tbuckley/cabot-search huggingface dataset:
OP09 TIPS outcomes for refractory ascites: a single centre experience
Authors: J. Macnaughtan, B. Hogan, G. Tritto, M. Mullan, D. Yu, D. Thorburn, J. O'Beirne, R. Jalan, D. Patch, A. Burroughs
Journal: Gut (2011)

<h3>Introduction</h3> Transjugular intrahepatic portosystemic shunt (TIPS) insertion is established as an important intervention in the management of refractory ascites. We conducted a retrospective analysis of a large series of patients undergoing TIPS insertion for this indication. <h3>Aim</h3> The aims of this study were to describe the series of patients undergoing TIPS insertion for refractory ascites at the Royal Free Hospital particularly with regards to survival and procedural success. <h3>Method</h3> A retrospective analysis of the Royal Free Hospital radiology database was conducted to identify all patients who underwent all TIPS procedures between January 1991 and January 2011. Patient records were used to subsequently identify those patients in whom refractory ascites was the principal indication for TIPS insertion and to characterise this patient cohort. Patients were excluded if hydrothorax was the primary indication for TIPS insertion. All patients underwent baseline EEG/echocardiography and cross sectional imaging as part of their pre-procedural work up. Patients were requiring regular paracentesis and were either diuretic insensitive or intolerant. <h3>Results</h3> 1073 TIPS-related procedures were conducted at the Royal Free Hospital between January 1991 and January 2011. Of these, 159 patients underwent TIPS insertion for refractory ascites. Within this patients cohort, the underlying aetiology of cirrhosis was: alcohol 56.0% (89/159), hepatitis C 12.6% (20/159), cryptogenic 8.8%(14/159) and other causes 22.6% (36/159). 29% (46/159) of the patients were female, 71% (113/159) were male. The mean age at the time of TIPS insertion was 54.3 (±0.94) yrs. The mean pre-TIPS MELD score was 15.26 (±0.57) with a mean pre-TIPS EEG frequency of 7.51 Hz (±0.20). The mean post-procedural portal pressure gradient was 11.0 mm Hg (±0.57). Six month, 12 month and 2-year survival post-TIPS insertion was 78%, 50% and 50% respectively. At 6 months, 63% of patients had no or minimal ascites, 29% had moderate volume ascites and only 8% had persistent large volume ascites. At 12 months, 69% of patients had no or minimal ascites, 21% had moderate volume ascites and 10% had persistent ascites requiring paracentesis. <h3>Conclusion</h3> In a carefully selected group of patients, TIPS is an effective intervention in the management of refractory ascites.
P1133 COMPARISON OF 24 AND 48 WEEKS OF TREATMENT WITH FALDAPREVIR AND PEGYLATED INTERFERON/RIBAVIRIN IN PATIENTS WITH DETECTABLE BUT NOT QUANTIFIABLE HCV RNA AT WEEK 4
Authors: J. Mallolas, M. Battegay, J.M. Guardiola, J.K. Rockstroh, V. Soriano, C. Leen, M. Núñez, J. Valdez Madruga, A. Rauch, J.O. Stern, A.-M. Quinson, R. Vinisko, M. Manero, D. Dieterich
Journal: Journal of Hepatology (2014)
Complete esophageal obstruction after endoscopic variceal band ligation
Authors: Reyna Elizondo-Rivera, José González-González, Diego Garcia-Compean, Hector Maldonado-Garza
Journal: Endoscopy (2014)

Endoscopic variceal band ligation (EVL) is the endoscopic therapy of choice for esophageal varices. We present a very rare complication of EVL: complete esophageal obstruction [1].
Treatment of Hypertensive Crisis
Authors: Jane F. Desforges, Jane F. Desforges, David A. Calhoun, Suzanne Oparil
Journal: New England Journal of Medicine (1990)

OF the estimated 60 million Americans with hypertension, less than 1 percent will ever have a hypertensive crisis.1 The infrequency of such events can be attributed to improvements in the management of hypertension over the past 10 years. When patients do arrive at the emergency department or the physician's office with a critical elevation in blood pressure, proper management is essential to avoid catastrophic injury to the central nervous system, the heart, and the kidneys as a result of a delay in initiating effective therapy or of overzealous therapy leading to a too-rapid reduction in blood pressure.Hypertensive crisis is . . .
Abstract 717: Aldo-keto reductase family 1B10 (AKR1B10): Novel biomarker and molecular target of hepatocellular carcinoma
Authors: Han Bai, Wanying Zhang, Haonan Li, Kristina A. Matkowskyj, Allison L. Yang, Jie Liao, Guang-Yu Yang
Journal: Cancer Research (2012)

Abstract Aldo -keto reductase family 1B10 (AKR1B10) is a member of aldo-keto reducase (AKR) superfamily with biologic functions involved in osmolytic regulation, carbonyl detoxification, and carcinogenesis. Overexpression of AKR1B10 is identified in tumors of liver, lung, cervix and pancreas. However, the functional role of AKR1B10 in cancer remains unclear. In the present studies, we determined the expression and function of AKR1B10 in human hepatocellular carcinoma (HCC) using ex vivo HCC tissues and HCC cell lines. Thirty nine of HCC surgical resected specimens have been analyzed for the expression of AKR1B10 using immunohistochemistry method and revealed that 92.3% (36/39) of HCC expressed AKR1B10, including 100% (10/10) well differentiated, 95.2% (20/21) moderate differentiated, and 75% (6/8) poor differentiated HCC. No expression was observed in the adjacent morphologically normal liver. Expression of AKR1B10 in HCC confined to the cytoplasm. In order to investigate the oncogenic role of AKR1B10 in HCC, silence or inhibition of AKR1B10 in HCC cells (Huh 7) was approached using lentivirus mediated shRNA method or AKR1B10 inhibitor epalrestat. The results showed that the expression of AKR1B10 protein was significantly decreased in the AKR1B10 silenced cell lines with three different shRNA sequences using western blot approach. Knockdown AKR1B10 resulted in a significant inhibition of Huh 7 cell proliferation/tumorigenesis by colony formation assay and showed the average clone number was 174±25 of pGIPZ vector control Huh7 cell, and 86±32 of the AKR1B10 shRNA silencing cells (p&amp;lt;0.05). The average clone size was also significantly decreased in AKR1B10 shRNA silencing cells. A slightly increased cell apoptosis was found in AKR1B10 silenced cells as detected with both caspase-3 immunohistochemistry (IHC) and Annexin V flow cytometry. Furthermore, AKR1B10 silenced cells or pGIPZ vector control Huh7 cells pretreated with AKR1B10 inhibitor epalrestat significantly increased sensitivity to doxorubicin and 4-hydroxy Hexenal-induced cell death as measured with Annexin V flow cytometry. Reduction of GTP-KRAS activity and its downstream MAPK signals were observed in AKR1B10 silencing cells as measured by western bolt approach. Our results indicated that AKR1B10 is involved in the process of cell proliferation, apoptosis, and Kras activation, and further imply that AKR1B10 is a novel biomarker and crucial molecular target of HCC. 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 717. doi:1538-7445.AM2012-717
Non-Endemic Burkitt's Lymphoma
Authors: Risa B. Mann, Elaine S. Jaffe, Raul C. Braylan, Koji Nanba, Michael M. Frank, John L. Ziegler, Costan W. Berard
Journal: New England Journal of Medicine (1976)

To investigate the nature of non-endemic Burkitt's lymphoma, we examined neoplastic cells from eight American patients for receptors for sheep erythrocytes (E), complement (EAC), and Fc fragment of lgG (igGEA), and for surface immunoglobulins (Slg) and hydrolytic enzymes. In addition, we reviewed 47 biopsies and 17 autopsies from American patients to ascertain patterns of involvement by tumor in lymph nodes, spleens and Peyer's patches. Neoplastic cells in all cases studies bore monoclonal surface immunoglobulins of the igM class. Receptors for EAC and igGEA were identified on a minority of the cells. Little or no hydrolytic enzyme activity was demonstrable. These results indicate that, like Burkitt's lymphoma in Africans, this histologically identical tumor in American patients consists of B lymphocytes. In 10 biopsies and two autopsies, germinal centers were selectively involved by tumor, suggesting that these neoplastic cells may be related to some B lymphocytes of normal germinal centers.
THU0107 Hypoxia-Inducible Factor 2A is Preferentially Expressed by M2-Like Synovial Macrophages in Rheumatoid Arthritis
Authors: W. J. Hardy, S. Aynsley, U. Fearon, D. Veale, A. G. Wilson, M. Muthana
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> In rheumatoid arthritis (RA), the influx of inflammatory cells as well as the aggressive proliferation of fibroblast-like synovial cells (FLS) outstrips the oxygen supply from blood vessels leading to joint hypoxia. Macrophages accumulate in hypoxic disease sites including RA joints where they possess broad pro-inflammatory, destructive and remodelling potential leading to inflammation and joint destruction. Macrophages respond to hypoxia by up regulating the hypoxia inducible transcription factors– HIF-1 and -2, which leads to the up-regulation of genes involved in proliferation, angiogenesis, and glucose metabolism. <h3>Objectives</h3> The objective of our study was to characterise the HIF-1 and HIF-2 expressing macrophage populations in response to joint hypoxia, and in particular to dissect out the effects of HIF-2 in a murine model of arthritis. <h3>Methods</h3> Arthroscopy sections (5 microns) from RA patients with mild (~40mmHg), moderate (~15mmHg) &amp; severe (~3mmHg) joint hypoxia were immunostained with anti-HIF 1 and 2 and co-localised with the pan-macrophage marker CD68 as well as other macrophage markers. Murine arthritis using K/BxN serum transfer was induced in 10 – 12 week old mice bearing a targeted deletion of HIF-2 in myeloid cells (HIF2fl/fl; LysM-Cre+' mice) or control mice (HIF2fl/fl; LysM-Cre-). Mice were given 100ul injections of serum on day 0 and 2 and inflammation was monitored daily. <h3>Results</h3> In patients with mildly hypoxic joints, macrophages expressed HIF-1+ and CD147 and were found in small clusters localised to the lining layer. Macrophages in patients with severely hypoxic joints predominately expressed HIF-2+ and the VEGF receptor Flt-1. These macrophages also expressed the angiopoietin receptor 'Tie2' and the mannose receptor 'CD206' both associated with M2-like macrophages. The significance of HIF-2 was evaluated in a murine arthritis model where macrophages having a genetic deletion of HIF-2 developed less severe arthritis compared to control mice. <h3>Conclusions</h3> HIF-2+ macrophages expressing M2-like markers were predominantly expressed in patients with severely hypoxic joints and loss of HIF-2 expression by macrophages in a mouse model of arthritis prevented disease development. Taken together, these findings suggest that HIF-2 is the major hypoxia-inducible transcription factor in synovial macrophages and targeting HIF-2 is likely to be an effective therapeutic strategy. <h3>Disclosure of Interest</h3> None Declared
Abstract LB-14: Low connexin-26 predicts the development of metastasis after radical prostatectomy
Authors: Irene V. Bijnsdorp, Laurence Rozendaal, R. Jeroen A. van Moorselaar, Albert A. Geldof
Journal: Cancer Research (2011)

Abstract Prostate cancer is the second most common cause of death in males. Not all tumors will become metastatic within a patients life time, but when metastasized no curative therapy is available. It is therefore important to identify molecules that predict whether the tumor will become metastatic. Connexin-26 (Cx26) is a gap-junction protein that is involved in cell-cell contacts and in cell adhesion. Cx26 is involved as a tumor suppressor in various tumor types. The aim of the present study was to determine Cx26 expression in localized prostate cancer and relate the expression to the development of metastasis. Cx26 was stained by immunohistochemical staining in radical prostatectomy tissues of 43 patients. The expression levels were scored by a pathologist. Cx26 expression was observed in 95% of the patients. No relation was found to Cx26 expression in the tumor and the development of metastasis (p=0.2). Interestingly, a clear relation was found between low Cx26 expression in benign epithelial cells within the same sections and the development of metastasis (p&amp;lt;0.03). These metastases developed in about 5–40 months after radical prostatectomy. Kaplan Meier analysis showed a relation between a low Cx26 (score &amp;lt;75) expression in benign epithelial cells and time to PSA progression (p=0.01). Time to progression was associated with PSA and Cx26 expression in benign epithelial cells (Multivariate Cox proportional hazards analysis, p=0.05). In conclusion, Cx26 expression in the benign epithelial cells was associated with the development of metastasis. Cx26 expression could therefore be used as a predictor of outcome after radical prostatectomy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-14. doi:10.1158/1538-7445.AM2011-LB-14
Nanopowder spray for temporary hemostasis in a patient presenting with esophago-carotid fistula after radiation and surgery for a head and neck cancer
Authors: Mikael Sawatzki, Lukas Hechelhammer, Christa Meyenberger, Ursula Schoenenberger, Sandro Stoeckli
Journal: Endoscopy (2014)

Hemospray (Cook Medical, Winston-Salem, North Carolina, USA), a locally applicable hemostatic agent, was introduced in 2011 for the management of upper gastrointestinal bleeding [1] [2]. In contact with moisture, Hemospray becomes cohesive and adhesive, creating a mechanical barrier and effective hemostasis.
Abstract 4173: <i>In vivo and in vitro propagation of Intraductal Papillay Mucinous Neoplasms</i>
Authors: Hirohiko Kamiyama, Mihoko Kamiyama, Seung-Mo Hong, Collins Karikari, Ming-Tseh Lin, Margaret Griffith, Angela Young, Alexis Kirby, Michael Borges, Conrad Lubek, Masamichi Mizuma, Georg Feldman, Chanjuan Shi, Hong Liang, Michael Goggins, Anirban Maitra, Ralph Hruban, James Eshleman
Journal: Cancer Research (2010)

Abstract Background Intraductal Papillary Mucinous Neoplasms (IPMNs) are one of the 3 known curable precursor lesions (IPMN, MCN (Mucinous Cystic Neoplasm), and PanIN (Pancreatic Intraepithelial Neoplasm)) of invasive pancreatic ductal adenocarcinoma, an almost uniformly fatal disease. Methods To advance the study of the biological features of IPMNs, we attempted in vivo and in vitro growth of selected IPMNs, based on the hypothesis that IPMNs could be grown in the most severely immunodeficient mice. We examined fourteen cases by implanting them into nude, severe combined immunodeficient (SCID), and NOD/SCID/IL2Rγnull (NOG) mice, in addition to direct culture, to generate tumor xenografts and cell lines. Results Thirteen tumors were implanted into the 3 types of mice, including 10 tumors implanted into the triple immunodeficient NOG mice, where the majority (8 of 10) grew including 5 IPMNs lacking invasive components. One of the explanted IPMNs, with an associated invasive carcinoma, was successfully established as a cell line. Growth in soft agar, growth in mice and homozygous deletion of P16/cdkn2a confirmed its tumorigenicity. The expression of cytokeratin confirmed the epithelial differentiation of the cell line, and DNA fingerprinting confirmed its human origin. Future directions Isolating cell lines from IPMNs and their invasion counterparts should be valuable to identify gene mutations critical to IPMN carcinogenesis, and permit drug screening to identify compounds that cause regression of those lesions. 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 4173.
Abstract 4516: Gene expression analysis as a biomarker study for ACTS-CC trial (TRICC0706), a phase III trial for adjuvant chemotherapy of S-1 and UFT/LV against stage III colon cancer in Japan
Authors: Hiroyuki Uetake, Toshiaki Ishikawa, Shigeyuki Matsui, Kenichi Sugihara
Journal: Cancer Research (2012)

Abstract Background: The ACTS-CC trial is a phase III trial designed to validate non-inferiority of S-1 to UFT/ LV, a standard treatment in Japan as adjuvant chemotherapy for stage III colon cancer and the initial safety report of the trial was reported in ASCO 2011. In biomarker study of ACTS-CC trial, gene expression levels were studied using formalin fixed and paraffin embedded (FFPE) specimens. Methods: Blocks from resected colorectal cancer specimens were obtained under informed consent for this biomarker study from 892 patients enrolled between Apr.2009 and Jan.2010. Gene expression levels of 11 enzymes (TS, DPD, TP, OPRT, FPGS, GGH, DHFR, MTHFR, MTHFD, FOLRA, GART), that correlate to 5-FU and folic acid metabolism, are studied according to Danenberg Tumor ProfileTM method (Shirota, Y. JCO 2001). Correlation coefficients between gene expressions of the 11 enzymes were computed using Spearman rank correlation test (Rs). Results: Gene expression levels were successfully estimated in 521-808 samples (84.0-90.0%, 89.4% in median). Highest Rs was observed between DPD and TP (0.68. 95% confidence interval; 0.64-0.71). Classifying Rs value into 3 groups (positive (0.5&amp;lt;), week (0.31-0.50) and negative (0.3 or less)), TS and OPRT had positive or week correlation with 4 of 7 metabolic enzymes of folic acid (DHFR, MTHFR, MTHFD, and GART). Conclusions: This is the first and largest gene expression analysis for metabolic enzymes of 5-FU and folic acid. Positive correlation was observed between gene expression level of DPD and TP, which are DNA catabolic enzymes. Gene expression level of TS and OPRT, which are DNA synthetic enzymes, had correlation with metabolic enzymes of folic acid. 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 4516. doi:1538-7445.AM2012-4516
Abstract 1191: Flotillin-2 overexpression is associated with an invasive urothelial cell carcinoma phenotype
Authors: Abhimanyu Veerakumarasivam, Kasra Saeb-Parsy, Helen E. Scott, David E. Neal, John D. Kelly
Journal: Cancer Research (2010)

Abstract Invasive urothelial cell carcinoma (UCC) is associated with poor clinical outcome and is characterized by a genotype that is distinct from superficial disease. Exploiting a multi-component mining strategy on a set of high-throughput genome-wide experimental data, we probed for genes associated with an invasive phenotype. Fresh frozen UCC tissues were profiled using global expression microarrays and array-based comparative genomic hybridization (aCGH). Differentially expressed genes were functionally annotated by gene ontology and compared to available SAGE libraries and expression array datasets. We identified overexpression of a lipid raft associated protein, Flotillin 2 (FLOT2) in invasive UCC. The FLOT2 locus (17q11-q12) was associated with copy number gains in 15% of the tumors. We further characterized Flot2 protein expression in an independent tissue microarray series by immunohistochemistry. Flot2 protein expression increased with clinical risk. Interestingly, carcinoma in situ (CIS) tumors demonstrated highest level of expression. In vitro, FLOT2 expression increased with the degree of invasiveness of the UCC cell lines. Knockdown of FLOT2 lead to a significant reduction in the invasive phenotype; whilst overexpression of wild-type FLOT2 enhanced invasion in non-invasive cells. The precise mode of action of Flot2 remains to be elucidated but it is predicted to play an important role in transmembrane signal transduction, cell adhesion and endocytosis. FLOT2 overexpression has also been shown to enhance the spreading of cells, formation of filopodia as well as melanoma progression and metastasis. Thus, the functional targeting experiments and gene-dosage dependent FLOT2 overexpression in invasive UCC confirm a link between FLOT2 and pro-invasive cancer phenotype. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. 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 1191.
AB0624 High Levels of Proinflammatory Biomarkers in Patients with Idiopathic Inflammatory Myopathies
Authors: K. Stefanantoni, I. Sciarra, M. Vasile, M. Pendolino, C. Alessandri, C. Giordano, G. D'Amati, C. Crescioli, G. Valesini, V. Riccieri
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Idiopathic Inflammatory myopathies (IIM) are an heterogeneous group of autoimmune diseases that include Polimyositis (PM), Dermatomyositis (DM), Inclusion Body Myositis (IBM) and Connective Tissue Disease-related Myositis (CTD-M). Several molecules, such as cytokines, chemokines and growth factors can play an important role in triggering and substain inflammation and the consequent muscle damage (1,2,3). <h3>Objectives</h3> To measure serum levels of some proinflammatory molecules to assess their hypothetical role in the development of chronic inflammatory myositis and the hypothetical differences among the different forms of myopathies. <h3>Methods</h3> We enrolled 24 patients (M/F =7/17; mean age =55,75yrs; mean disease duration =105,2 months) affected by PM (n=7), DM (n=10), IBM (n=2), and CTD-M (n=5), diagnosed according to clinical and histological criteria. We also enrolled 12 age and sex matched healthy controls. In all patients we investigated serum levels of 17 molecules: CTACK, β-NGF, HGF, IFNα, IL 2rα, M-CSF, MIG, SCFG-β, IL-1α, IL-3, LIF, MCP, SCF, SDF-1α, TNF-β and TRAIL, using a multiplex method (Human Cytokine Standard 23-Plex, Bio-Rad Laboratories). <h3>Results</h3> We detected a statistically significant increase of β-NGF (median 1,72 pg/ml vs 0,94 pg/ml; p=0.0051), HGF (median 625 pg/ml vs 400 pg/ml; p=0,0053), IFNα (median 46,61 pg/ml vs 29,63 pg/ml; p=0,05), IL-2 rα (median 139,9 pg/ml vs 82,7 pg/ml; p=0,018), LIF (median 15pg/ml vs 4,13 pg/ml; p=0,05), M-CSF (median 30,87 pg/ml vs 19,15 pg/ml; p=0,033), MIG (median 2492,49 pg/ml vs 900,84 pg/ml; p=0,0008) and SCFG- β (median 20198,1 pg/ml vs 13976,65 pg/ml; p=0,0066) serum levels in patients with IIM respect to healthy controls. We didn9t find any significant difference among the various forms of myopathies nor for the main clinical and laboratory features. <h3>Conclusions</h3> Our study shows that several proinflammatory molecules can be involved in the pathogenesis of IIM. Their exact role needs to be better assessed and requires further investigations assuming that these molecules may be used, in addition to the histopathological analysis, as a useful diagnostic tool for these rare diseases. <h3>References</h3> Salomonsson S, Lundberg IE: Cytokines in idiopathic inflammatory myopathies. Autoimmunity 2006. Dalakas MC: Mechanism of disease: signaling pathways and immunology of inflammatory myopathies. Nat Clin Pract Rheumatol. 2006. Baird S, Montine T.J: Multiplex Immunoassay Analysis of Cytokines in Idiopathic Inflammatory Myopathy. Arch Pathol Med. 2008. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5311
Lung Cancer in Patients Under 40 Years: a Prospective Observational Multicenter Study (Groupe Français De Pneumo-Cancérologie (Gfpc) 1001 Study)
Authors: L. Bigay-Gamé, S. Bota, L. Greillier, I. Monnet, A. Madroszyk, R. Corre, B. Mastroianni, L. Falchero, C. Chouaid, C. Audigier-Valette, N. Baize, C. Daniel, G. Fraboulet, D. Gossot, C. Raynaud, J. Mazières, H. Colineaux, B. Lepage, G. Robinet
Journal: Annals of Oncology (2014)