bluuebunny/crossref_metadata_2025_split huggingface dataset:
Genetic Variants in the Vitamin D Receptor Are Associated with Advanced Prostate Cancer at Diagnosis: Findings from the Prostate Testing for Cancer and Treatment Study and a Systematic Review
Authors: Chen Lina , Davey Smith George , Evans David M. , Cox Angela , Lawlor Debbie A. , Donovan Jenny , Yuan Wei , Day Ian N. M. , Martin Richard M. , Lane Athene , Rodriguez Santi , Davis Michael , Zuccolo Luisa , Collin Simon M. , Hamdy Freddie , Neal David , Lewis Sarah J. 
Published: November 2009

Abstract
Low levels of plasma vitamin D have been implicated as a possible risk factor for both prostate cancer incidence and advanced disease, and recent phase II trials suggest that vitamin D supplementation might delay progression of prostate cancer. Common polymorphisms in the vitamin D receptor (VDR) are associated with VDR activity and are therefore potentially useful proxies for assessing whether vitamin D is causally related to advanced prostate cancer. We genotyped five well-known VDR polymorphisms in 1,604 men with prostate cancer from the Prostate Testing for Cancer and Treatment study. Our aim was to examine the association between VDR polymorphisms and cancer stage (localized versus advanced) as well as cancer grade (Gleason score &lt;7 versus ≥7). Moreover, we also carried out a systematic review and meta-analysis of 13 similar studies. As a result of our meta-analysis, we revealed three polymorphisms, BsmI, ApaI, and TaqI, associated with high Gleason score with an overall summary odds ratios (95% confidence intervals) of 1.12 (1.00-1.25; bb versus BB + Bb), 1.25 (1.02-1.53; aa versus AA + Aa), and 0.82 (0.69-0.98; Tt + tt versus TT), respectively. The haplotype analysis revealed that the BsmI (B)-ApaI (A)-TaqI (t) participants compared with BsmI (b)-ApaI (a)-TaqI (T) individuals were less likely to have high Gleason scores (odds ratio, 0.84; 95% confidence interval, 0.71-1.00; Punadjusted = 0.050; Padjusted = 0.014). Our finding provides some support for the hypothesis that low levels of vitamin D may increase the risk of prostate cancer progression. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2874–81)
Elevated Cancer Mortality in the Relatives of Patients with Pancreatic Cancer
Authors: Wang Li , Brune Kieran A. , Visvanathan Kala , Laheru Daniel , Herman Joseph , Wolfgang Christoper , Schulick Richard , Cameron John L. , Goggins Michael , Hruban Ralph H. , Klein Alison P. 
Published: November 2009

Abstract
Most inherited cancer syndromes are characterized by the familial clustering of cancers at several organ sites. To determine if cancers, other than pancreatic cancer, cluster in pancreatic cancer kindreds, we examined mortality patterns among the relatives of National Familial Pancreatic Tumor Registry probands. Over 200,000 person-years of follow-up from 8,564 first-degree relatives of probands and 1,007 spouse controls were included in these analyses. We compared mortality rates of National Familial Pancreatic Tumor Registry participants to US population rates using weighed standardized mortality ratios (wSMR). Analyses were stratified by family history of pancreatic cancer (sporadic versus familial), family history of young onset pancreatic cancer (&lt;50 years), and family history score. Cancer mortality was increased in both the relatives of sporadic probands [wSMR 1.55, 95% confidence interval (95% CI) 1.39-1.73] and familial probands (wSMR 1.41, 95% CI 1.26-1.58). Relatives of familial probands had a significantly increased risk of dying from breast (wSMR 1.66, 95% CI 1.15-2.34), ovarian (wSMR 2.05, 95% CI 1.10-3.49), and bile duct cancers (wSMR 2.89, 95% CI 1.04-6.39). Relatives of sporadic probands were at increased risk of dying from bile duct cancer (wSMR 3.01, 95% CI 1.09-6.67). Relatives of young onset probands were at higher risk of dying from cancers of the breast (wSMR 1.98, 95% CI 1.01-3.52), colon (wSMR 2.31, 95% CI 1.30-3.81) and prostate (wSMR 2.31, 95% CI 1.14-4.20). Increased cancer mortality was not observed in the spouse controls. Our results show that relatives of pancreatic cancer patients are at higher risk of developing cancers at other sites and highlight the importance of complete family history in clinical risk assessment. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2829–34)
Enrichment of Low Penetrance Susceptibility Loci in a Dutch Familial Colorectal Cancer Cohort
Authors: Middeldorp Anneke , Jagmohan-Changur Shantie , van Eijk Ronald , Tops Carli , Devilee Peter , Vasen Hans F. A. , Hes Frederik J. , Houlston Richard , Tomlinson Ian , Houwing-Duistermaat Jeanine J. , Wijnen Juul T. , Morreau Hans , van Wezel Tom 
Published: November 2009

Abstract
Recent genome-wide association studies have identified several loci that confer an increased risk of colorectal cancer (CRC). We studied the role of the 8q24.21 (rs6983267), 18q21.1 (rs12953717), 15q13.3 (rs4779584), 11q23.1 (rs3802842), 8q23.3 (rs16892766), and 10p14 (rs10795668) risk variants in a series of 995 Dutch CRC cases and 1340 controls. The CRC cases were selected on basis of having a family history of CRC and/or early-onset disease. The detailed clinical and molecular data available on the cases allowed us to examine the relationship between risk variants and clinicopathologic characteristics. We replicated the association with an increased risk of CRC cancer for all loci, except 10p14. The association with the variant on chromosome 15q13.3 was confirmed for the first time. The risks associated with variants in our series were higher (not significant) than those previously reported, consistent with our series reflecting genetic enrichment. Moreover, we show that familial CRC cases possess an increased number of risk alleles compared with solitary CRC cases (early-onset; mean age at diagnosis of 48.5 years). We also identified a significant increase in the number of risk alleles in families with early-onset disease (≤50 years) compared with late-onset families (&gt;50 years). In solitary CRC patients, enrichment for risk alleles was not observed, suggesting that other causes of increased CRC risk play a role in these cases. Overall, our results suggest that clustering of low-risk variants may explain part of the excess risk in CRC families. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3062–7)
DNA Hypermethylation ofESR1andPGRin Breast Cancer: Pathologic and Epidemiologic Associations
Authors: Gaudet Mia M. , Campan Mihaela , Figueroa Jonine D. , Yang Xiaohong R. , Lissowska Jolanta , Peplonska Beata , Brinton Louise A. , Rimm David L. , Laird Peter W. , Garcia-Closas Montserrat , Sherman Mark E. 
Published: November 2009

AbstractImproved understanding of the etiology of estrogen receptor-α (ERα)–negative and progesterone receptor (PR)–negative breast cancers may permit improved risk prediction. In vitro studies implicate DNA hypermethylation of the ERα and PR promoters in the pathogenesis of ERα-negative and PR-negative tumors, but results are not definitive. We evaluated 200 invasive breast cancers selected from a population-based case-control study. DNA extracted from fixed tumor tissue cores was tested using MethyLight to assess DNA methylation at four CpG islands: ESR1 promoters A and B; PGR promoters A and B; and a CpG shore, ESR1 promoter C. DNA methylation results were compared with levels of ERα and PR, tumor characteristics, and breast cancer risk factors. We observed mild to moderate DNA methylation levels in most tumors for ESR1 promoters A and B and PGR promoter B, and a few tumors showed mild methylation in PGR promoter A. In contrast, ESR1 promoter C showed a wide range of methylation and was weakly correlated with lower expression levels of ERα (β = −0.26; P &lt; 0.0001) and PR (β = −0.25; P &lt; 0.0001). The percentage of tumors with methylated PGR promoters A and B was significantly higher for tumors with low ERα (A, Fisher's test P = 0.0001; B, P = 0.033) and PR levels (A, P = 0.0006; B, P = 0.001). Our data suggest that the relationships between DNA methylation of ESR1 and PGR promoters and protein expression are weak and unlikely to represent a predominant mechanism of receptor silencing. In contrast to CpG islands, ESR1 promoter C showed a wider range of methylation levels and inverse associations with ERα and PR expression. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3036–43)
Urinary Prostaglandin E2 Metabolite and Gastric Cancer Risk in the Shanghai Women's Health Study
Authors: Dong Linda M. , Shu Xiao-Ou , Gao Yu-Tang , Milne Ginger , Ji Bu-Tian , Yang Gong , Li Hong-Lan , Rothman Nathaniel , Zheng Wei , Chow Wong-Ho , Abnet Christian C. 
Published: November 2009

Abstract
Chronic inflammation has been implicated in the etiology of gastric cancer. Prostaglandin E2 (PGE2) is one of the major end-products of the cyclooxygenase-2 pathway, an enzyme that is an important mediator of inflammation. Using a novel method of quantifying the primary urinary metabolite of PGE2 (PGE-M; 11α-hydroxy-9,15-dioxo-2,3,4,5-tetranorprostane-1,20-dioic acid), we evaluated urinary PGE-M concentrations in association with subsequent risk of development of gastric cancer in the Shanghai Women's Health Study, a large population-based prospective cohort, using a nested case-control study design. Controls were matched (1:1) to 153 gastric cancer cases by menopausal status; age, time, and date of sample collection; time interval since last meal; and availability of urine sample. Odds ratios (95% confidence intervals) were calculated using conditional logistic regression adjusted for potential confounders. Baseline urinary PGE-M levels were slightly higher among gastric cancer cases with a median of 6.4 ng/mg creatinine (interquartile range, 3.4-11.2) compared with 5.4 ng/mg creatinine among controls (interquartile range, 2.8-9.0), but this difference was not statistically significant (P = 0.34, Wilcoxon). With increasing quartiles of urinary PGE-M levels, the odds ratios (95% confidence intervals) for risk of gastric cancer increased in quartiles 2 to 4: 1.00 (0.48-2.08), 1.40 (0.67-2.91), and 1.98 (0.95-4.13), with a statistically significant test for trend (P = 0.04). The association persisted after additional adjustment for Helicobacter pylori status and was slightly strengthened among non–nonsteroidal anti-inflammatory drug users, subjects with positive H. pylori status, and for cases diagnosed within 46 months after study enrollment. Our findings suggest that higher levels of urinary PGE-M, a marker of inflammation, may be associated with gastric cancer risk. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3075–8)
Modulation of Human Serum Glutathione S-Transferase A1/2 Concentration by Cruciferous Vegetables in a Controlled Feeding Study Is Influenced by GSTM1 and GSTT1 Genotypes
Authors: Navarro Sandi L. , Chang Jyh-Lurn , Peterson Sabrina , Chen Chu , King Irena B. , Schwarz Yvonne , Li Shuying S. , Li Lin , Potter John D. , Lampe Johanna W. 
Published: November 2009

Abstract
Glutathione S-transferases (GST) detoxify a wide range of carcinogens. Isothiocyanates (ITC), from cruciferous vegetables, are substrates for and inducers of GST. GST variants may alter ITC clearance such that response to crucifers varies by genotype. In a randomized cross-over trial, we tested the hypothesis that changes in serum GSTA1/2 concentration in response to cruciferous vegetable feeding depends on GSTM1/GSTT1 genotype. Thirty-three men and 34 women (age 20-40 years) ate four 14-day controlled diets—basal (vegetable-free), basal supplemented with two different doses of crucifers (“single dose” and “double dose”), and single-dose cruciferous-plus-apiaceous vegetables—fed per kilogram of body weight. Fasting bloods from days 0, 7, 11, and 14 of each diet period were analyzed for serum GSTA1/2 by ELISA. GSTA1/2 increased with single- and double-dose cruciferous compared with basal diet (10% and 13%, respectively; P = 0.02 and 0.004), but cruciferous-plus-apiaceous did not differ from basal (P = 0.59). Overall, GSTA1/2 was higher in GSTM1-null/GSTT1-null than GSTM1+/GSTT1+ individuals (4,198 ± 338 and 3,372 ± 183 pg/mL; P = 0.03). The formal interaction of genotype-by-diet was not statistically significant, but the GSTA1/2 increase during the single-dose cruciferous diet was among GSTM1-null/GSTT1-null individuals (by 28%; P = 0.008), largely explained by GSTM1-null/GSTT1-null men (by 41%; P = 0.01). GSTA1/2 increased during the double-dose cruciferous diet in both GSTM1-null/GSTT1-null men (by 35%; P = 0.04) and GSTM1+/GSTT1+ men (by 26%; P = 0.01) but not in women. In summary, cruciferous vegetable supplementation increased GSTA1/2, but the effect was most marked in GSTM1-null/GSTT1-null men. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2974–8)
Rates of Atypical Ductal Hyperplasia Have Declined with Less Use of Postmenopausal Hormone Treatment: Findings from the Breast Cancer Surveillance Consortium
Authors: Menes Tehillah S. , Kerlikowske Karla , Jaffer Shabnam , Seger Deborah , Miglioretti Diana L. 
Published: November 2009

Abstract
Aim: To examine risk factors and rates of atypical ductal hyperplasia (ADH) with and without associated breast cancer over time and tumor characteristics of breast cancer with and without associated ADH in women previously screened with mammography.
Methods: Data on screening mammograms done between 1996 and 2005 were collected from mammography registries that participate in the Breast Cancer Surveillance Consortium. Associations between age, family history of breast cancer, postmenopausal hormone treatment (HT), and final pathology result (ADH or cancer with or without ADH in the same breast) were examined. Rates of different outcomes were calculated per exam year. Tumor characteristics of cancers with and without associated ADH were compared.
Results: A total of 2,453,483 screening mammograms were associated with 1,064 biopsies with ADH, 833 breast cancers with ADH, and 8,161 cancers with no ADH. Postmenopausal HT use decreased significantly from 35% to 11% during the study period. Rates of ADH decreased from a peak of 5.5/10,000 mammograms in 1999 to 2.4/10,000 in 2005. Rates of cancer with ADH decreased from a peak of 4.3/10,000 mammograms in 2003 to 3.3/10,000 in 2005. ADH and breast cancer were significantly associated with use of postmenopausal HT. Cancer associated with ADH was of lower grade and stage and more estrogen receptor positive than cancer with no ADH.
Summary: Postmenopausal HT is associated with an increased risk of ADH with or without cancer. Rates of ADH have decreased over the past decade, which may be partially explained by the significant reduction in use of postmenopausal HT. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2822–8)
Identifying Genes for Establishing a Multigenic Test for Hepatocellular Carcinoma Surveillance in Hepatitis C Virus-Positive Cirrhotic Patients
Authors: Archer Kellie J. , Mas Valeria R. , David Krystle , Maluf Daniel G. , Bornstein Karen , Fisher Robert A. 
Published: November 2009

Abstract
In this study, we used the Affymetrix HG-U133A version 2.0 GeneChips to identify genes capable of distinguishing cirrhotic liver tissues with and without hepatocellular carcinoma by modeling the high-dimensional dataset using an L1 penalized logistic regression model, with error estimated using N-fold cross-validation. Genes identified by gene expression microarray included those that have important links to cancer development and progression, including VAMP2, DPP4, CALR, CACNA1C, and EGR1. In addition, the selected molecular markers in the multigenic gene expression classifier were subsequently validated using reverse transcriptase-real time PCR, and an independently acquired gene expression microarray dataset was downloaded from Gene Expression Omnibus. The multigenetic classifier derived herein did similarly or better than standard abdominal ultrasonography and serum α-fetoprotein, which are currently used for hepatocellular carcinoma surveillance. Because early hepatocellular carcinoma diagnosis increases survival by increasing access to therapeutic options, these molecular markers may prove useful for early diagnosis of hepatocellular carcinoma, especially if prospectively validated and translated into gene products that can be reproducibly and reliably tested noninvasively. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2929–32)
Predisposition for TMPRSS2-ERG Fusion in Prostate Cancer by Variants in DNA Repair Genes
Authors: Luedeke Manuel , Linnert Carmen M. , Hofer Matthias D. , Surowy Harald M. , Rinckleb Antje E. , Hoegel Josef , Kuefer Rainer , Rubin Mark A. , Vogel Walther , Maier Christiane 
Published: November 2009

Abstract
The somatic fusion of TMPRSS2 to ETS oncogenes is a common event in prostate cancer (PCa). We hypothesized that defects in DNA repair may lead to an increase of chromosomal rearrangements and thus to the occurrence of ETS oncogene fusion. We have previously conducted a genome-wide linkage analysis in TMPRSS2-ERG fusion-positive PCa families, revealing potential susceptibility loci on chromosomes 5q14, 9q21, 10q26, 11q24, 12q15, 13q12, 18q, and Xq27. In the present study, nine candidate genes from these regions were selected from the context of DNA repair and screened for mutations in TMPRSS2-ERG fusion-positive families. Thirteen nonsynonymous variants, 5 of which had a minor allele frequency of &lt;0.05, were genotyped in 210 familial cases, 47 of which with a known TMPRSS2-ERG status, 329 sporadic cases, and 512 controls. Significant association of TMPRSS2-ERG fusion-positive PCa was found with rare variants in the genes for POLI [variant F532S: P = 0.0011; odds ratios (OR), 4.62; 95% confidence interval (95% CI), 1.84-11.56] and ESCO1 (variant N191S: P = 0.0034; OR, 4.27; 95% CI, 1.62-11.28). Additional findings, regardless of TMPRSS2-ERG status, were the overrepresentation of a rare BRCA2 variant (V2728I: P = 0.03; OR, 6.16; 95% CI, 1.19-32.00) in familial PCa and of a common allele of RMI1 (variant N455S: P = 0.02; OR, 1.33; 95% CI, 1.04-1.70) in unselected PCa cases. The DNA repair genes POLI and ESCO1 are proposed as susceptibility genes for TMPRSS2-ERG fusion-positive PCa that warrant further investigation. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3030–5)
Dietary Patterns and Prostate Cancer Risk
Authors: Muller David C. , Severi Gianluca , Baglietto Laura , Krishnan Kavitha , English Dallas R. , Hopper John L. , Giles Graham G. 
Published: November 2009

Abstract
Recent studies report that certain dietary patterns, especially those high in red and processed meats, are associated with prostate cancer risk. We prospectively investigated associations between empirically derived dietary patterns and prostate cancer risk using the Melbourne Collaborative Cohort Study. We followed 14,627 men of ages 34 to 75 years for an average of 13.6 years, and identified 1,018 incident prostate cancers. Factor analysis of the 121-item food frequency questionnaire identified four factors with eigenvalues &gt;2 that explained 67% of the total variance. Using Cox proportional hazard models, we found no association between any dietary pattern and prostate cancer risk overall (all Ptrend ≥ 0.2). The hazard ratios for quartiles of the dietary pattern scores ranged from 0.87 to 1.14 and all 95% confidence intervals included 1. The analyses by aggressiveness, Gleason score groups, and age at diagnosis did not show any association (all Ptrend &gt; 0.07). (Cancer Epidemiol Biomarkers Prev 2009;18(11):3126–9)
Global and Seasonal Assessment of Interactions between Climate and Vegetation Biophysical Processes: A GCM Study with Different Land–Vegetation Representations
Authors: Xue Yongkang , De Sales Fernando , Vasic Ratko , Mechoso C. Roberto , Arakawa Akio , Prince Stephen 
Published: November 2009

Abstract
A global and seasonal assessment of regions of the earth with strong climate–vegetation biophysical process (VBP) interactions is provided. The presence of VBP and degree of VBP effects on climate were assessed based on the skill of simulations of observed global precipitation by two general circulation models of the atmosphere coupled to three land models with varying degrees of complexity in VBP representation. The simulated VBP effects on precipitation were estimated to be about 10% of observed precipitation globally and 40% over land; the strongest impacts were in the monsoon regions. Among these, VBP impacts were highest on the West African, South Asian, East Asian, and South American monsoons. The specific characteristics of vegetation–precipitation interactions in northern high latitudes were identified. Different regions had different primary impact season(s) depending on regional climate characteristics and geographical features. The characteristics of VBP effects on surface energy and water balance as well as their interactions were also analyzed. The VBP-induced change in evaporation was the dominant factor in modulating the surface energy and water balance. The land–cloud interaction had substantial effects in the feedback. Meanwhile, the monsoon regions, midlatitudes lands, and high-latitude lands each exhibited quite different characteristics in circulation response to surface heating changes. This study is the first to compare simulations with observations to identify and assess global seasonal mean VBP feedback effects. It is concluded that VBPs are a major component of the global water cycle.
Uncertainty in Scatterometer-Derived Vorticity
Authors: Bourassa Mark A. , McBeth Ford Kelly 
Published: November 2009

Abstract
A more versatile and robust technique is developed for determining area-averaged surface vorticity based on vector winds from swaths of remotely sensed wind vectors. This technique could also be applied to determine the curl of stress, and it could be applied to any gridded dataset of winds or stresses. The technique is discussed in detail and compared to two previous studies that focused on early development of tropical systems. Error characteristics of the technique are examined in detail. Specifically, three independent sources of error are explored: random observational error, truncation error, and representation error. Observational errors are due to random errors in the wind observations and determined as a worst-case estimate as a function of averaging spatial scale. The observational uncertainty in the Quick Scatterometer (QuikSCAT)-derived vorticity averaged for a roughly circular shape with a 100-km diameter, expressed as one standard deviation, is approximately 0.5 × 10−5 s−1 for the methodology described herein. Truncation error is associated with the assumption of linear changes between wind vectors. Uncertainty related to truncation has more spatial organization in QuikSCAT data than observational uncertainty. On 25- and 50-km scales, the truncation errors are very large. The third type of error, representation error, is due to the size of the area being averaged compared to values with 25-km length scales. This type of error is analogous to oversmoothing. Tropical and subtropical low pressure systems from three months of QuikSCAT observations are used to examine truncation and representation errors. Representation error results in a bias of approximately −1.5 × 10−5 s−1 for area-averaged vorticity calculated on a 100-km scale compared to vorticity calculated on a 25-km scale. The discussion of these errors will benefit future projects of this nature as well as future satellite missions.