bluuebunny/crossref_metadata_2025_split huggingface dataset:
Clinical Biology of Esophageal Adenocarcinoma after Surgery Is Influenced by Nuclear Factor-κB Expression
Authors: Izzo Julie G. , Malhotra Usha , Wu Tsung-Teh , Luthra Rajalakshmi , Correa Arlene M. , Swisher Stephen G. , Hofstetter Wayne , Chao K.S. Clifford , Hung Mien-Chie , Ajani Jaffer A. 
Published: June 2007

Abstract
Background: The expression of transcriptional factor nuclear factor κB (NF-κB) in untreated esophageal cancer specimens from patients who receive preoperative chemoradiation is associated with aggressive clinical biology. We hypothesized that nuclear NF-κB would define clinical biology even when surgery is used as primary therapy.
Methods: Consecutive patients who did not receive any preoperative therapy were selected. Surgical cancer specimens were examined for nuclear NF-κB and correlated with overall survival (OS) and disease-free survival (DFS).
Results: One hundred twenty-three patients (stage I, 9%; stage II, 24%; stage III, 53%; stage IV, 15%) with adenocarcinoma who underwent surgery as primary therapy were analyzed. Most patients were men (90%) and the median age was 63 years. For all 123 patients, the median DFS was 21 months and the median OS was 28 months. Nuclear NF-κB was associated with shortened DFS (P = 0.001) in 123 patients but also in stage II (P = 0.03) and stage III (P = 0.04). Nuclear NF-κB was associated with shortened OS (P = 0.002) in 123 patients and in stage II (P = 0.04) and showed trend in stage III (P = 0.17). Numbers are too small for stages I and IV. In multivariate models, nuclear NF-κB was an independent predictor for both DFS and OS (P = 0.005 and P = 0.01).
Conclusions: Our data are the first to show that NF-κB status significantly correlates with DFS and OS for patients with esophageal adenocarcinoma undergoing surgery as primary therapy. NF-κB is an independent prognosticator of outcome, even for individual stages (e.g., stages II and III). More comprehensive molecular studies could help the design of strategies to individualize therapy of esophageal adenocarcinoma. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1200–5)
Phase I Dose Escalation Pharmacokinetic Study in Healthy Volunteers of Resveratrol, a Potential Cancer Chemopreventive Agent
Authors: Boocock David J. , Faust Guy E.S. , Patel Ketan R. , Schinas Anna M. , Brown Victoria A. , Ducharme Murray P. , Booth Tristan D. , Crowell James A. , Perloff Marjorie , Gescher Andreas J. , Steward William P. , Brenner Dean E. 
Published: June 2007

AbstractThe red grape constituent resveratrol possesses cancer chemopreventive properties in rodents. The hypothesis was tested that, in healthy humans, p.o. administration of resveratrol is safe and results in measurable plasma levels of resveratrol. A phase I study of oral resveratrol (single doses of 0.5, 1, 2.5, or 5 g) was conducted in 10 healthy volunteers per dose level. Resveratrol and its metabolites were identified in plasma and urine by high-performance liquid chromatography-tandem mass spectrometry and quantitated by high-performance liquid chromatography-UV. Consumption of resveratrol did not cause serious adverse events. Resveratrol and six metabolites were recovered from plasma and urine. Peak plasma levels of resveratrol at the highest dose were 539 ± 384 ng/mL (2.4 μmol/L, mean ± SD; n = 10), which occurred 1.5 h post-dose. Peak levels of two monoglucuronides and resveratrol-3-sulfate were 3- to 8-fold higher. The area under the plasma concentration curve (AUC) values for resveratrol-3-sulfate and resveratrol monoglucuronides were up to 23 times greater than those of resveratrol. Urinary excretion of resveratrol and its metabolites was rapid, with 77% of all urinary agent-derived species excreted within 4 h after the lowest dose. Cancer chemopreventive effects of resveratrol in cells in vitro require levels of at least 5 μmol/L. The results presented here intimate that consumption of high-dose resveratrol might be insufficient to elicit systemic levels commensurate with cancer chemopreventive efficacy. However, the high systemic levels of resveratrol conjugate metabolites suggest that their cancer chemopreventive properties warrant investigation. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1246–52)
A Prospective Cohort Study of Cancer Incidence Following the Diagnosis of Parkinson's Disease
Authors: Driver Jane A. , Logroscino Giancarlo , Buring Julie E. , Gaziano J. Michael , Kurth Tobias 
Published: June 2007

Abstract
Background: Prior studies suggest a decreased risk of cancer among patients with Parkinson's disease (PD).
Methods: Matched cohort analysis among the 22,071 participants in the Physician's Health Study. A total of 487 incident cases of PD without preceding cancer were identified by self-report. Each PD case was matched by age to a reference participant who was alive and cancer free at the time of PD diagnosis. Both cohorts were followed for incident cancer. We used proportional hazards models to calculate adjusted relative risks (RR) for cancer.
Results: A total of 121 cancers were confirmed during a median follow-up of 5.2 years (PD) and 5.9 years (reference). Those with PD developed less cancer (11.0% versus 14.0%), with an adjusted RR of 0.85 [95% confidence interval (95% CI), 0.59-1.22]. Reduced risk was present for smoking-related cancers such as lung (RR, 0.32), colorectal (RR, 0.54), and bladder (RR, 0.68), as well as for most non–smoking-related cancers such as prostate cancer (RR, 0.74). In contrast, PD patients were at significantly increased risk (RR, 6.15; 95% CI, 1.77-21.37) for melanoma. PD patients who smoked were at reduced risk for smoking-related cancer (RR, 0.33; 95% CI, 0.12-0.92), whereas nonsmokers with PD were at increased risk (RR, 1.80; 95% CI, 0.60-5.39). This interaction was statistically significant (Pinteraction = 0.02).
Conclusions: Our results suggest a decreased incidence of most cancers in patients with PD. PD patients had a significantly increased risk of malignant melanoma, a finding consistent with prior studies. We confirmed an interaction between smoking and the relationship of PD to smoking-related cancer that may fit the pattern of a gene-environment interaction. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1260–5)
Allergy-Related Polymorphisms Influence Glioma Status and Serum IgE Levels
Authors: Wiemels Joseph L. , Wiencke John K. , Kelsey Karl T. , Moghadassi Michelle , Rice Terri , Urayama Kevin Y. , Miike Rei , Wrensch Margaret 
Published: June 2007

Abstract
Previous studies have shown that glioma patients report allergies less frequently than controls, harbor lower atopy-associated IgE levels, and harbor different frequencies of polymorphisms in the IL13 and IL4 pathways than controls. We sought to confirm this latter result and extend the analysis to IgE levels. Glioma patients (n = 456) and controls (n = 541) were genotyped for genetic variants in IL4, IL4R, and IL13 and tested for total IgE levels (n = 248 controls and 289 cases). Among Whites, IL4 and IL4R polymorphisms and haplotypes were neither significantly associated with IgE levels in controls nor associated with glioma status. IL13 R110G and C-1112T were associated with increased IgE levels in controls (P &lt; 0.001 and P = 0.04, respectively), and IL13 C-1112T was inversely associated with case-control status (P = 0.05, test for trend in dose model). An IL4R haplotype was borderline associated with increased risk in case-control analysis [odds ratio (OR), 1.5; 95% confidence interval (95% CI), 1.0-2.3]. In addition, a rare haplotype for IL4 was associated with decreased risk (OR, 0.23; 95% CI, 0.07-0.83), and a common haplotype in IL13 was associated with decreased risk (OR, 0.73; 95% CI, 0.53-1.00). Our data provide evidence for a role of IL13 polymorphisms on IgE levels and a role for IL4, IL4R, and IL13 haplotypes on case-control status. We did not find any evidence that the interleukin (IL) polymorphisms exerted their effect on glioma risk via their effects on IgE levels. Further exploration of immune susceptibility factors, including genetics, in glioma etiology is advisable. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1229–35)
Risk of Germ Cell Tumors among Men with HIV/Acquired Immunodeficiency Syndrome
Authors: Goedert James J. , Purdue Mark P. , McNeel Timothy S. , McGlynn Katherine A. , Engels Eric A. ,   for the HIV/AIDS Cancer Match Study
Published: June 2007

Abstract
Background: Men with HIV/acquired immunodeficiency syndrome (AIDS) are reported to be at increased risk for germ cell tumors (GCT), particularly testicular seminoma. We investigated correlates of this association to improve understanding of GCTs.
Methods: Testicular and extratesticular seminoma and nonseminoma cases were found by linking population-based cancer and HIV/AIDS registry data for 268,950 men who developed AIDS in 1980 to 2003. Standardized incidence ratios (SIR) with 95% confidence intervals (95% CI) were used to compare these cases with the number of cases expected in the demographically matched population.
Results: Overall, seminoma risk (161 cases: SIR, 1.9; 95% CI, 1.6-2.2) was increased significantly with HIV/AIDS, whereas nonseminoma risk was not (56 cases: SIR, 1.3; 95% CI, 0.96-1.7). Extratesticular GCT risk also was increased (11 cases: SIR, 2.1; 95% CI, 1.1-3.7). Seminoma risk was elevated regardless of age, race, or HIV/AIDS transmission group. It was highest for disseminated disease (SIR, 4.7; 95% CI, 2.9-7.2) and within 9 months of AIDS onset (SIR, 7.6; 95% CI, 5.8-9.6), but it was unrelated to CD4 count and duration of HIV/AIDS. The excess risk of seminoma declined in more recent calendar periods, and it was no longer elevated (SIR, 1.4; 95% CI, 0.9-1.9) in the highly active antiretroviral treatment era.
Conclusions: Men with HIV/AIDS had an increased risk of seminoma, but this risk may have attenuated with improving anti-HIV/AIDS treatments. Although detection bias could partly explain the excess of this cancer, various lines of evidence support a causal relationship. Possible mechanisms underlying this association include impaired tumor immunosurveillance or AIDS-related testicular atrophy. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1266–9)
Dietary Iron and Heme Iron Intake and Risk of Breast Cancer: A Prospective Cohort Study
Authors: Kabat Geoffrey C. , Miller Anthony B. , Jain Meera , Rohan Thomas E. 
Published: June 2007

Abstract
Recent studies suggest that elevated body iron levels may contribute to breast carcinogenesis; however, epidemiologic evidence is lacking. We used data from a large cohort study of Canadian women to assess breast cancer in association with total iron and heme iron intake. Among 49,654 women ages 40 to 59 followed for an average of 16.4 years, we identified 2,545 incident breast cancer cases. Data from a food frequency questionnaire administered at baseline were used to calculate total dietary iron and heme iron intake. Using Cox proportional hazards models, we found no association of iron or heme iron intake with risk of breast cancer overall, in women consuming 30+ g of alcohol per day, or in women who had ever used hormone replacement therapy. The present study offers no support for an association of iron or heme iron intake with breast cancer risk or for a modification by iron of the effect of alcohol or estrogen. However, further cohort studies with repeated measurement of iron intake are warranted. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1306–8)
Different Risk Factor Profiles for Mucinous and Nonmucinous Ovarian Cancer: Results from the Danish MALOVA Study
Authors: Soegaard Marie , Jensen Allan , Høgdall Estrid , Christensen Lise , Høgdall Claus , Blaakær Jan , Kjaer Susanne K. 
Published: June 2007

Abstract
Objectives: The aim of the study was to examine the overall risk factors for epithelial ovarian cancer and according to histologic subtypes.
Materials and Methods: Ovarian cancer cases and controls were recruited from 1995 to 1999, and personal interviews were conducted. A total of 554 cases and 1,564 randomly selected controls were included. The analyses were done using multiple logistic regression models.
Results: The overall risk of ovarian cancer decreased with ever being pregnant [odds ratios (OR), 0.40; 95% confidence intervals (CI), 0.30-0.55], with increasing pregnancies (OR, 0.63; 95% CI, 0.45-0.87 and OR, 0.51; 95% CI, 0.37-0.69 for two and three pregnancies as compared with one), and with older age at first and last pregnancy, respectively. Increasing years of ovulation was a very strong risk factor with a 7% to 8% increase in risk for each year of ovulation. Use of oral contraceptives (OR, 0.67, 95% CI, 0.53-0.85) and longer duration of use were associated with a decreased risk of ovarian cancer. Ever use of hormone replacement therapy increased the overall risk (OR, 1.30; 95% CI, 1.05-1.61). For all those variables, the effect was present for serous tumors, endometrioid tumors, and tumors of other histologies, but not for mucinous tumors. In contrast, current smoking was a risk factor only for mucinous tumors (OR, 1.78; 95% CI, 1.01-3.15) and increasing body mass index tended to increase the risk especially for mucinous and endometrioid tumors.
Conclusions: We confirmed already known risk factors for ovarian cancer, and we observed significant differences in the risk profiles between mucinous and nonmucinous tumors indicating different etiologies. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1160–6)
Associations of Circulating C-Reactive Protein and Interleukin-6 with Survival in Women with and without Cancer: Findings from the British Women's Heart and Health Study
Authors: Heikkilä Katriina , Ebrahim Shah , Rumley Ann , Lowe Gordon , Lawlor Debbie A. 
Published: June 2007

Abstract
Background: Inflammation is associated with worse prognosis and survival in many cancers. Our aim was to investigate the associations of circulating C-reactive protein (CRP) and interleukin-6 (IL-6) concentrations with all-cause mortality in cancer patients and to determine whether any associations were specific to malignancy.
Method: We used data from the British Women's Heart and Health Study, a cohort of 4,286 women aged 60 to 79 years. We investigated the associations between CRP, IL-6, and survival in women with and without cancer using Cox regression and assessed the interaction between cancer status and these inflammatory markers to determine whether these associations differed according to cancer status.
Results: Elevated CRP and IL-6 were associated with decreased survival in women with cancer [unadjusted hazard ratio per doubling of CRP, 1.22, 95% confidence interval (95% CI), 1.03, 1.46; and per doubling of IL-6, 1.52, 95% CI, 1.25, 1.86] and in women without cancer [CRP: 1.24 (1.12, 1.37); IL-6: 1.53 (1.35, 1.75)]. Adjustment for age, body mass index, physical activity level, socioeconomic position, HRT use, and tobacco smoking did not change these associations. After mutual adjustment, IL-6 but not CRP was independently associated with survival. We found no strong evidence that these associations differed between cancer patients and cancer-free women.
Conclusions: Elevated CRP and IL-6 concentrations were similarly associated with an increased risk of death in elderly women with and without cancer. Thus, in this group, these markers are likely to be indicators of non-cancer comorbidities rather than related to the malignancy itself. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1155–9)
Honeycomb-type Solid Oxide Fuel Cells Using La0.9Sr0.1Ga0.8Mg0.2O3 Electrolyte
Authors: Zhong Hao , Matsumoto Hiroshige , Ishihara Tatsumi , Toriyama Akira 
Published: June 2007

Abstract
La0.9Sr0.1Ga0.8Mg0.2O3 (LSGM)-based honeycomb cell was first time successfully built and power generation property of the single-wall and the 4-wall-used cells was measured. The achieved maximum power density is 390 and 250 mW/cm2 at 1073 and 973 K, respectively, when the single wall is used for the cell fabrication. The power generations of 4-wall-used cell also succeed in this study, and about 200 mW/cm2, which is high volumetric power density as high as 300 W/L, is achieved.
Zinc-Finger Transcription Factor Odd-Skipped Related 2 Is One of the Regulators in Osteoblast Proliferation and Bone Formation
Authors: Kawai Shinji , Yamauchi Masashi , Wakisaka Satoshi , Ooshima Takashi , Amano Atsuo 
Published: June 2007

Abstract
We report that Osr2 is one of the regulators of osteoblast function, because dominant-negative Osr2 transgenic mice exhibited decreased osteoblast activity and delayed mineralization in calvarial and tibial bone tissues. Our results indicate that Osr2 functions in regulation of osteoblast proliferation.
Introduction: Molecular mechanisms that control bone formation have received attention with increasing knowledge related to genetic control of osteoblast differentiation. The odd-skipped related (Osr) gene is a zinc-finger transcription factor recently suggested to be involved in bone formation, although little is known about its role.
Materials and Methods: To elucidate the in vivo function of Osr2, we generated transgenic mice overexpressing dominant-negative Osr2.
Results: In this study, N-terminal–deleted Osr2 was found to act as a dominant-negative mutant toward both Osr1 and Osr2. Dominant-negative Osr2 (Osr2ΔN) transgenic mice showed delayed mineralization in calvarial and cortical bone tissues. Furthermore, soft X-ray analysis of transgenic mice bones revealed distinctly increased radiolucency. Examinations of newborn Osr2ΔN transgenic mice skeletons stained with alcian blue and alizarin red showed reduced intensities in the skull and skeletal elements. Morphologically, calvariae and tibias of Osr2ΔN transgenic mice were composed of markedly thinner parietal and cortical bones and lower numbers of osteoblastic cells on bone surfaces, indicating a reduced proliferation of osteoblasts. Furthermore, calvarial osteoblasts obtained from Osr2ΔN transgenic mice showed highly attenuated osteoblast differentiation and proliferation, confirming that Osr2 is needed for osteogenesis. Finally, results of Runx2-deficient cell assays suggested that Osr2 induces alkaline phosphatase (ALP) expression, but to a lesser degree than Runx2-expressing cells.
Conclusions: Our genetic observations showed that the Osr2 gene plays a key role in osteoblastic cell proliferation.
Strontium Ranelate Treatment Improves Trabecular and Cortical Intrinsic Bone Tissue Quality, a Determinant of Bone Strength
Authors: Ammann Patrick , Badoud Isabelle , Barraud Sébastien , Dayer Romain , Rizzoli René 
Published: June 2007

Abstract
Beside its influence on determinants of bone strength (geometry, microarchitecture), which is likely to be related to a cellular effect, strontium ranelate improves bone tissue quality as evaluated by nanoindentation, increasing elastic modulus, hardness, and dissipated energy in vertebrae of rats treated for 104 wk with daily dose from 0 to 900 mg/kg.
Introduction: We previously showed that strontium ranelate treatment improves the mechanical properties of the vertebral body and long bone midshaft in intact rats. The increased energy to failure obtained with strontium ranelate is essentially caused by an increase in plastic energy, suggesting that bone formed during treatment can withstand greater deformation before fracture. In the bone mineral phase, strontium is mainly located in the hydrated shell and could thus potentially influence intrinsic bone tissue quality.
Materials and Methods: To study whether strontium ranelate treatment could positively influence intrinsic bone tissue quality (elastic modulus, hardness, and dissipated energy), nanoindentation tests were performed at the level of trabecular nodes and cortex under physiological or dry conditions in vertebrae of rats treated for 104 wk with strontium ranelate at a daily dose of 0, 225, 450, or 900 mg/kg (n = 12 per group). Ex vivo μCT measurements and axial compression tests of adjacent vertebral bodies were also performed. Significance of difference was evaluated using ANOVA.
Results: In agreement with previous results, strontium ranelate (900 mg/kg/d) significantly increased versus controls in maximal load (+23%), total energy (+71%), and plastic energy (+143%). At the level of trabecular bone, strontium ranelate treatment resulted in a significant increase in elastic modulus (+15.1%, p &lt; 0.01), hardness (+11.5%, p &lt; 0.05), and dissipated energy (+16.2%, p &lt; 0.001) versus controls in physiological, but not in dry, conditions. The effect was less pronounced in cortex.
Conclusions: These results show for the first time a direct action of strontium ranelate on bone tissue quality. Beside its shown influence on classical determinants of bone strength (geometry, microarchitecture), which is likely to be related to a cellular effect, strontium ranelate improves bone tissue quality. This could contribute to the increase in bone strength and thus be involved in the reduction of fracture risk in postmenopausal osteoporotic patients treated with strontium ranelate.
Two‐Year Changes in Bone Mineral Density and T Scores in Patients Treated at a Pharmacist‐Run Teriparatide Clinic
Authors: Stroup Jeffrey S. , Rivers Shannon M. , Abu‐Baker Asim M. , Kane Michael P. 
Published: June 2007

Study Objectives. To determine changes in bone mineral density (BMD) and T scores of patients after 2 years of teriparatide therapy, and to determine the number of fractures that occurred during therapy.Design. Prospective, observational study.Setting. Pharmacist‐run teriparatide clinic in a private‐practice endocrinology group.Patients. Sixty patients with osteoporosis who experienced fractures or adverse events while receiving antiresorptive therapy and were referred by the endocrinologists to the clinic between January 1, 2002, and January 1, 2004.Intervention. After a 1‐hour counseling and training session with a clinical pharmacist, patients self‐administered subcutaneous teriparatide 20 μg/day for the next 2 years.Measurements and Main Results. Primary outcome measures were dual x‐ray absorptiometry–determined BMDs and T scores for the total hip, spine, and wrist at baseline and at 1 and 2 years. Patients' BMDs for the hip significantly increased by 3.5% at 1 year and by 3.9% at 2 years. In addition, BMD for the spine significantly increased by 7.2% at 1 year and 10.9% at 2 years. In 56 (93%) patients, BMD for the spine increased after 2 years of treatment. For the wrist, BMD decreased by 0.75% at 1 year and by 2.4% at 2 years, but the change was only significant at 2 years (p=0.011). At both 1 and 2 years, T scores for the total hip and spine significantly improved from baseline (p≤0.019), whereas T scores for the wrist significantly declined after 2 years of therapy (p<0.003). No new fractures were documented in any of the patients.Conclusion. In patients with osteoporosis, the use of teriparatide in a pharmacist‐run clinic significantly increased BMD at the total hip and spinal sites and significantly decreased BMD in the wrist.