tbuckley/cabot-search huggingface dataset:
Abstract P3-09-04: The associations between body mass index and breast cancer intrinsic subtypes in Japanese women
Authors: K Kimura, S Tanaka, M Iwamoto, K Uchiyama
Journal: Cancer Research (2012)

Abstract Purpose: The purpose of this study was to examine the associations between body mass index (BMI) and breast cancer intrinsic subtypes in Japanese women. A more complete understanding of the subtypes of breast cancer may help elucidate mechanisms affecting etiology and mortality associated with each subtype. Methods: Tumor data on 531 invasive breast cancer cases subtyped by estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 (Her2) status were obtained (luminal A, luminal B, TN, and Her2-type). Demographics (age at diagnosis, menopausal status, and BMI) were collected from medical records. Case-only odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using logistic regression, adjusting for age at diagnosis. Results: In all cases, the patients were Japanese. Of the 531 cases with IHC marker data, 333 (62.7%) were classified as luminal A, 85 (16.0%) were luminal B, 43 (8.1%) were Her2-type, and the remaining 70 cases (13.2%) were TN. The distribution of patient demographics (age at diagnosis, menopausal status, and BMI) did not differ significantly by breast cancer tumor subtype. Case-only ORs comparing each subtype to luminal A were caluculated. Of the TN cases, postmenopausal TN cases were more likely to be underweight (OR = 3.14, 95% CI = 1.19 to 8.01). Although some epidemiological studies have reported that higher BMI was associated with premenopausal TN cases compared with luminal A cases, this association was not found among premenopausal TN cases analyzed using BMI 18.5 to 24.9 kg/m2 as the reference in this analysis. However, there were no underweight cases (BMI &amp;lt; 18.5 kg/m2) among the premenopausal TN cases in the present study. Therefore, the association between BMI and the TN subtype was also analyzed using BMI &amp;lt; 25 kg/m2 as the reference. Compared to luminal A cases, premenopausal TN cases were more likely to be obese (OR = 4.11, 95% CI = 1.10 to 14.40), similar to reports from Western countries. Compared to luminal A cases, premenopausal luminal B cases were likely to be underweight (OR = 3.27, 95% CI = 0.88 to 11.39) or obese (≥ 25 kg/m2) (OR = 3.32, 95% CI = 0.98 to 10.81), yet this association was of borderline significance. Compared to luminal A cases, luminal B and Her2-type cases were likely to be underweight (BMI &amp;lt; 18.5 kg/m2), yet this association was of borderline significance (luminal B: OR = 2.12, 95% CI = 0.97 to 4.46; Her2-type: OR = 2.53, 95% CI = 0.92 to 6.36). Conclusions: In the present study, significant heterogeneity of associations between BMI and tumor subtypes was observed. Breast cancer subtypes may have different etiologies associated with each subtype. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P3-09-04.
Alcohol-Induced Hepatic Injury in Nonalcoholic Volunteers
Authors: Emanuel Rubin, Charles S. Lieber
Journal: New England Journal of Medicine (1968)

Isocaloric substitution of alcohol for carbohydrate in young nonalcoholic volunteers rapidly led to hepatic fat accumulation and ultrastructural changes, both on a standard diet and on a diet high in protein and low in fat. The addition of alcohol to a normal diet for two days resulted in similar changes, which could not be prevented by a diet high in protein with minimal fat (5 per cent of total calories). Blood alcohol levels in every subject studied were almost all well below accepted legal limits for intoxication. The data indicate that in normal nonalcoholic people, alcohol itself is hepatotoxic, independent of nutritional factors. Nonalcoholic people are not less susceptible than alcoholic patients to the injurious effects of alcohol. Amounts of alcohol consumed by many "social" drinkers are enough to damage the liver, and one need never have been drunk to sustain alcohol-induced hepatic injury.
Epidemic Profile of Shiga-Toxin–Producing<i>Escherichia coli</i>O104:H4 Outbreak in Germany
Authors: Christina Frank, Dirk Werber, Jakob P. Cramer, Mona Askar, Mirko Faber, Matthias an der Heiden, Helen Bernard, Angelika Fruth, Rita Prager, Anke Spode, Maria Wadl, Alexander Zoufaly, Sabine Jordan, Markus J. Kemper, Per Follin, Luise Müller, Lisa A. King, Bettina Rosner, Udo Buchholz, Klaus Stark, Gérard Krause
Journal: New England Journal of Medicine (2011)

We describe an outbreak of gastroenteritis and the hemolytic-uremic syndrome caused by Shiga-toxin-producing Escherichia coli in Germany in May, June, and July, 2011. The consumption of sprouts was identified as the most likely vehicle of infection.We analyzed data from reports in Germany of Shiga-toxin-producing E. coli gastroenteritis and the hemolytic-uremic syndrome and clinical information on patients presenting to Hamburg University Medical Center (HUMC). An outbreak case was defined as a reported case of the hemolytic-uremic syndrome or of gastroenteritis in a patient infected by Shiga-toxin-producing E. coli, serogroup O104 or serogroup unknown, with an onset of disease during the period from May 1 through July 4, 2011, in Germany.A total of 3816 cases (including 54 deaths) were reported in Germany, 845 of which (22%) involved the hemolytic-uremic syndrome. The outbreak was centered in northern Germany and peaked around May 21 to 22. Most of the patients in whom the hemolytic-uremic syndrome developed were adults (88%; median age, 42 years), and women were overrepresented (68%). The estimated median incubation period was 8 days, with a median of 5 days from the onset of diarrhea to the development of the hemolytic-uremic syndrome. Among 59 patients prospectively followed at HUMC, the hemolytic-uremic syndrome developed in 12 (20%), with no significant differences according to sex or reported initial symptoms and signs. The outbreak strain was typed as an enteroaggregative Shiga-toxin-producing E. coli O104:H4, producing extended-spectrum beta-lactamase.In this outbreak, caused by an unusual E. coli strain, cases of the hemolytic-uremic syndrome occurred predominantly in adults, with a preponderance of cases occurring in women. The hemolytic-uremic syndrome developed in more than 20% of the identified cases.
Abstract 3308: Differential expression of Notch-1 and Notch-2 correlates to invasive phenotype in bladder cancer cell lines
Authors: Kilian M. Gust, Shannon Awrey, Susan Ettinger, Estelle Li, Ladan Fazli, Peter C. Black
Journal: Cancer Research (2010)

Abstract The Notch pathway plays a critical role in growth and differentiation, and is involved in cancer progression in different organ sites. Little is known about Notch in bladder cancer. In this study, we evaluated Notch-1 and Notch-2 expression in a panel of bladder cancer cell lines. Thirteen bladder cancer cell lines with previously described invasive properties and epithelial/mesenchymal characteristics were screened for Notch-1 and Notch-2 expression by Western blot and real-time PCR. Immunohistochemistry (IHC) was performed on a tissue microarray (US Biomax, Inc., Rockville, MD) that included cores from 152 patients with bladder cancer. Alterations in gene expression after Notch-2 silencing with siRNA were measured by expression microarray in 3 cell lines. Genes that changed by at least 2-fold in all 3 cell lines were selected for further analysis. Wound healing assays were performed after treatment with Notch-2 siRNA versus scrambled siRNA. The Mann-Whitney test was performed for statistical analysis. Epithelial cell lines with low invasive potential expressed Notch-1 at high and Notch-2 at low relative levels (P=0.03 and P&amp;lt;0.01, respectively, compared to invasive cell lines). Highly invasive, mesenchymal cell lines expressed high levels of Notch-2 and low levels of Notch-1. These results were validated by Western blot and IHC (TMA). Microarray analysis revealed altered expression of genes related to epithelial to mesenchymal transition (EMT), protein and endosome trafficking, and cell-cell connections, when Notch-2 was silenced with siRNA. Notch-2 silencing decreased the migration of UC3 cells in the wound healing assay (P=0.02). These results provide preliminary evidence for a role for Notch in the progression of bladder cancer and it is suggested that this may be related to EMT. Further investigation is needed to assess the suitability of Notch as a therapeutic target, and it would appear that selective inhibition of individual Notch receptors may be preferential over global inhibition. 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 3308.
Intramural hematoma with gastric outlet obstruction: a rare complication of endoscopic injection therapy for bleeding anastomotic ulcer
Authors: Lei Shi, Fu Liu, Qiu Jia, Hang Guang, Zhao Lu
Journal: Endoscopy (2014)

A 66-year-old man was admitted to our department because of severe hematemesis and melena for 2 days. He had a history of gastric ulcer, which had been treated by a Billroth I partial gastrectomy 15 years previously. His hemoglobin was 3.4 g/dL and he was transfused with 5 units of packed red blood cells. Laboratory tests revealed normal platelet count and coagulation profile. Endoscopy showed blood oozing from an anastomotic ulcer ([Fig. 1 a]). The bleeding was arrested by injecting approximately 8 mL of diluted epinephrine (1 : 10 000) into and around the bleeding site ([Fig. 1 b]).
Abstract 33: Implementing CAD cells quantify the relationships between Ig-CAM-mediated adhesion, force transduction, and actin dynamics
Authors: Miles H. Fuller, Andrew Schaefer, Cecile Mejean, Paul Forscher
Journal: Cancer Research (2012)

Abstract Several neuro-degenerative diseases and motor defects have been linked to malfunctions in the motility of neurons. This project is focused on the determining whether the roles of the transmembrane proteins NCAM and L1-CAM can be studied using the CAD cell line as a model. CAD cells are a cancer cell line that come from mice and can be stimulated to grow as either neurons or glial cells. In addition, this cell line has been shown to be an easily transfected line. In order to determine usefulness of this cell line several techniques were used. Western blots were implemented in order to determine if the NCAM and/or L1-CAM and proteins known to be involved in their signaling pathways were present in the cell line. Western blots were then confirmed by immunocytochemistry staining. Next, the CAD cell line was transfected with photoactivateable actin. Finally, immuno beads were attached to the membranes of these CAD cells and then holographic optical tweezers were used to determine whether or not thsee ligands coupled to the retrograde actin flow in the cells. The combination of these experiments should provide the evidence for whether or not the CAD cells would be a feasible model to study the nature of the NCAM and L1-CAM proteins and their relationship to the movement of actin in the cytoskeleton of neurons. 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 33. doi:1538-7445.AM2012-33
Abstract 4685: Multiplexed methylation profiles of urinary DNA for non-invasive bladder cancer diagnostics
Authors: Maria Jose Cabello, Laura Grau, Esteban Orenes-Piñero, Noreli Franco, Miguel Alvarez, Ana Blanca-Pedregosa, Oscar Heredero, Jesus Fernandez, Alberto Palacios, Antonio Lopez-Beltran, Marta Sanchez-Carbayo
Journal: Cancer Research (2010)

Abstract Changes in DNA methylation of crucial cancer genes including tumor suppressors can occur early in carcinogenesis, being potentially important early indicators of cancer. The objective of this study was to examine a multiplexed approach to assess the methylation of tumor suppressor genes as urinary diagnostic markers for bladder cancer. A multicandidate probe panel interrogated DNA for aberrant methylation status in 25 tumor suppressor genes using a methylation-specific multiplex ligation-dependent probe amplification assay (MS-MLPA). Initial analyses in bladder cancer cell lines (n=14), and fresh-frozen primary bladder tumor specimens (n=31) supported the panel of genes selected to be altered in bladder cancer. MS-MLPA was then optimized for its application in body fluids using two sets of urinary specimens (n=146) including bladder cancer patients (n=96) and controls (n=50). Genes previously reported to be methylated such as BRCA1, CDH13 and RARB, were confirmed to be methylated in the three types of samples analyzed. WT1 and PAX5A were identified as novel tumor suppressor candidates methylated in bladder cancer specimens. The most frequently methylated genes in the bladder tumors analyzed were BRCA1 (71.0%), WT1 (38.7%), and RARB (38.7%), being WT1 methylation significantly associated with tumor stage (p=0.011). BRCA1, WT1 and RARB were also as the most frequently methylated genes in two independent training and validation sets of urinary specimens (n=146). ROC curves analyses revealed significant diagnostic accuracies over 70% in both sets of urinary specimens for BRCA1, RARB, WT1, PAX5A and CDH13. In summary, the novelty of this report deals with applying a multiplexed methylation technique for bladder cancer, and also in body fluids. MS-MLPA represents a promising methylation profiling tool for histopathologic stratification of bladder tumors, and diagnosis using urinary samples. This latter is clinically relevant by offering a non-invasive strategy for the clinical management of patients affected with uroepithelial neoplasias 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 4685.
P445 CLIF-SOFA SCORING SYSTEM ACCURATELY PREDICTS IMMINENT MORTALITY OF ACUTELY DECOMPENSATED PATIENTS WITH ALCOHOLIC CIRRHOSIS
Authors: M. Lee, J.-H. Lee, J.H. Yoon, S. Oh, Y. Jang, W. Lee, H.J. Lee, J.-J. Yoo, W.-M. Choi, Y.Y. Cho, D.H. Lee, Y.B. Lee, S.J. Yu, N.-J. Yi, K.-W. Lee, Y.J. Kim, K.-S. Suh, H.-S. Lee
Journal: Journal of Hepatology (2014)
Abstract 354: PI-103 and TCN as proliferative inhibitors of the RTK/PI3K/ATK signaling pathways in astrocytomas
Authors: Yvette Connell-Albert, Demir Gursel, Robert Tuskan, Theonie Anastassiadis, Jessica Hawes, Jessica Van Schaick, Karlyne Reilly
Journal: Cancer Research (2010)

Abstract INTRODUCTION: Glioblastomas (GBMs), the most aggressive of malignant astrocytomas, are recurrent, infiltrative, and fatal. In GBMs, receptor tyrosine kinases (RTKs) are often mutated and activated, leading to the dysregulation of normal cell signaling pathways. The PI3K/Akt1/mTOR pathway, which is important in normal biological events such as proliferation, survival, invasion, migration and angiogenesis, is often deregulated in malignant cancers, resulting from the simultaneous loss of tumor suppressor PTEN, and the hyperactivation of the Akt pathway. Therefore, pharmacological inhibition of the PI3K/Akt1/mTOR may prove beneficial in arresting the proliferation of astrocytomas and glioblastomas. METHODS: In order to determine if the selected inhibitors PIA-6, OSU03012, Rapamycin, Tricribine (TCN), and PI-103 had an effect on the PI3K/Akt-1/mTOR pathway, we examined their inhibitory effects on mouse astrocytoma cell lines K1861-10 Grade II; KR158 Grade III; K130G#3 Grade IV; human astrocytoma cell lines, U87MG and SF295, both Grades IV; and normal proliferating mouse primary astrocytes using the Alamar blue assay as a measure of metabolic activity and proliferation. Inhibitors with low IC50 values in tumor cells as compared to normal primary astrocytes were favored. RESULTS: From the select panel of inhibitors, only the AKT inhibitor TCN and dual PI3K/mTor inhibitor PI-103 showed low IC50 values in the nM or pM range, suggesting strong inhibition of proliferation in the astrocytoma cell lines tested. Rapamycin, an mTOR inhibitor, showed inconsistent inhibition of cell proliferation on the cell lines tested, although mTor activity was effectively inhibited, suggesting that inhibitory effects of rapamycin at higher concentrations may be acting via different pathways. CONCLUSIONS: Our results support the hypothesis that the PI3K/Akt1/mTOR pathway is a potential druggable target in astrocytomas and glioblastomas. 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 354.
AB0497 Comparison of quality of life in patients with systemic sclerosis and rheumatoid arthritis
Authors: E. Kilic, G. Kilic, O. Akgul, S. Ozgocmen
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Systemic sclerosis (SSc) is a multisystem disease associated with impaired health-related quality of life (HR-QOL). <h3>Objectives</h3> The aim of this study was to compare HR-QOL in systemic sclerosis (SSc) and rheumatoid arthritis (RA). <h3>Methods</h3> Forty-five patients with SSc, and 48 with RA were recruited from our rheumatology out patient-clinic. Patients were assessed for detailed clinical history and physical examination. HR-QOL and functional limitations were evaluated by Short Form 36 (SF-36) and Nottingham Health Profile (NHP); disability by Health Assessment Questionnaire (HAQ); depression and anxiety risk by the Hospital Anxiety and Depression Scale (HAD) and hand functions by Duruoz Hand Index (DHI). <h3>Results</h3> Mean age of the patients with SSc was 49.9±12.1 and RA was 47.8±11.4. Mean disease duration in SSc and RA was 10.1±8.2 and 10.2±7.5 respectively (p&gt;0.05). Mean BMI of SSc and RA was 25.7±6.1 and 29.5±5.2, respectively (p&lt;0.05). The mean diagnostic delay in SSc and RA was 5.2±5.3 and 2.8±3.7 years, respectively and was statistically longer in SSc (p&lt;0.05). All component scores of SF36 as well as NHP were similar between patients with SSc and RA, except emotional reaction subscores of NHP, which was higher in RA. Mean total score of DHI was similar in SSc and RA groups (23.7±25.4 and 21.1±20.8, p&gt;0.05, respectively). Anxiety and depression scores of HAD were relatively higher in SSc, but not statistically significant. Mean handgrip strength in SSc was relatively higher than RA (p&gt;0.05). There was positive correlation between Rodnan skin score and DHI (r:0.57, p:0.001), HAQ (r:0.44, p:0.009), sleep subscore of NHP (r:0,37, p:0.004), and negative correlation with SF-36 physical function (r:-0,35, p:0.02), handgrip strength (r:-0.39, p:0.04). Medical Research Council dyspnea score was positively correlated with DHI (r:0.389, p&lt;0.05), HAQ (r:0.55, p:0.001), all component of NHP (pain;r:0.44, p:0.008, physical activity; r:0.54, p:0.001, fatigue; r:0.53 p:0.001, social isolation;r: 0.38, p:0.02, emotional rection; r:0.457, p:0.006) except sleep subscore, depression score (r:0.37, p:0.03) of HAD and negatively correlated with physical component scores of SF-36 (r:-0,45, p:0.005). <h3>Conclusions</h3> This study indicates similar impairment in HR-QOL, hand function, and disability, depression and anxiety risks in patients with SSc and RA. This study is the first comparing patients with SSc vs RA by using different functional and psychometric scales. <h3>Disclosure of Interest</h3> None Declared
Two Cases of Vaccine-Derived Poliovirus Infection in an Oncology Ward
Authors: Axel Schubert, Sindy Böttcher, Anna M Eis-Hübinger
Journal: New England Journal of Medicine (2016)

The oral poliovirus vaccine strains can revert to virulent forms and establish chronic infection in persons with a weakened immune system. The authors describe such infection in two children and clearance of infection through immune recovery.
SP0085 Building Successful Alliances with Other Stake Holders in the Field of Chronic Diseases
Authors: J. Church
Journal: Annals of the Rheumatic Diseases (2014)

<h3></h3> Many hands make light work, so the saying goes and when it comes to making a big impact in the area of arthritis patient support, this also is true. Arthritis Ireland is a small charity working within a very big disease area that has mutiple co-morbities and many patients experience other chronic diseases in addition to their arthritis. In order to make a big impact with a new or existing service, often involving small budgets and small staff numbers, collabortaions and partnerships are very important. During the course of this presentation, Arthritis Ireland will demonstarte some of the collaborations that they employed in order to develop and implement impactful services in the community. Some of these collaborations involved partrnering with the pharmaceutical industry whilst others involved partnering with other chronic disease organisations. However all had the objective of utilising expertise, human resources and financial support that ensured the programmes were a greater success than had they simply involved the staff or resources of Arthritis Ireland alone. Th sum of the parts is often greater than the individual elements and can ensure greater success for any organisation but especially for smaller volunteer led organisations or for those with limited staff numbers. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.6177
SP0047 Role of fibroblasts in scleroderma
Authors: C.P. Denton
Journal: Annals of the Rheumatic Diseases (2013)

Scleroderma (systemic sclerosis) is an autoimmune rheumatic disease of high morbidity and mortality. Much of the clinical burden results from organ-based or vascular fibrosis, and scarring is a pathological hallmark of the disease. It can be regarded s a disease in which there is dysregulated connective tissue repair and inappropriate resolution of fibrosis that has been triggered by inflammation of vascular dysfunction. There is growing evidence to support a genetic basis for the disease that relates to autoimmunity but the basis for altered repair processes is less clear, it appears that there is fibroblast-dependent dysregulated connective tissue repair and this may involve a number of distinct cellular lineages. There are important lessons from developmental biology and also from studies of normal wound healing. Genetic models are no established that replicate key features of scleroderma in mutant mice and some of these provide a platform to explore the broad range of organ based pathologies that occur in the disease, notably lug fibrosis and pulmonary hypertension. Thus fibroblasts in scleroderma are both effecter cells of the disease and also key regulators of normal connective tissue repair. This lecture will explore these issues and review emerging evidence that may permit better understanding of key molecular pathways in scleroderma that could ultimately be targeted as novel forms of disease modifying therapy. <h3>Disclosure of Interest</h3> C. Denton Consultant for: Actelion Pharmaceuticals, GSK, Sanofi-Aventis, Serono, Pfizer