bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nonsteroidal Anti-inflammatory Drugs and Subsite-Specific Colorectal Cancer Incidence in the Iowa Women's Health Study
Authors: Mahipal Amit , Anderson Kristin E. , Limburg Paul J. , Folsom Aaron R. 
Published: October 2006

Abstract
Background: Previous epidemiologic studies have shown that regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with decreased colorectal cancer risk. However, few studies have examined associations between NSAID use and subsite-specific colorectal cancer risks. Because tumors of the proximal and distal colon differ with respect to their genetic alterations, clinicopathologic features, and demographic distribution, further investigation of subsite-specific colorectal cancer risks may be rewarding.
Methods: Data about aspirin and nonaspirin-NSAID use were recorded by self-report in 1992 among the initially cancer-free cohort of postmenopausal women in the Iowa Women's Health Study (n = 27,160). In total, 637 women developed colorectal cancer during the 11 years of follow-up, including 365 proximal colon, 132 distal colon, and 120 rectal cancer cases (11 overlapping and 9 not specified).
Results: For colon cancer, the multivariable-adjusted hazard ratios (HR) for women reporting use of aspirin two to five times and six or more times weekly (compared with nonusers of aspirin) were 0.79 [95% confidence interval (95% CI), 0.59-1.04] and 0.76 (95% CI, 0.58-1.00), respectively. The corresponding HRs for nonaspirin NSAIDs were 0.63 (95% CI, 0.41-0.96) and 0.85 (95% CI, 0.63-1.15), respectively. For proximal colon cancer, the multivariable-adjusted HRs for women reporting use of aspirin or nonaspirin NSAIDs two or more times weekly (compared with nonusers of each) were 0.67 (95% CI, 0.51-0.87) and 0.71 (95% CI, 0.52-0.97), respectively. No statistically significant association was found between either distal colon or rectal cancer and aspirin or nonaspirin NSAID use.
Discussion: Our study is consistent with a limited number of prior reports that have observed stronger associations between NSAID use and proximal versus distal colorectal cancer. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1785–90)
Comparison of Polymorphisms in Genes Involved in Polycyclic Aromatic Hydrocarbon Metabolism with Urinary Phenanthrene Metabolite Ratios in Smokers
Authors: Hecht Stephen S. , Carmella Steven G. , Yoder Andrea , Chen Menglan , Li Zhong-ze , Le Chap , Dayton Rachel , Jensen Joni , Hatsukami Dorothy K. 
Published: October 2006

AbstractThe hypothesis that interindividual differences among smokers in the metabolism of polycyclic aromatic hydrocarbons (PAH) are related to lung cancer risk has been extensively investigated in the literature. These studies have compared lung cancer risk in groups of smokers with or without polymorphisms in genes involved in PAH metabolism. We believe that carcinogen metabolite phenotyping, involving the actual measurement of PAH metabolites, would be a better way to investigate differences in lung cancer risk. With this goal in mind, we have developed methods for quantifying phenanthrene metabolites in urine. Phenanthrene is the simplest PAH with a bay region, a feature closely associated with carcinogenicity. The urinary metabolite r-1,t-2,3,c-4-tetrahydroxy-1,2,3,4-tetrahydrophenanthrene (PheT) is a measure of metabolic activation, whereas phenanthrols (HOPhe) are a measure of detoxification. In this study, we quantified urinary PheT/HOPhe ratios in 346 smokers who were also genotyped for 11 polymorphisms in genes involved in PAH metabolism: CYP1A1MspI, CYP1A1I462V, CYP1B1R48G, CYP1B1A119S, CYP1B1L432V, CYP1B1N453S, EPHX1Y113H, EPHX1H139R, GSTP1I105V, GSTP1A114V, and GSTM1 null. The geometric mean molar PheT/3-HOPhe ratio was 4.08 (95% confidence interval, 3.79-4.39). Ten percent of the smokers had PheT/3-HOPhe ratios of ≥9.90. We found a significant association between the presence of the CYP1A1I462V polymorphism and high PheT/3-HOPhe ratios (P = 0.02). This effect was particularly strong in females and in combination with the GSTM1 null polymorphism. In contrast, the CYP1B1R48G and CYP1B1A119S polymorphisms were associated with significantly lower PheT/3-HOPhe ratios, particularly in Blacks. There were no consistent significant effects of any of the other polymorphisms on PheT/3-HOPhe ratios. The highest 10% of PheT/3-HOPhe ratios could not be predicted by the presence of any of the 11 polymorphisms individually or by certain combinations. The effects of the CYP1A1I462 polymorphism observed here, particularly in combination with GSTM1 null, are quite consistent with reports in the literature. However, the results of this study indicate that genotyping is not an effective way to predict PAH metabolism at least as represented by PheT/HOPhe ratios. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1805–11)
The Risk of Cancer following Hospitalization for Infection in Infancy: A Population-Based Cohort Study
Authors: Paltiel Ora , Laniado David E. , Yanetz Rivlca , Deutsch Lisa , Calderon-Margalit Ronit , Harlap Susan , Friedlander Yehiel 
Published: October 2006

Abstract
Background: The relation between infections in infancy and subsequent cancer risk in children and young adults is controversial. Our aim was to examine this association in the Jerusalem Perinatal Study, a population-based cohort comprising all offspring from western Jerusalem and surroundings born from 1964 to 1976.
Methods: Identity numbers of nonmalformed singletons with recorded data about hospital admission in the 1st year of life (n = 24,554) were linked to the Population and Cancer Registries. Person-year incidence rates were calculated for the exposed (admitted for infection) and nonexposed (not admitted for infection) groups from birth to date of cancer diagnosis, death, or December 31, 2004. We used Cox proportional hazards models to adjust for covariates associated with hospitalization.
Results: The median follow-up was 36 years. Cancer developed in 283 individuals. Hospitalization for infection was not associated with overall cancer risk [risk ratio (RR), 0.88; 95% confidence interval (95% CI), 0.56-1.37]. The incidence rate for non–Hodgkin's lymphoma was higher in the exposed compared with the nonexposed group (RR, 3.46; 95% CI, 1.38-8.68), remaining unchanged after controlling for birth weight, gender, and maternal education. Leukemia risk was not significantly associated (RR, 0.44; 95% CI, 0.06-3.24) with hospitalization for infection.
Conclusions: Hospital admission in the 1st year of life due to infection is associated with an increased risk of non–Hodgkin's lymphoma. This is consistent with observations that mild immunodeficiencies predispose to lymphoma. Survival of infants with subtle immune defects, who may have previously succumbed to their infection, may contribute to the increased incidence of non–Hodgkin's lymphoma observed over the last 50 years. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1964–8)
Haplotype-Based Association Studies of IGFBP1 and IGFBP3 with Prostate and Breast Cancer Risk: The Multiethnic Cohort
Authors: Cheng Iona , Penney Kathryn L. , Stram Daniel O. , Le Marchand Loic , Giorgi Elena , Haiman Christopher A. , Kolonel Laurence N. , Pike Malcolm , Hirschhorn Joel , Henderson Brian E. , Freedman Matthew L. 
Published: October 2006

Abstract
Collective evidence suggests that the insulin-like growth factor (IGF) system plays a role in prostate and breast cancer risk. IGF-binding proteins (IGFBP) are the principal regulatory molecules that modulate IGF-I bioavailability in the circulation and tissues. To examine whether inherited differences in the IGFBP1 and IGFBP3 genes influence prostate and breast cancer susceptibility, we conducted two large population-based association studies of African Americans, Native Hawaiians, Japanese Americans, Latinos, and Whites. To thoroughly assess the genetic variation across the two loci, we (a) sequenced the IGFBP1 and IGFBP3 exons in 95 aggressive prostate and 95 advanced breast cancer cases to ensure that we had identified all common missense variants and (b) characterized the linkage disequilibrium patterns and common haplotypes by genotyping 36 single nucleotide polymorphisms (SNP) spanning 71 kb across the loci (∼20 kb upstream and ∼40 kb downstream, respectively) in a panel of 349 control subjects of the five racial/ethnic groups. No new missense SNPs were found. We identified three regions of strong linkage disequilibrium and selected a subset of 23 tagging SNPs that could accurately predict both the common IGFBP1 and IGFBP3 haplotypes and the remaining 13 SNPs. We tested the association between IGFBP1 and IGFBP3 genotypes and haplotypes for their associations with prostate and breast cancer risk in two large case-control studies nested within the Multiethnic Cohort [prostate cases/controls = 2,320/2,290; breast cases (largely postmenopausal)/controls = 1,615/1,962]. We observed no strong associations between IGFBP1 and IGFBP3 genotypes or haplotypes with either prostate or breast cancer risk. Our results suggest that common genetic variation in the IGFBP1 and IGFBP3 genes do not substantially influence prostate and breast cancer susceptibility. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1993–7)
Validity of Self-reported Smoking Status among Participants in a Lung Cancer Screening Trial
Authors: Studts Jamie L. , Ghate Sameer R. , Gill Jaime L. , Studts Christina R. , Barnes Christopher N. , LaJoie A. Scott , Andrykowski Michael A. , LaRocca Renato V. 
Published: October 2006

Abstract
Lung cancer remains a devastating disease associated with substantial morbidity and mortality. Recent research has suggested that lung cancer screening with spiral computed tomography scans might reduce lung cancer mortality. Studies of lung cancer screening have also suggested that significant numbers of participants quit smoking after screening. However, most have relied solely on self-reported smoking behavior, which may be less accurate among participants in lung cancer screening. To assess the validity of self-reported smoking status among participants in a lung cancer screening trial, this study compared self-reported smoking status against urinary cotinine levels. The sample included 55 consecutive participants enrolled in a randomized clinical trial comparing annual spiral computed tomography and chest X-ray for lung cancer screening. Participants were a mean of 59 years of age and predominantly Caucasian (96%) and male (55%). Self-reported smoking status was assessed before and after participants learned of the purpose of the biochemical verification study. Using urinary cotinine as the “gold standard,” the sensitivity and specificity of self-reported smoking status were 91% and 95%, respectively (κ = 0.85, P &lt; 0.001, 95% confidence interval = 0.71-0.99). Total misclassification rate was 7%. However, three of the four misclassified participants reported concurrent use of nicotine replacement strategies. Eliminating these cases from the analysis revealed sensitivity of 100% and specificity of 95% (κ = 0.96, P &lt; 0.001, 95% confidence interval = 0.88-1.00). In conclusion, self-reported smoking status among participants in a lung cancer screening trial was highly consistent with urinary cotinine test results. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1825–8)
Building the New African Eco-Industrial Economy: Circulating Brains and Recycling Materials
Authors: Patterson Rubin 
Published: October 2006

AbstractThis paper develops an original proposition for debate in the fields of African studies, transnationalism, environmental studies, and technology studies. Essentially, the paper posits that, for a few key reasons, Sub-Saharan Africa will not likely have an opportunity to experience industrialization with the reigning "destructo-industrial" technologies pioneered by Europeans and Americans. An industrial experience appears achievable for Sub-Saharan Africans only in the context of a new ecological economy. Not only are there no unassailable national frontrunners in this future area, but Sub-Saharan Africans have a credible opportunity of being among the leaders in the future. The process would commence with "brain circulation," the movement of Africans into rich, technologically advanced countries to have their human, economic, and social capital enhanced, some of which to be reinvested in their respective homelands, particularly in ecological industrial areas.
Targeting mitochondrial factor Smac/DIABLO as therapy for multiple myeloma (MM)
Authors: Chauhan Dharminder , Neri Paola , Velankar Mugdha , Podar Klaus , Hideshima Teru , Fulciniti Mariateresa , Tassone Pierfrancesco , Raje Noopur , Mitsiades Constantine , Mitsiades Nicholas , Richardson Paul , Zawel Leigh , Tran Mary , Munshi Nikhil , Anderson Kenneth C. 
Published: October 2006

AbstractSecond mitochondria–derived activator of caspases (Smac) promotes apoptosis via activation of caspases. Here we show that a low-molecular-weight Smac mimetic LBW242 induces apoptosis in multiple myeloma (MM) cells resistant to conventional and bortezomib therapies. Examination of purified patient MM cells demonstrated similar results, without significant cytotoxicity against normal lymphocytes and bone marrow stromal cells (BMSCs). Importantly, LBW242 abrogates paracrine MM cell growth triggered by their adherence to BMSCs and overcomes MM cell growth and drug-resistance conferred by interleukin-6 or insulinlike growth factor-1. Overexpression of Bcl-2 similarly does not affect LBW242-induced cytotoxicity. Mechanistic studies show that LBW242-induced apoptosis in MM cells is associated with activation of caspase-8, caspase-9, and caspase-3, followed by PARP cleavage. In human MM xenograft mouse models, LBW242 is well tolerated, inhibits tumor growth, and prolongs survival. Importantly, combining LBW242 with novel agents, including tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) or the proteasome inhibitors bortezomib and NPI-0052, as well as with the conventional anti-MM agent melphalan, induces additive/synergistic anti-MM activity. Our study therefore provides the rationale for clinical protocols evaluating LBW242, alone and together with other anti-MM agents, to improve patient outcome in MM.
GOLEM: an interactive graph-based gene-ontology navigation and analysis tool
Authors: Sealfon Rachel SG , Hibbs Matthew A , Huttenhower Curtis , Myers Chad L , Troyanskaya Olga G 
Published: October 2006

Abstract

Background
The Gene Ontology has become an extremely useful tool for the analysis of genomic data and structuring of biological knowledge. Several excellent software tools for navigating the gene ontology have been developed. However, no existing system provides an interactively expandable graph-based view of the gene ontology hierarchy. Furthermore, most existing tools are web-based or require an Internet connection, will not load local annotations files, and provide either analysis or visualization functionality, but not both.

Results
To address the above limitations, we have developed GOLEM (Gene Ontology Local Exploration Map), a visualization and analysis tool for focused exploration of the gene ontology graph. GOLEM allows the user to dynamically expand and focus the local graph structure of the gene ontology hierarchy in the neighborhood of any chosen term. It also supports rapid analysis of an input list of genes to find enriched gene ontology terms. The GOLEM application permits the user either to utilize local gene ontology and annotations files in the absence of an Internet connection, or to access the most recent ontology and annotation information from the gene ontology webpage. GOLEM supports global and organism-specific searches by gene ontology term name, gene ontology id and gene name.

Conclusion
GOLEM is a useful software tool for biologists interested in visualizing the local directed acyclic graph structure of the gene ontology hierarchy and searching for gene ontology terms enriched in genes of interest. It is freely available both as an application and as an applet at http://function.princeton.edu/GOLEM.
Analysis of the dermatophyte Trichophyton rubrum expressed sequence tags
Authors: Wang Lingling , Ma Li , Leng Wenchuan , Liu Tao , Yu Lu , Yang Jian , Yang Li , Zhang Wenliang , Zhang Qian , Dong Jie , Xue Ying , Zhu Yafang , Xu Xingye , Wan Zhe , Ding Guohui , Yu Fudong , Tu Kang , Li Yixue , Li Ruoyu , Shen Yan , Jin Qi 
Published: October 2006

Abstract

Background
Dermatophytes are the primary causative agent of dermatophytoses, a disease that affects billions of individuals worldwide. Trichophyton rubrum is the most common of the superficial fungi. Although T. rubrum is a recognized pathogen for humans, little is known about how its transcriptional pattern is related to development of the fungus and establishment of disease. It is therefore necessary to identify genes whose expression is relevant to growth, metabolism and virulence of T. rubrum.

Results
We generated 10 cDNA libraries covering nearly the entire growth phase and used them to isolate 11,085 unique expressed sequence tags (ESTs), including 3,816 contigs and 7,269 singletons. Comparisons with the GenBank non-redundant (NR) protein database revealed putative functions or matched homologs from other organisms for 7,764 (70%) of the ESTs. The remaining 3,321 (30%) of ESTs were only weakly similar or not similar to known sequences, suggesting that these ESTs represent novel genes.

Conclusion
The present data provide a comprehensive view of fungal physiological processes including metabolism, sexual and asexual growth cycles, signal transduction and pathogenic mechanisms.
Phase III Trial Comparing Three Doses of Docetaxel for Second-Line Treatment of Advanced Breast Cancer
Authors: Harvey Vernon , Mouridsen Henning , Semiglazov Vladimir , Jakobsen Erik , Voznyi Edouard , Robinson Bridget A. , Groult Vanina , Murawsky Michael , Cold Soeren 
Published: October 2006

Purpose To evaluate whether a relationship exists between docetaxel dose and clinical response in the treatment of patients with advanced breast cancer. Patients and Methods Patients whose cancer had progressed after one prior chemotherapy regimen for advanced breast cancer or had recurred during or within 6 months of adjuvant chemotherapy were randomly assigned to docetaxel 60, 75, or 100 mg/m2 intravenously every 3 weeks. Results Five hundred twenty-seven patients were randomly assigned (intent to treat [ITT]), and 524 were assessable for toxicity. In the population assessable for efficacy (n = 407), logistic regression analysis showed that increasing docetaxel dose was significantly associated with higher response rate (P = .007) and improved time to progression (TTP; P = .014). In the ITT analysis, a significant dose-response relationship was observed for tumor response (P = .026) but not for TTP (P = .067). The incidences of most hematologic and nonhematologic toxicities were related to increasing dose, with grade 3 to 4 neutropenia occurring in 76.4%, 83.7%, and 93.4% and febrile neutropenia occurring in 4.7%, 7.4%, and 14.1% of patients administered the 60, 75, and 100 mg/m2 doses, respectively. One death was considered treatment related. Conclusion A relationship between increasing dose of docetaxel and increased tumor response was observed across the dose range of 60 to 100 mg/m2 every 3 weeks. Toxicities were related to increasing dose. Depending on the therapy goal, any of the doses studied may be appropriate for second-line treatment of advanced breast cancer.
Thyroid Hormone Increases mRNA and Protein Expression of Na+-K+-ATPase α2 and β1 Subunits in Human Skeletal Muscles
Authors: Phakdeekitcharoen Bunyong , Phudhichareonrat Suchart , Pookarnjanamorakot Chathchai , Kijkunasathian Chusak , Tubtong Nattha , Kittikanokrat Wassana , Radinahamed Piyanuch 
Published: October 2006

AbstractContext: Thyroid hormone regulates specific Na+-K+-ATPase isoforms in rodent skeletal muscles. No study has examined this relationship in human tissues.Objective: This study investigated the effect of hyperthyroid status on the expression of the α- and β-subunits of the Na+-K+-ATPase.Design: The vastus lateralis muscles from eight hyperthyroid patients were biopsied before and after treatment. Ten age-matched euthyroid subjects served as controls.Results: In hyperthyroid patients, the average T3 level was three times higher in pretreatment compared with posttreatment (262 ± 75 vs. 86 ± 21 ng/dl, P = 0.001). The relative mRNA expression of the α2, but not α1 or α3, subunit was increased approximately 3-fold in pretreatment (2.98 ± 0.52 vs. 0.95 ± 0.40, P &lt; 0.01), whereas that of β1, not β2 or β3, subunit was increased approximately 2.8-fold in pretreatment (2.83 ± 0.38 vs. 1.10 ± 0.27, P &lt; 0.01). The relative mRNA expression of the α2 and β1 subunits was positively correlated with the serum T3 (r = 0.75, P = 0.001 and r = 0.66, P = 0.003, respectively). Immunohistochemistry studies revealed an increase in protein abundance of the α2 and β1, but not α1 or β2, subunits in the plasma membrane of muscle fibers of hyperthyroid patients, which decreased after treatment.Conclusions: This provides the first evidence that, in human skeletal muscles, thyroid hormone up-regulates the Na+-K+-ATPase protein expression at least, in part, at mRNA level, and the α2 and β1 subunits play the important role in this regulation.
The Ghrelin Response to Exercise before and after Growth Hormone Administration
Authors: Vestergaard E. T. , Dall R. , Lange K. H. W. , Kjaer M. , Christiansen J. S. , Jorgensen J. O. L. 
Published: October 2006

Abstract
Context: We have previously shown that exercise-induced GH release is not mediated by ghrelin, but it remains to be studied whether the increase in GH may suppress postexercise ghrelin levels.
Objective: The objective of this study was to characterize systemic ghrelin levels after exercise with and without concomitant GH administration.
Design, Participants, and Intervention: Group A: Twenty-nine elite athletes (age, 18–37 yr) were studied after a maximal exercise test. Group B: In a double blind, placebo-controlled, parallel study, 32 healthy subjects (age, 18–33 yr) were randomized to placebo, GH 0.1 IU/kg per day, or GH 0.2 IU/kg per day for 4 wk. These subjects performed a multistage fitness test to assess maximum oxygen uptake at baseline and after 4 wk. We measured total circulating ghrelin levels before and immediately after exercise and at 15, 30, 60, 90, and 120 min after exercise.
Results: Group A: Serum ghrelin levels after exercise decreased significantly (P &lt; 0.01). Group B: Exercise at baseline was associated with a significant lowering of ghrelin levels after exercise (P &lt; 0.0001). In addition, 4 wk of high-dose GH were followed by a further approximately 20% reduction in basal and after exercise serum ghrelin (micrograms per liter): 0.78 (range 0.52–1.17) vs. 0.63 (range 0.50–0.91), P &lt; 0.05.
Conclusions: 1) Ghrelin levels decrease significantly after exercise in elite athletes and healthy subjects. 2) High-dose GH suppresses ghrelin levels. 3) These data support the hypothesis that GH feedback inhibits ghrelin secretion.