tbuckley/cabot-search huggingface dataset:
OP0100 Gout in patients with stable coronary heart disease and the impact of serum uric acid levels on adverse cardiovascular outcomes: A long-term follow-up study
Authors: D. Rothenbacher, A. Kleiner, W. Koenig, P. Primatesta, L.P. Breitling, H. Brenner
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> A relationship between hyperuricemia or gout and cardiovascular disease has been described in many studies. However, it is unclear whether the association between serum uric acid (SUA), inflammatory cytokines and risk of atherosclerosis is causal or an epiphenomenon. <h3>Objectives</h3> To investigate the independent prognostic relationship of SUA and inflammatory markers with adverse cardiovascular outcomes in a patient population with stable coronary heart disease (CHD) at baseline under special consideration of gout. <h3>Methods</h3> CHD patients aged 30-70 from two cooperating German hospitals were enrolled (January 1999 - May 2000) and followed up for 8 years. Self-reported gout diagnosis was ascertained at baseline. The relation of SUA and inflammatory markers (CRP; IL-6) with subsequent CVD (fatal or non-fatal MI or stroke) was assessed by Kaplan-Meier and Cox proportional hazards, adjusting for know confounders for CVD events. <h3>Results</h3> 1,056 patients were included, of whom 229 reported at baseline a diagnosis of gout. Patients with gout at baseline had a less favourable cardiometabolic profile: higher CRP, IL-6 and SUA. Overall, 151 patients out of 1,056 (incidence 21.1 per 1000 patient-years) experienced subsequent fatal or non-fatal CVD. This incidence was positively correlated with SUA and CRP in Kaplan-Meier plots (p=0.003 and p=0.002 respectively). After adjustment for age, gender and hospital site the hazard ratio (HR) for SUA increased from 1.53 to 1.74 and 2.80 in the second, third, and top quartile, when compared to the bottom one (p for trend &lt;0.0001). The presence of clinical diagnosis of gout did not enhance this association. The relationship between CRP and subsequent CVD was not statistically significant. <h3>Conclusions</h3> The data suggest that, irrespective of the presence of gout, SUA (in contrast to CRP) predicts future CVD risk in patients with stable CHD with a risk increase even at levels considered normal, and therefore may contribute independently to the pathophysiology of CVD events. <h3>Disclosure of Interest</h3> D. Rothenbacher: None Declared, A. Kleiner: None Declared, W. Koenig: None Declared, P. Primatesta Employee of: Novartis, L. Breitling: None Declared, H. Brenner: None Declared
1291 IN SLEEP APNEA SYNDROME, NONALCOHOLIC FATTY LIVER DISEASE (NAFLD) IS ASSOCIATED WITH THE SEVERITY OF INTERMITTENT HYPOXIA AND MORE SEVERE ENDOTHELIAL DYSFUNCTION
Authors: M.N. Hilleret, C. Minville, R. Tamisier, P. Levy, J.P. Zarski, J.L. Pepin
Journal: Journal of Hepatology (2012)
Abstract 1194: The splicing isoform osteopontin-c contributes to ovarian cancer progression
Authors: Tatiana M. Tilli, Vanessa Franco, Bruno Robbs, João Wanderley, Fabrício Borges, João Viola, Georg Weber, Etel Gimba
Journal: Cancer Research (2010)

Abstract Introduction: Osteopontin (OPN) is a secreted glycophosphoprotein that is involved in tumorigenesis and metastasis in many solid tumors. Alternative splicing of OPN mRNA generates 3 known species and proteins, OPNa, OPNb and OPNc. Objective and Methodology: The aim of the present work was to investigate the expression profiling and the functional roles of OPN isoforms in ovarian carcinoma. Here we investigate the expression of each OPN isoform in ovarian cell lines and ovarian tissues, by quantitative real-time PCR using OPN splice variants specific primer pairs. We then investigated the roles of each one of these isoforms by using in vitro and in vivo models. Cell proliferation, migration and anchorage independent cell growth analysis were performed using OvCAr-3 cells overexpressing OPNa, OPNb or OPNc isoforms. Tumor formation was evaluated in athymic nude mice inoculated with OvCar3 cells overexpressing each oisoform as compared to empty vector controls. Results: We show that OPNa and OPNb are expressed in all ovarian tissues analyzed. However, the isoform OPNc is selectively present in malignant and borderline ovarian tumors and malignant tumor cell lines, but not in benign and normal ovarian tissues. Cell proliferation, migration, anchorage-independent growth and tumor growth in vivo are dramatically increased in OvCar-3 cells overexpressing OPNc. In contrast, OPNa and OPNb do not present these same pro-tumorigenic properties. Conclusions: These results together provide compelling evidence that OPNc plays important roles in ovarian cancer progression. Firstly, OPNc is specifically expressed in borderline and malignant ovarian tumors. Secondly, OPNc expression facilitates tumor progression towards an aggressive phenotype. Targeting OPNc in ovarian cancer has potential as a novel therapeutic strategy. Financial Support: CNPq, CAPES, FAPERJ, Swiss Bridge Foundation, FAF/MS Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1194.
Policy Gains Speed America's Flight From Tobacco
Authors: J. McKenna
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Policy Gains Speed America's Flight From Tobacco Get access Jeff McKenna Jeff McKenna Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 3, 6 February 1991, Pages 166–167, https://doi.org/10.1093/jnci/83.3.166 Published: 06 February 1991
Abstract 3422: N-α-acetyltransferase 10 protein suppresses cancer cell metastasis by binding PIX proteins and inhibiting Cdc42/Rac1 activity
Authors: Kuo-Tai Hua, Ching-Ting Tan, Chi-Kuan Chen, Min-Wei Chen, Michael Hsiao, Min-Liang Kuo
Journal: Cancer Research (2012)

Abstract 80%-90% of eukaryotic proteins are N-α-terminally acetylated. They are mediated by specific N-α-acetyltransferases. However, the biological importance of these N-α-acetyltransferases remains largely unknown. Recently, these N-α-acetyltransferases have been recognized as important characters in many biological processes, including embryonic development, neuron disease and cancer. N-α-acetyltransferase A (Nat A) was first characterized in yeast, it composed of Naa10p, also known as hARD1 (human Arrest defective 1), and Naa15p, also known as NATH (N-acetyl transferase human), are responsible for the N-α-acetylation of majority proteins in mammalian cells. Naa10p is known to be involved in cell cycle control and apoptosis. However, the role of Naa10p in human cancers is elusive. In this study, we found that elevated Naa10p levels are associated with less metastasis to lymph nodes and better prognosis of cancer patients. Naa10p significantly suppressed migration, tumor growth, and metastasis independent of its enzymatic activity. Instead, Naa10p binds to the GIT-binding domain of PIX, thereby preventing the formation of the GIT-PIX-Paxillin complex, resulting in reduced intrinsic Cdc42/Rac1 activity and decreased cell migration. Forced expression of PIX in Naa10-transfected tumor cells restored the migration and metastasis ability. We suggest that Naa10p functions as a tumor metastasis suppressor by disrupting the migratory complex, PIX-GIT- Paxillin, in cancer cells. Our study not only highlights the potential of Naa10p as a therapeutic target for tumor metastasis, but also identifies Naa10p as a regulatory component of the migration complex PIX-GIT-Paxillin. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3422. doi:1538-7445.AM2012-3422
EARLY ONSET PERIPARTUM CARDIOMYOPATHY FOLLOWING DILATION AND EVACUATION FOR COMPLETE HYDATIDIFORM MOLE COEXISTENT WITH LIVE FETUS
Authors: Yuichi Saito, Hiroyuki Takaoka, Nobusada Funabashi, Hiroshi Hasegawa, Akiko Omoto, Hirokazu Usui, Makio Shozu, Yoshio Kobayashi
Journal: Journal of the American College of Cardiology (2015)
DCIS-Associated Myoepithelial Cells Expressing the αvβ6 Integrin Modify Tumour Cell Behaviour: A Predictor of Invasive Progression?
Authors: J. Jones, M. Allen, G. Thomas, M. Dawoud, S. Vallath, S. Payne, D. Edwards, C. Pennington, J. Marshall, I. Hart
Journal: Cancer Research (2009)

Abstract Ductal carcinoma in-situ (DCIS) now accounts for up to 25% of breast cancer presentations. DCIS will progress to invasive breast cancer in 25-40% of cases, though the mechanisms involved in this progression are poorly understood. Understanding the factors that promote progression to invasive disease is of importance both in terms of developing better prognostic and predictive markers, and also in the development of novel therapies.One of the key features in the progression of DCIS to invasive disease is penetration of the myoepithelial-basement membrane barrier. As well as being a physical barrier myoepithelial cells (MEC) also have been described as tumour suppressors exerting their effects through autocrine and paracrine pathways, but there is evidence that these cells change in DCIS.The integrin αvβ6 is an epithelial-restricted protein, not usually expressed in normal adult tissue, which has been demonstrated to be up-regulated in invasive cancer where it activates TGF-β. Here we show that αvβ6 is up-regulated in the myoepithelial cell compartment of high grade DCIS (∼ 100% in ∼200 cases) especially where invasion also is present. To understand the relevance of this observation we have created a model for DCIS-associated MEC by introducing β6 cDNA into an immortalised MEC line (1089) to create the αvβ6 expressing derivative, β6-1089. Using Transwell assays we demonstrate increased invasive activity of a panel of breast cancer cell lines exposed to conditioned media from β6-1089 cells relative to the control cell line. Using our organotypic assay, to examine invasion in a more physiological manner, we also found that the invasive capacity of MDA-MB-231 cells is enhanced after they are co-cultured with β6-1089 cells. Furthermore, in-vivo experiments demonstrate increased growth of tumour cells injected with β6-1089 MEC compared to control 1089 cells. Expression of αvβ6 de novo in β6-1089 cells caused an increase in MMP9 expression while a chemical inhibitor of MMP9 was able to block the observed increased invasion. Tissue studies revealed a highly significant correlation between MEC expression of αvβ6 and of MMP-9 (p&amp;lt;0.001), supporting these in vitro findings.These results show that up-regulation of αvβ6 expression in MEC from DCIS with associated invasion is a common event and promotes invasion of breast cancer cells through increased elaboration of MMP-9. This suggests expression of αvβ6 by myoepithelial cells may be an important prognostic marker for the progression of DCIS. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 4159.
AB0660 Predictive Factors of Treatment Response to A Second Tnf-α Inhibitor in Patients with Ankylosing Spondylitis - Results from the Portuguese Register Reuma.Pt
Authors: F. Araújo, A. Sepriano, P. Madureira, R. Aguiar, A. Bernardo, C. Silva, E. Sousa, F. Santos, G. Sequeira, H. Canhão, H. Santos, J. Garcia, J.A. Pereira Silva, J. Canas Silva, M. Oliveira, M.J. Salvador, P. Nero, P. Monteiro, T. Nόvoa, J. Branco
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Approximately one-third of patients with ankylosing spondylitis (AS) treated with tumor necrosis factor inhibitors (TNFi) need to switch their biological therapy. However, a significant clinical response only occurs in half of switcher patients. <h3>Objectives</h3> To determine predictive factors of treatment response at 12 weeks in AS patients switching treatment to a second TNFi. <h3>Methods</h3> Patients with AS (1984 modified New York classification criteria) switching treatment to a second TNFi were identified in the Rheumatic Diseases Portuguese Register, Reuma.pt. Data was extracted at baseline (at second TNFi start) and at 12 weeks of follow-up. Variables included in the analysis were age, race, gender, BMI, education level, work status, tobacco and alcohol consumption, disease duration, time to diagnosis, peripheral arthritis, extra-articular manifestations, ESR, CRP, HLA-B27 positivity, previous DMARD and steroid therapy, BASDAI, ASDAS, BASFI, BASMI, first TNFi used, reason and time to switch. Univariable logistic regression analysis of baseline predictors of BASDAI response (improvement ≥2 units or ≥50%) was performed and variables with a p-value&lt;0.25 were re-tested in multivariable regression models. <h3>Results</h3> Of the 334 AS patients treated with biologicals, 85 (25.4%) switched to a second TNFi. Reasons for switch included treatment failure (16; 18.8%), adverse events (25; 29.4%) and other reasons (44; 51.8%) like refractory extra-articular manifestations, surgery or patient preferences. Patients were included in the analysis if they stayed in therapy at least for 3 months and have BASDAI at baseline and at 3 months available. Forty-nine patients were analyzed, 22 responders (44.9%) and 27 non-responders (55.1%). BASDAI clinical response at 12 weeks was predicted by BASMI (p=0.04; OR 3.8 [95% CI 1.0, 14.1]) adjusting for gender, erythrocyte sedimentation rate and age at biological treatment onset. No other statistical significant demographical, clinical or laboratorial predictors were found. <h3>Conclusions</h3> We found 44.9% switchers who responded to the second TNFi. An increased BASMI score was an independent predictor of BASDAI clinical response to a second TNFi in AS patients. The inclusion of a greater number of patients in future studies may allow the determination of further predictive factors. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5590
Abstract P3-08-03: Urinary levels of prostaglandin E2 metabolite and postmenopausal breast cancer
Authors: S Kim, JA Taylor, DP Sandler
Journal: Cancer Research (2012)

Abstract Estrogens are considered a key player in the mammary carcinogenesis. In postmenopausal women, peripheral aromatization of androgens is the predominant source of estrogens. Given that prostaglandin E2 (PGE2) is a potent activator of aromatase expression, we hypothesized that endogenous level of PGE2 would influence estrogen bioavailability and subsequent breast cancer risk in postmenopausal women. In addition, because PGE2 synthesis is suppressed by treatment of non-steroidal anti-inflammatory drugs (NSAIDs) via inhibition of cyclooxygenase enzyme activity, we further hypothesized that regular use of NSAIDs may modify the association between PGE2 and postmenopausal breast cancer risk. We carried out a case-cohort analysis within the NIEHS Sister Study, a prospective cohort study of 50,884 women. Postmenopausal women who were aged 50 or older and did not report current use of hormones were eligible for the present analysis (N = 11,338). Urinary levels of a major PGE2 metabolite (PGE-M), which is generally accepted as the most accurate index of endogenous PGE2 formation, were quantified using liquid chromatography/tandem mass spectrometry in 302 incident breast cancer cases and 305 subcohort members who were randomly selected by frequency matching for age among cases. Hazard ratios (HR) and 95% confidence intervals (95% CI) were estimated using Prentice's pseudo-likelihood approach with Barlow's weighting scheme. Several factors were associated with higher levels of urinary PGE-M in the multivariable analysis, including current smoking, obesity, high caloric intake from saturated fat and surgical menopause. No associations were observed for dietary intake of omega 3 fatty acids, use of vitamin supplements and physical activity. Overall, there was no association between urinary PGE-M and postmenopausal breast cancer risk. After including the interaction terms between NSAID use and urinary levels of PGE-M in the model, however, high levels of urinary PGE-M were associated with an increased risk of breast cancer in postmenopausal women who did not regularly use NSAIDs (likelihood ratio test p &amp;lt;0.01). Taking into account use of NSAIDs 1 day prior to urine collection did not change results. NSAID use may modify the conversion of androgens to estrogen and thereby lower breast cancer risk. Expected data on estrogen and estrogen metabolites will help us better understand these findings. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P3-08-03.
SP0125 Modern Treatment of Rheumatoid Arthritis
Authors: M. L. Hetland
Journal: Annals of the Rheumatic Diseases (2013)

<h3></h3> In this lecture, recent scientific evidence on the optimum treatment of rheumatoid arthritis (RA) in primary care will be addressed. Despite substantial research effort many aspects of how to best manage RA are at dispute. This includes the role of non-biologic disease-modifying drugs (nbDMARDs) versus biologic DMARDs (bDMARDs) in early as well as in established disease. Conflicting data exist as to whether nbDMARD should be used in monotherapy or in combination. Also, recent studies questionmark the role of glucocorticoids as well as their route of administration. With recent guidelines, tight disease control is central. This opens for a shift in focus from <i>type of drug</i> to <i>treatment strategy</i> with interesting implications for routine care, which will be discussed. It is, however, a challenge to meet the treatment goals in routine care. One question is how patient-reported outcomes and web-solutions may aid the rheumatologist in this effort? Recent studies have demonstrated that also economic and regulatory barriers in different countries challenge the rheumatologist both in primary and in secondary care. These and other questions, which are highly relevant for the treatment of RA, will be presented and discussed. <h3>Disclosure of Interest</h3> None Declared
THE ROLE OF OESOPHAGEAL STENTS IN THE MANAGEMENT OF OESOPHAGEAL ANASTOMOTIC LEAKS AND BENIGN OESOPHAGEAL PERFORATIONS
Authors: B Dasari, D Neely, A Kennedy, G Spence, P Rice, E Mackle, E Epanomeritakis
Journal: Gut (2013)

<h3>Introduction</h3> Endoscopic placement of oesophageal stent across the benign oesophageal perforation and postoperative oesophageal anastomotic leak might help to control the sepsis and reduce the associated mortality and morbidity. <h3>Aims/Background</h3> The aim of this review is to assess the safety and effectiveness of oesophageal stents in the management of benign oesophageal perforation and oesophageal anastomotic leaks. <h3>Method</h3> All the published case series reporting the use of metallic and plastic stents in the management of postoperative anastomotic leaks, spontaneous oesophageal perforations, iatrogenic oesophageal perforations were identified from MEDLINE, EMBASE and PUBMED (1990–2012). Primary outcomes assessed were technical success rates and complete healing rates. Secondary outcomes assessed were stent migration rates, stent perforation rates, duration of hospital stay, time to stent removal and mortality rates. A pooled analysis was performed and subgroup analysis was performed for plastic vs metallic stents and anastomotic leaks vs perforations separately. <h3>Results</h3> 27 case series with 340 patients were included. Technical and clinical success rates of stenting were 91% and 81% respectively. Stent migration rates were significantly higher with plastic stents compared to metallic stents (40/148 vs 13/117 patients respectively; p=0.001). Patients with metallic stents had significantly higher incidence of post procedure strictures (p=0.006). There was no significant difference in the primary or secondary outcomes when stenting was performed for anastomotic leaks or perforations. <h3>Conclusion</h3> Endoscopic management of oesophageal anastomotic leaks and perforations with the use of oesophageal stents is technically feasible. It appears to be safe and effective when performed along with mediastinal or pleural drainage.
Abstract 1162: SIX1 protein expression selectively identifies blastemal elements in Wilms tumor
Authors: Daniel Sehic, Jenny Karlsson, Bengt Sandstedt, David Gisselsson
Journal: Cancer Research (2012)

Abstract Background. Wilms tumour (WT) is the most common renal neoplasm in children. Histologically, most WTs consist of three tissue elements: blastema, epithelium, and stroma. Some cases also show diffuse or focal anaplastic features. Previous studies have shown that a predominance of blastemal cells in post-chemotherapy WT specimens is associated with a poor clinical course. However, there is currently no molecular marker for blastemal cells, and risk stratification for post-nephrectomy treatment is therefore often based on clinico-histological parameters alone. Procedure. In the present study, three public gene expression microarray datasets, including 82 WTs and 8 normal foetal kidneys, were used to establish a consensus gene expression profile of WT. By bioinformatic analyses, 17 genes overexpressed in WT compared to foetal kidney were then selected for evaluation of their protein expression in WT cell lines and in the different histological components in paraffin-embedded WT tissue sections by immunofluorescence. Results. Most of the evaluated proteins were expressed in all three common histological components. A prominent exception was SIX1, being expressed predominantly in blastemal elements in 24/25 paediatric cases containing blastema. Anaplastic elements exhibited highly variable SIX1-positivity. The SIX2 protein, known to be co-expressed with SIX1 during nephrogenesis, only exhibited blastemal-predominant expression in half of the SIX2 evaluated cases. Conclusions. Genes highly expressed in WT compared to foetal kidney are generally overexpressed in all of the three common WT tissue elements. An exception is the predominant expression of SIX1 in blastemal cells, hereby identifying this protein as a candidate marker for blastema. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1162. doi:1538-7445.AM2012-1162
Analgesic Effect of Intraarticular Morphine after Arthroscopic Knee Surgery
Authors: Christoph Stein, Karin Comisel, Elisabeth Haimerl, Alexander Yassouridis, Klaus Lehrberger, Albert Herz, Klaus Peter
Journal: New England Journal of Medicine (1991)

Opioids can produce potent antinociceptive effects by interacting with local opioid receptors in inflamed peripheral tissue. In this study we examined the analgesic effects of the intraarticular, as compared with intravenous, administration of morphine after arthroscopic knee surgery.
18F-FDG Hepatic Superscan in a Patient With Chronic Myeloid Leukemia
Authors: Bulin Du, Xuena Li, Na Li, Yaming Li, Bailing Hsu
Journal: Clinical Nuclear Medicine (2014)

A 62-year-old man with a history of breakpoint cluster region-ABL-positive chronic myeloid leukemia treated with hydroxyurea and interferon alfa for 4 years presented a lesion in the left lateral lobe of the liver. Besides an FDG-avid lesion, his 18F-FDG PET/CT study showed intense and diffuse FDG uptake (reminiscent of a hepatic superscan) throughout the rest of the left lobe and the right anterior lobe of the liver. This interesting superscan indicated that patients with chronic myeloid leukemia may show hepatic involvement by leukemia cells.