman Ellen 
Published: September 2005

Abstract
We investigated the associations between dietary intake of folate and vitamin B2, MTHFR C677T genotype, and colorectal adenomas in a Dutch case-control study. Data of cases with at least one histologically confirmed colorectal adenoma (n = 768) and controls with no history of any type of colorectal polyp (n = 709) were included. Dietary intake was assessed using a food-frequency questionnaire. Multivariable models included age and, if appropriate, dietary folate and calcium intake. The adjusted odds ratio (OR) and 95% confidence interval (CI) for the highest compared with the lowest sex-specific tertile of intake were 1.32 (95% CI, 1.01-1.73) for folate and 0.51 (95% CI, 0.36-0.73) for vitamin B2. Folate seemed to be a risk factor, especially when vitamin B2 intake was low; vitamin B2 was inversely associated with adenomas, especially with relatively high folate intake. No association was observed between MTHFR C677T genotype and colorectal adenomas. The inverse association between vitamin B2 intake and colorectal adenoma risk seemed to be more pronounced among those with the MTHFR TT genotype. We conclude that this study does not provide evidence for a decreased colorectal adenoma risk for subjects with high dietary intake of folate. It suggests, however, an inverse association between vitamin B2 and colorectal adenomas, which may be more relevant for those with the MTHFR TT genotype.