bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sun and Solarium Exposure and Melanoma Risk: Effects of Age, Pigmentary Characteristics, and Nevi
Authors: Veierød Marit Bragelien , Adami Hans-Olov , Lund Eiliv , Armstrong Bruce Konrad , Weiderpass Elisabete 
Published: January 2010

AbstractBackground: Few prospective studies have analyzed solar and artificial (solarium) UV exposure and melanoma risk. We investigated these associations in a Norwegian-Swedish cohort study and addressed effect modification by age, pigmentary characteristics, and nevi.Methods: The cohort included women ages 30 to 50 years at enrollment from 1991 to 1992. Host factors and exposure to sun and solariums in life decades were collected by questionnaire at enrollment. Relative risks (RR) with 95% confidence intervals (CI) were estimated by Poisson regression.Results: Among 106,366 women with complete follow-up through 2005, 412 melanoma cases were diagnosed. Hair color and large, asymmetric nevi on the legs were strongly associated with melanoma risk (Ptrend &lt; 0.001), and the RR for ≥2 nevi increased from brown/black to blond/yellow to red-haired women (RRs, 1.72, 3.30, and 4.95, respectively; Pinteraction = 0.18). Melanoma risk increased significantly with the number of sunburns and bathing vacations in the first three age decades (Ptrend ≤ 0.04) and solarium use at ages 30 to 39 and 40 to 49 years [RRs for solarium use ≥1 time/mo 1.49 (95% CI, 1.11-2.00) and 1.61 (95% CI 1.10-2.35), respectively; Ptrend ≤ 0.02]. Risk of melanoma associated with sunburns, bathing vacations, and solarium use increased with accumulating exposure across additional decades of life.Conclusions: Melanoma risk seems to continue to increase with accumulating intermittent sun exposure and solarium use in early adulthood. Apparently, super-multiplicative joint effects of nevi and hair color identify people with red hair and multiple nevi as a very high risk group and suggest important gene-gene interactions involving MC1R in melanoma etiology. Cancer Epidemiol Biomakers Prev; 19(1);111–20
Dietary Glucosinolate Intake, Polymorphisms in Selected Biotransformation Enzymes, and Risk of Prostate Cancer
Authors: Steinbrecher Astrid , Rohrmann Sabine , Timofeeva Maria , Risch Angela , Jansen Eugène , Linseisen Jakob 
Published: January 2010

Abstract
A protective role of glucosinolates in prostate cancer development might be mediated by the induction of biotransformation enzymes. These enzymes, enhancing the elimination of carcinogens from the body, are known to be polymorphic. Therefore, we evaluated whether a possible association between glucosinolate intake and prostate cancer risk is modified by polymorphisms in GSTT1, GSTM1, GSTA1, GSTP1, or NOQ1 genes. A case-control study including 248 prostate cancer cases and 492 matched controls was nested in the prospective European Prospective Investigation into Cancer and Nutrition-Heidelberg cohort. At baseline, participants provided dietary and lifestyle data and blood samples, which were used for genotyping and measurement of serum glutathione S-transferase-α concentration. Odds ratios and 95% confidence intervals were calculated by conditional logistic regression. We found an inverse association of glucosinolate intake with prostate cancer risk (adjusted odds ratio, 0.72 per 10 mg/d increment; 95% confidence interval, 0.53-0.96). Stratification by genotype showed significantly reduced risks for subjects with wild-type of NQO1 (C609T) compared with CT or TT carriers (Pinteraction = 0.04). Those with deletions in both GSTM1 and GSTT1 genes combined had a significantly reduced risk with increasing glucosinolate intake (Pinteraction = 0.01). There was no effect modification of glucosinolate intake and cancer risk by GSTA1 (G-52A) or GSTP1 (A313G) genotype, but serum glutathione S-transferase-α concentrations were inversely associated with prostate cancer. This study showed that the inverse association between glucosinolate intake and prostate cancer risk was modified by NQO1 (C609T) and GSTM1 and GSTT1 deletion polymorphisms. This information will help to further elucidate the mechanism of action of potentially protective substances in vivo. Cancer Epidemiol Biomarkers Prev; 19(1); 135–43
Genetic Variability in theMTHFRGene and Colorectal Cancer Risk Using the Colorectal Cancer Family Registry
Authors: Levine A. Joan , Figueiredo Jane C. , Lee Won , Poynter Jenny N. , Conti David , Duggan David J. , Campbell Peter T. , Newcomb Polly , Martinez Maria Elena , Hopper John L. , Le Marchand Loic , Baron John A. , Limburg Paul J. , Ulrich Cornelia M. , Haile Robert W. 
Published: January 2010

AbstractBackground: The MTHFR C677T TT genotype is associated with a 15% to 18% reduction in colorectal cancer risk, but it is not clear if other variants of the gene are associated with colorectal cancer risk.Methods: We used a tagSNP approach to comprehensively evaluate associations between variation in the MTHFR gene and colorectal cancer risk using a large family-based case-control study of 1,750 population-based and 245 clinic-based families from the Colon Cancer Family Registry. We assessed 22 TagSNPs, selected based on pairwise r2 &gt;95%, using the Haploview Tagger and genotyped the TagSNPs on the Illumina GoldenGate or Sequenom platforms. The association between single nucleotide polymorphisms and colorectal cancer was assessed using log-additive, codominant, and recessive models.Results: From studying the population-based families, the C677T (rs1801133) and A1298C (rs1801131) polymorphisms were associated with a decreased colorectal cancer risk overall [odds ratio (OR), 0.81; 95% confidence interval (95% CI), 0.63-1.04; and OR, 0.82; 95% CI, 0.64-1.07, respectively]. The 677 TT genotype was associated with a decreased risk of microsatellite-stable/microsatellite-low tumors (OR, 0.69; 95% CI, 0.49-0.97) and an increased risk of microsatellite-high tumors (OR, 2.22; 95% CI, 0.91-5.43; Pinteraction = 0.01), as well as an increased risk of proximal cancers and a decreased risk of distal and rectal cancers (Pinteraction = 0.02). No other single nucleotide polymorphism was associated with risk overall or within subgroups.Conclusion: The 677 TT and 1298 CC genotypes may each be associated with a decrease in colorectal cancer risk. We observed little evidence of additional genetic variability in the MTHFR gene relevant to colorectal cancer risk. Cancer Epidemiol Biomarkers Prev; 19(1); 89–100
ESR1/SYNE1 Polymorphism and Invasive Epithelial Ovarian Cancer Risk: An Ovarian Cancer Association Consortium Study
Authors: Doherty Jennifer A. , Rossing Mary Anne , Cushing-Haugen Kara L. , Chen Chu , Van Den Berg David J. , Wu Anna H. , Pike Malcolm C. , Ness Roberta B. , Moysich Kirsten , Chenevix-Trench Georgia , Beesley Jonathan , Webb Penelope M. , Chang-Claude Jenny , Wang-Gohrke Shan , Goodman Marc T. , Lurie Galina , Thompson Pamela J. , Carney Michael E. , Hogdall Estrid , Kjaer Susanne Kruger , Hogdall Claus , Goode Ellen L. , Cunningham Julie M. , Fridley Brooke L. , Vierkant Robert A. , Berchuck Andrew , Moorman Patricia G. , Schildkraut Joellen M. , Palmieri Rachel T. , Cramer Daniel W. , Terry Kathryn L. , Yang Hannah P. , Garcia-Closas Montserrat , Chanock Stephen , Lissowska Jolanta , Song Honglin , Pharoah Paul D.P. , Shah Mitul , Perkins Barbara , McGuire Valerie , Whittemore Alice S. , Di Cioccio Richard A. , Gentry-Maharaj Aleksandra , Menon Usha , Gayther Simon A. , Ramus Susan J. , Ziogas Argyrios , Brewster Wendy , Anton-Culver Hoda ,   The Australian Ovarian Cancer Study Management Group,   The Australian Cancer Study (Ovarian Cancer), Pearce Celeste Leigh ,   on behalf of the Ovarian Cancer Association Consortium (OCAC)
Published: January 2010

Abstract
We genotyped 13 single nucleotide polymorphisms (SNPs) in the estrogen receptor alpha gene (ESR1) region in three population-based case-control studies of epithelial ovarian cancer conducted in the United States, comprising a total of 1,128 and 1,866 non-Hispanic white invasive cases and controls, respectively. A SNP 19 kb downstream of ESR1 (rs2295190, G-to-T change) was associated with invasive ovarian cancer risk, with a per-T-allele odds ratio (OR) of 1.24 [95% confidence interval (CI), 1.06-1.44, P = 0.006]. rs2295190 is a nonsynonymous coding SNP in a neighboring gene called spectrin repeat containing, nuclear envelope 1 (SYNE1), which is involved in nuclear organization and structural integrity, function of the Golgi apparatus, and cytokinesis. An isoform encoded by SYNE1 has been reported to be downregulated in ovarian and other cancers. rs2295190 was genotyped in an additional 12 studies through the Ovarian Cancer Association Consortium, with 5,279 invasive epithelial cases and 7,450 controls. The per-T-allele OR for this 12-study set was 1.09 (95% CI, 1.02-1.17; P = 0.017). Results for the serous subtype in the 15 combined studies were similar to those overall (n = 3,545; OR, 1.09; 95% CI, 1.01-1.18; P = 0.025), and our findings were strongest for the mucinous subtype (n = 447; OR, 1.32; 95% CI, 1.11-1.58; P = 0.002). No association was observed for the endometrioid subtype. In an additional analysis of 1,459 borderline ovarian cancer cases and 7,370 controls, rs2295190 was not associated with risk. These data provide suggestive evidence that the rs2295190 T allele, or another allele in linkage disequilibrium with it, may be associated with increased risk of invasive ovarian cancer. Cancer Epidemiol Biomarkers Prev; 19(1); 244–50
Occupational Exposure to Formaldehyde, Hematotoxicity, and Leukemia-Specific Chromosome Changes in Cultured Myeloid Progenitor Cells
Authors: Zhang Luoping , Tang Xiaojiang , Rothman Nathaniel , Vermeulen Roel , Ji Zhiying , Shen Min , Qiu Chuangyi , Guo Weihong , Liu Songwang , Reiss Boris , Freeman Laura Beane , Ge Yichen , Hubbard Alan E. , Hua Ming , Blair Aaron , Galvan Noe , Ruan Xiaolin , Alter Blanche P. , Xin Kerry X. , Li Senhua , Moore Lee E. , Kim Sungkyoon , Xie Yuxuan , Hayes Richard B. , Azuma Mariko , Hauptmann Michael , Xiong Jun , Stewart Patricia , Li Laiyu , Rappaport Stephen M. , Huang Hanlin , Fraumeni Joseph F. , Smith Martyn T. , Lan Qing 
Published: January 2010

Abstract
There are concerns about the health effects of formaldehyde exposure, including carcinogenicity, in light of elevated indoor air levels in new homes and occupational exposures experienced by workers in health care, embalming, manufacturing, and other industries. Epidemiologic studies suggest that formaldehyde exposure is associated with an increased risk of leukemia. However, the biological plausibility of these findings has been questioned because limited information is available on the ability of formaldehyde to disrupt hematopoietic function. Our objective was to determine if formaldehyde exposure disrupts hematopoietic function and produces leukemia-related chromosome changes in exposed humans. We examined the ability of formaldehyde to disrupt hematopoiesis in a study of 94 workers in China (43 exposed to formaldehyde and 51 frequency-matched controls) by measuring complete blood counts and peripheral stem/progenitor cell colony formation. Further, myeloid progenitor cells, the target for leukemogenesis, were cultured from the workers to quantify the level of leukemia-specific chromosome changes, including monosomy 7 and trisomy 8, in metaphase spreads of these cells. Among exposed workers, peripheral blood cell counts were significantly lowered in a manner consistent with toxic effects on the bone marrow and leukemia-specific chromosome changes were significantly elevated in myeloid blood progenitor cells. These findings suggest that formaldehyde exposure can have an adverse effect on the hematopoietic system and that leukemia induction by formaldehyde is biologically plausible, which heightens concerns about its leukemogenic potential from occupational and environmental exposures. Cancer Epidemiol Biomarkers Prev; 19(1); 80–8.
Diabetes and Outcomes After Radical Prostatectomy: Are Results Affected by Obesity and Race? Results from the Shared Equal-Access Regional Cancer Hospital Database
Authors: Jayachandran Jayakrishnan , Aronson William J. , Terris Martha K. , Presti Joseph C. , Amling Christopher L. , Kane Christopher J. , Freedland Stephen J. 
Published: January 2010

Abstract
Background: Diabetes is associated with lower prostate cancer risk. The association of diabetes with prostate cancer outcomes is less clear. We examined the association between diabetes and outcomes after radical prostatectomy and tested whether associations varied by race and/or obesity.
Materials and Methods: This study is a retrospective analysis of 1,262 men treated with radical prostatectomy between 1988 and 2008 within the Shared Equal-Access Regional Cancer Hospital database. We examined the multivariate association between diabetes at surgery and adverse pathology, biochemical recurrence (BCR), and prostate-specific antigen doubling time at recurrence using logistic, proportional hazards, and linear regression, respectively. Data were examined as a whole and stratified by race and obesity.
Results: Diabetes was more prevalent among black (22% versus 15%, P &lt; 0.001) and more obese men (P &lt; 0.001). Diabetes was associated with higher tumor grade (odds ratio, 1.73; P = 0.002), seminal vesicle invasion (odds ratio, 1.73; P = 0.04), but not BCR (P = 0.67) or PSADT at recurrence (P = 0.12). In the secondary analysis, among white obese men, diabetes was associated with 2.5-fold increased BCR risk (P = 0.002) and a trend toward shorter PSADT, whereas among all other men (nonobese white men and black men), diabetes was associated with 23% lower recurrence risk (P = 0.09) and longer PSADT (P = 0.04).
Conclusion: In a radical prostatectomy cohort, diabetes was not associated with BCR. In the secondary analysis, diabetes was associated with more aggressive disease in obese white men and less aggressive disease for all other subsets. If externally validated, these findings suggest that among men with prostate cancer, the association between diabetes and prostate cancer aggressiveness may vary by race and obesity. Cancer Epidemiol Biomarkers Prev; 19(1); 9–17
Nutrient-Based Dietary Patterns and Laryngeal Cancer: Evidence from an Exploratory Factor Analysis
Authors: Edefonti Valeria , Bravi Francesca , Garavello Werner , La Vecchia Carlo , Parpinel Maria , Franceschi Silvia , Dal Maso Luigino , Bosetti Cristina , Boffetta Paolo , Ferraroni Monica , Decarli Adriano 
Published: January 2010

AbstractBackground: The issue of diet and laryngeal cancer has been rarely addressed considering the potential role of dietary patterns.Methods: We examined this association using data from a case-control study carried out between 1992 and 2000. Cases were 460 histologically confirmed incident laryngeal cancers hospitalized in two Italian areas. Controls were 1,088 subjects hospitalized for acute nonneoplastic diseases unrelated to tobacco or alcohol consumption. Dietary habits were investigated through a 78-item food frequency questionnaire. A posteriori dietary patterns were identified through principal component factor analysis carried out on a selected set of 28 major nutrients. The internal reproducibility, robustness, and reliability of the identified patterns were evaluated. Odds ratios (OR) of laryngeal cancer and 95% confidence intervals (95% CI) were estimated using unconditional multiple logistic regression models on quartiles of factor scores.Results: We identified five major dietary patterns named “animal products,” “starch-rich,” “vitamins and fiber,” “vegetable unsaturated fatty acids,” and “animal unsaturated fatty acids.” The vitamins and fiber dietary pattern was inversely associated with laryngeal cancer (OR, 0.35; 95% CI, 0.24-0.52 for the highest versus the lowest score quartile), whereas the animal products (OR, 2.34; 95% CI, 1.59-3.45) and the animal unsaturated fatty acids (OR, 2.07; 95% CI, 1.42-3.01) patterns were directly associated with it. There was no significant association between the vegetable unsaturated fatty acids and the starch-rich patterns and laryngeal cancer risk.Conclusion: These findings suggest that diets rich in animal products and animal fats are directly related, and those rich in fruit and vegetables inversely related, to laryngeal cancer risk. Cancer Epidemiol Biomarkers Prev; 19(1); 18–27
Preclinical In vivo Evaluation of Efficacy, Pharmacokinetics, and Pharmacodynamics of a Novel MEK1/2 Kinase Inhibitor RO5068760 in Multiple Tumor Models
Authors: Daouti Sherif , Higgins Brian , Kolinsky Kenneth , Packman Kathryn , Wang Huisheng , Rizzo Christine , Moliterni John , Huby Nicholas , Fotouhi Nader , Liu Mei , Goelzer Petra , Sandhu Harpreet K. , Li Jia Kui , Railkar Aruna , Heimbrook David , Niu Huifeng 
Published: January 2010

Abstract
Targeting the Ras/Raf/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway represents a promising anticancer strategy. Recently, we have reported a novel class of potent and selective non–ATP-competitive MEK1/2 inhibitors with a unique structure and mechanism of action. RO5068760 is a representative of this class showing significant efficacy in a broad spectrum of tumors with aberrant mitogen-activated protein kinase pathway activation. To understand the relationship between systemic exposures and target (MEK1/2) inhibition as well as tumor growth inhibition, the current study presents a detailed in vivo characterization of efficacy, pharmacokinetics, and pharmacodynamics of RO5068760 in multiple xenograft tumor models. For inhibition of MEK1/2 as measured by the phosphorylated ERK levels, the estimated EC50s in plasma were 1.36 μmol/L (880 ng/mL) and 3.35 μmol/L (2168 ng/mL) in LOX melanoma and HT-29 colorectal cancer models, respectively. A similar EC50 (1.41 μmol/L or 915 ng/mL) was observed in monkey peripheral blood lymphocytes. To achieve tumor growth inhibition (≥90%), an average plasma drug concentration of 0.65 or 5.23 μmol/L was required in B-RafV600E or K-Ras mutant tumor models, respectively, which were remarkably similar to the IC90 values (0.64 or 4.1 μmol/L) determined in vitro for cellular growth inhibition. With equivalent in vivo systemic exposures, RO5068760 showed superior efficacy in tumors harboring B-RafV600E mutation. The plasma concentration time profiles indicate that constant p-ERK suppression (&gt;50%) may not be required for optimal efficacy, especially in highly responsive tumors. This study may facilitate future clinical trial design in using biochemical markers for early proof of mechanism and in selecting the right patients and optimal dose regimen. Mol Cancer Ther; 9(1); 134–44
A Conserved Lysine in the Thyroid Hormone Receptor–α1 DNA-Binding Domain, Mutated in Hepatocellular Carcinoma, Serves as a Sensor for Transcriptional Regulation
Authors: Chan Ivan H. , Privalsky Martin L. 
Published: January 2010

Abstract
Nuclear receptors are hormone-regulated transcription factors that play key roles in normal physiology and development; conversely, mutant nuclear receptors are associated with a wide variety of neoplastic and endocrine disorders. Typically, these receptor mutants function as dominant negatives and can interfere with wild-type receptor activity. Dominant-negative thyroid hormone receptor (TR) mutations have been identified in over 60% of the human hepatocellular carcinomas analyzed. Most of these mutant TRs are defective for corepressor release or coactivator binding in vitro, accounting for their transcriptional defects in vivo. However, two HCC-TR mutants that function as dominant-negative receptors in cells display near-normal properties in vitro, raising questions about the molecular basis behind their transcriptional defects. We report here that a single amino acid substitution, located at the same position in the DNA-binding domain of both mutants, is responsible for their impaired transcriptional activation and dominant-negative properties. Significantly, this amino acid, K74 in TRα, is highly conserved in all known nuclear receptors and seems to function as an allosteric sensor that regulates the transcriptional activity of these receptors in response to binding to their DNA recognition sequences. We provide evidence that these two human hepatocellular carcinoma mutants have acquired dominant-negative function as a result of disruption of this allosteric sensing. Our results suggest a novel mechanism by which nuclear receptors can acquire transcriptional defects and contribute to neoplastic disease. Mol Cancer Res; 8(1); 15–23
Mobilising Ulster Unionism: new directions or old?
Authors: McAuley James White 
Published: January 2010

One consequence of the contemporary peace process in Ireland has been the surfacing from deep within working class loyalism of groupings openly challenging the traditional values of Unionism. For socialists one of the key questions is whether this marks some form of permanent change, or something that will be neutralised by the counter-positions taken by traditional supporters of Unionism. This article argues that while ‘new loyalism’ may modify the central themes of Unionism, it is unlikely in the foreseeable future to herald a break from them. (C)ultural identity has itself become a term much used and abused. In Ireland, it is thrown around like a frizbee. Terms such as Irish, British; nationalist, Unionist; protestant, catholic. But what does identity actually mean, or, more importantly, are people really so preoccupied with it in Ireland as compared with people in England, France or the US? (Gerald Dawe, The Rest is History, 1998: 113-114) (P)olitical-cultural identities are ways of reading enfolding structural circumstances. These subtle constructs are contested; they express a balance between private thoughts and public truths. The nature of political-cultural identity will be shaped by the exchange of powerful groups, established institutions and the informal resources of everyday life. (P. W. Preston, Political/Cultural Identity, 1997: 175)
The Dialectical Structure of Marx's Concept of ‘Revolution in Permanence’
Authors: Hudis Peter 
Published: January 2010

This article argues that while the limitations of Hegel's political reconciliation with existing reality has long been evident, the depth of Marx's challenge to capital cannot be fully comprehended, let alone restated for today, without a re-encounter with Marx's rootedness in and transcendence of Hegel's concept of absolute negativity. The need to go beyond critiques of private property and the market by projecting ground for the negation of capital creates a compulsion to return to Hegel at his most ‘abstract’ level—the Absolute. THE 150TH ANNIVERSARY of Marx's Communist Manifesto last year seemed to have brought with it a shock of recognition concerning the timeliness of Marx's critique of existing capitalism. For some, the Manifesto's discussion of the relentless drive of capital for self-expansion makes it ‘the most concise and thrilling account of a process that creates havoc in the contemporary world, the inexorable pressure of globalization.’ For others, the Manifesto's description of ‘a class of labourers who live only so long as they find work, and who find work only so long as their labour increases capital,’ makes it the best ‘characterization of capitalism at the end of the 20th century currently available.’
Why read Capital?
Authors: Holloway John 
Published: January 2010

Why learn Latin? Both Latin and Capital are dying languages. How many Capital reading groups are there now? How many courses on Capital in colleges or universities? How many individuals ploughing on their own through the three volumes? Yet it was reading Capital that brought many of us into the CSE. Now that Capital & Class is celebrating its twenty-fifth anniversary, it is worth recording that the change in the title of the journal of the CSE from the Bulletin of the CSE to Capital & Class had much to do with the influx of non-economists in to the CSE at about that time.