tbuckley/cabot-search huggingface dataset:
Abstract 364: Impact of glucocorticoid in patients with locally advanced esophageal cancer treated with concurrent chemoradiotherapy
Authors: Yen-Shen Lu, Chia-Chi Lin, Chih-Hung Hsu, Huang-Chun Lien, Pei-Yen Yeh, Ling-Chiun Yeh, Ann-Lii Cheng
Journal: Cancer Research (2011)

Abstract Background: Concerns about the effect of glucocorticoids (GC) on tumor growth and chemosensitivity have been raised recently. Our pervious study shows that GC receptor is highly expressed in esophageal squamous cell carcinoma (ESCC) tumor tissues (Histopathology 2008;52:314-324). This study sought to further characterize the GC effect on the efficacy of conventional anti-cancer therapy to ESCC. Materials and Methods:The in vitro study was performed in 2 esophagus cell lines: KYSE-70 and KYSE-410. The cell viability is determined by MTT assay and clonogenic assay. The effect of GC on cytotoxic treatment -induced apoptotic cell death was determined by flow cytometric and Western blot analysis. Further, we retrospectively analyzed impact of GC usage on the outcomes of 92 patients with locally advanced ESCC who received preoperative concurrent chemoradiotherapy in a prospective clinical trial. Among 92 locally advanced ESCC patients, 39 patients who received GC twice weekly for four to six weeks (a total of eight doses or more) and 53 patients who received GC only two doses in the first week at discretion of individual physicians. Results: In vitro study showed pretreatment of GC confer resistance to cytotoxic agents including paclitaxel, gemcitabine and 5-FU, and resistance to irradiation. The effect of increase chemo-resistance by GC may be through decrease of the apoptosis according to PI/annexin V staining flow cytometric study and Western blot study. In the retrospective clinical study, the two groups were well balanced with respect to disease stage and other prognostic factors. Multivariate analysis showed that corticosteroid usage and performance status were independently prognostic of survivals. The median overall survivals of the two-dose group the eight-dose-or-more group were 38.4 and 15.1 months, (p = 0.089), respectively. The median progression-free survivals were 27.5 and 9.4 months (p = 0.024), respectively. Conclusion: This data suggest that GC decrease chemo-sensitivity and radio-sensitivity of ESCC cells. Frequent usage of GC during concurrent chemoradiotherapy may have a detrimental effect on patients with locally advanced ESCC. 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 364. doi:10.1158/1538-7445.AM2011-364
Effectiveness of 23-valent pneumococcal polysaccharide vaccine in adults aged 60 years and over in the Region of Madrid, Spain, 2008–2011
Authors: M  A Gutiérrez Rodríguez, M A Ordobás Gavín, L García-Comas, J C Sanz Moreno, E Córdoba Deorador, M D Lasheras Carbajo, J A Taveira Jiménez, F Martín Martínez, D Iniesta Fornies, A Arce Arnaez
Journal: Eurosurveillance (2014)

Invasive pneumococcal disease (IPD) is a notifiable disease in the Region of Madrid. The 23-valent pneumococcal polysaccharide vaccine (PPV23) is recommended for children and adults aged two years or over with a high risk of disease, and for all adults aged 60 and over. We describe the evolution of IPD incidence from 2008 to 2011 in people aged 60 years and over and PPV23 vaccine effectiveness (VE). VE is estimated using both the screening method and indirect cohort method. The incidence of IPD varied from 20.0 in 2008 to 15.2 per 100,000 inhabitants in 2011 (RR: 0.8; 95% CI: 0.6–0.9). Adjusted VE estimated with the screening method was 68.2% (95% CI: 56.2–76.9). VE with the Broome method was 44.5% (95% CI: 23.8–59.6) for all PPV23 serotypes, and 64.4% (95% CI: 45.2–76.8) for PPV23 serotypes not included in conjugate vaccines. VE was lower in patients aged 80 years and older (25.5%; 95% CI:-23.2 to 55.0) and those with highrisk medical conditions (31.7%; 95% CI: -2.2 to -54.4). Adjusted VE was 44.5% (95% CI: 19.4-61.8) within 5 years of vaccination and 32.5% (95% CI: -5.6 to 56.9) after 5 years. These results are compatible with current recommendations for PPV23.
Abstract 203: Hotair, a long non-coding RNA, exhibits pro-oncogenic activity in pancreatic cancer
Authors: Kyounghyun Kim, Stephen Safe
Journal: Cancer Research (2012)

Abstract HOTAIR is a long intervening non-coding RNA (lincRNA) that represses specific gene transcription by interaction with the Polycomb Repressive Complex 2 (PRC2) that trimethylates histone H3 lysine 27, leading to reprograming of chromatin states. HOTAIR is a poor prognostic indicator for survival of breast, colon and liver cancer patients and is highly associated with cancer invasion and metastasis. In this study, we show that HOTAIR is more highly expressed in pancreatic tumors than normal tissue and is strongly correlated not only with cell invasiveness but also cell proliferation and death. Overexpression of HOTAIR increased cell invasion in pancreatic cancer cells expressing low levels of HOTAIR and this was previously observed in other cancer cell lines. However, unlike previous reports, HOTAIR knockdown in Panc1 and L3.6pL pancreatic cancer cells that overexpress this lincRNA decreased cell proliferation, altered cell cycle progression, and induced apoptosis, demonstrating an expanded function for HOTAIR in pancreatic cancer cells compared to other cancer cell lines. Results of gene profiling studies after HOTAIR knockdown showed that there was minimal overlap between HOTAIR-regulated genes in pancreatic vs. breast cancer cells and HOTAIR uniquely suppressed several interferon-related genes and genes related to cell cycle progression in pancreatic cancer cells. Consistently, Gene Set Enrichment Analysis (GSEA) shows that HOTAIR regulates gene sets relevant to cell proliferation using HOTAIR Knockdown gene profiling data and pancreatic patient gene expression data. Analysis of selected genes suppressed by HOTAIR in Panc1 and L3.6 pL cells showed by knockdown of EZH2 and chromatin immunoprecipitation assays that HOTAIR-mediated gene repression was both PRC-2-dependent and -independent. HOTAIR knockdown in L3.6pL cells also inhibited tumor growth in mouse xenograft model, further demonstrating the pro-oncogenic function of HOTAIR in pancreatic cancer. These results indicated that HOTAIR is a potential molecular target for inhibiting pancreatic cancer cell invasion, metastasis and proliferation for inducing cell death. 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 203. doi:1538-7445.AM2012-203
AB0715 Aspirin resistance in systemic lupus erythematosus patients
Authors: A. Akdogan, L. Kilic, U. Akman, I. Dogan, Ö. Karadag, S.A. Bilgen, Y. Büyükasık, S. Kiraz, I. Ertenli
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Aspirin inhibits platelet aggregation by blocking thromboxane synthesis and has an antithrombotic effect. Patients with systemic lupus erythematosus (SLE) are at increased risk for thrombotic events and are frequently on aspirin treatment. <h3>Objectives</h3> The aim of this study is to investigate the presence of aspirin resistance in SLE patients. <h3>Methods</h3> Aspirin resistance is determined by Multiplate<sup>R</sup> impedance aggregometer (Dynabyte GmbH, Munich, Germany). If the arachidonic acid induced testwas positive then it was repeated in presence of 1 mg/ml acetylic salicylic acid in the medium (ASA control, Dynabyte GmbH, Munich, Germany). Aspirin resistance was defined if TRAP induced and ASPI induced aggregation test values were between 800-1300 area under the curve and 300 AUC respectively. Disease activity in SLE patients were determined by using SELENA-Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). <h3>Results</h3> Twenty-six SLE patients (F/M: 24/2) who were on regular aspirin treatment were enrolled into the study. Mean age of the patients was 37,8±12,9 years. Twenty-five patients were on 100/day aspirin and one was on alternate day 100 mg aspirin. Aspirin resistance were determined in 5(19,2%) SLE patients. When the tests were performed by adding acetylic salicylic acid in the medium, all of these patients were responsive to the aspirin. The mean SELENA-SLEDAI score or the mean body mass index value was not different between the SLE patients with aspirin resistance and the SLE patients without aspirin resistance (p=NS for all). <h3>Conclusions</h3> Aspirin resistance is not infrequent in SLE. Patient’s compliance to the aspirin treatment should be checked periodically. <h3>Disclosure of Interest</h3> None Declared
High-Dose Pancreatic-Enzyme Supplements and Fibrosing Colonopathy in Children with Cystic Fibrosis
Authors: Stacey C. FitzSimmons, Greg A. Burkhart, Drucy Borowitz, Richard J. Grand, Thomas Hammerstrom, Peter R. Durie, John D. Lloyd-Still, Albert B. Lowenfels
Journal: New England Journal of Medicine (1997)

Fibrosing colonopathy has been reported in young children with cystic fibrosis, the majority of whom take high-strength pancreatic-enzyme supplements to control intestinal malabsorption. We conducted a case–control study in the United States to investigate the relation between dose and type of pancreatic-enzyme supplement and fibrosing colonopathy.
RM-05 * CASE OF GLIOBLASTOMA PATIENT TREATED WITH NovoTTF THERAPY AT RECURRENCE DEGENERATING TO SARCOMA
Authors: P. Majd, D. O'Connell, R. Kim, D. Bota, J. Carrillo
Journal: Neuro-Oncology (2014)

NovoTTF treatment is an FDA approved treatment strategy for recurrent Glioblastoma multiforme (GBM) management which employs alternating electric fields to the region of the malignant tumor through probes on the patient's head which is thought to improve time to disease progression of GBM via cell cycle mitosis disruption. A patient is described with recurrent GBM who had disease progression following initial standard surgical treatment and concomitant chemo-radiotherapy and was found to have sarcomatous transformation after initiation of NovoTTF-100A electrical device therapy with bevacizumab. Upon tumor progression, less than two years after initial diagnosis, the patient underwent surgical resection which revealed transformation from a GFAP-positive WHO grade IV astrocytoma into a GFAP-negative, reticulin-positive sarcoma with rhabdomyoid features following histopathological evaluation. The possibility of a causal connection between the NovoTTF therapy and sarcomatous transformation needs to be further evaluated. No such case of sarcoma progression in the CNS following chemo-radiotherapy and/or electrical current treatment for Glioblastoma multiforme has been reported in the literature.
Kidney Cancer: Current and Novel Treatment Options
Authors: Eric Jonasch
Journal: Journal of the National Comprehensive Cancer Network (2015)

Antiangiogenic therapies remain the standard of care in the front-line setting for renal cell carcinoma, although vascular endothelial growth factor (VEGF) blockade is not sufficient, and many patients do not respond to such treatment. With a host of approved agents, questions arise as to how best to use them in both initial and secondary treatments. Optimal sequences are currently being tested in various clinical trials. Because approximately 20% of patients exhibiting primary resistance to these anti-VEGF therapies, new therapies are needed. Novel therapies such as MET and AXL inhibitors as well as checkpoint antibodies hold promise for the future.
AB0321 Usefulness of tocilizumab therapy and changes in bone and cartilage metabolism markers in ra patients
Authors: K. Hiraku, S. Wataru, S. Masakatsu, S. Satoshi, K. Masato, U. Mitsuo, A. Masao, N. Fumiaki, N. Tohgo, O. Narihiro
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Some cases in RA, the use of biologics improved bone quality and formation. We try to demonstrate the TCZ suppresses RA activity and promotes bone formation. <h3>Objectives</h3> TCZ was administered to RA patients to suppress the inflammatory cytokine IL-6, and the correlation of clinical assessment (DAS28-ESR) with bone/cartilage markers (MMP-3, IL-6, OC, NTX, osteoprotegerin [OPG], Dickkopf-1 [DKK-1], CTX-2) and the Spearman rank-correlation coefficient (ρ) were examined. <h3>Methods</h3> Each marker and overall assessment was done pre-administration and at 12, 24 and 52 weeks in 20 RA patients from 2010 to 2012 at facilities associated with Kinki University. The subjects were 7 men and 13 women, average age 57.0±18.2 years, stages I (5), II (5), III (1) and IV (9), classes I (4), II (14), III (2) and IV (0), with disease duration of 8.8±8.0 years, rate of MTX use of 35% (7 patients) at 6.5±1.8 mg/week, rate of PSL use of 70% (14 patients) at 4.0±1.4 mg, with 11 subjects having used other biological agent. <h3>Results</h3> DAS28-ESR at 52 weeks (LOCF) significantly decreased from pre-administration 5.1±1.4 to 1.9±0.9, with 90% achieving the remission criteria, and of 9 patients using TCZ as the first-line choice, 8 met the remission criteria and 1 met the criteria for low disease activity. MMP-3 significantly decreased from pre-administration 192±174 ng/mL to 102±86 ng/mL, as well as PSL use to 2.5±2.1 mg. OC and DKK-1 significantly changed at 24 weeks, when the DKK-1 and OC/NTX ratio showed negative correlation by the Spearman rank-correlation coefficient (ρ): -0.8593 (p&lt;0.0001). Similarly, sigificant negative correlation of ρ=-0.4908 (p=0.0329) was also seen at 52 weeks (LOCF). DKK-1 at 52 weeks had significanly decreased from pre-administration 3194±797 pg/mL to 2451±734 pg/mL by TCZ administration, while the OC/NTX ratio increased 1.5 times from pre-administration. CTX-2, NTX and OPG showed no significant differences during this time. These changes related to bone formation were marked in first-line TCZ cases, and decrease was significantly greater in the remission group than in the non-remission group (p value). TCZ suppresses IL-6, which has various actions, and it may act on RANKL and have inhibitory effect on bone destruction through Wnt signal inhibitors. TCZ shows association with multiple mutual factors affecting inflammation, bone, joints, etc., and it was suggested that TCZ administration suppresses RA disease activity and promotes bone formation (particularly first-line choice &amp; early choice &gt; later choice). <h3>Conclusions</h3> TCZ suppresses RA activity and promotes bone formation. <h3>Disclosure of Interest</h3> None Declared
Abstract 691: Estrogen receptor mRNA level in breast cancer predicts response to tamoxifen
Authors: Jennifer Bordeaux, Huan Cheng, Allison Welsh, Bruce Haffty, Donald Lannin, Xingyong Wu, Nan Su, Xiao-Jun Ma, Yuling Luo, David Rimm
Journal: Cancer Research (2012)

Abstract PURPOSE: Quantification of mRNA has historically been done by reverse transcription polymerase chain reaction (RT-PCR). Recently, a robust method of detection of mRNA utilizing in situ hybridization has been described that is linear and shows high specificity with low background. Here we describe the use of the AQUA method of quantitative immunofluorescence (QIF) for measuring mRNA in situ using ESR1 (the estrogen receptor alpha gene) in breast cancer to determine its predictive value compared to Estrogen Receptor ≤ (ER) protein. METHODS: Messenger RNA for ER (ESR1) and Ubiquitin C (UbC) were visualized using RNAscope probes and levels were quantified by quantitative in situ hybridization (qISH) on two Yale breast cancer cohorts on tissue microarrays. ESR1 levels were compared to ER protein levels measured by QIF using the SP1 antibody. RESULTS: ESR1 mRNA is reproducibly and specifically measurable by qISH on tissue collected from 1993 or later. ESR1 levels were correlated to ER protein levels in a non-linear manner on two Yale cohorts. High levels of ESR1 were found to be predictive of response to tamoxifin. CONCLUSION: Quantification of mRNA using qISH may allow assessment of large cohorts with minimal formalin fixed, paraffin embedded tissue. Exploratory data using this method suggests that measurement of ESR1 mRNA levels may be predictive of response to endocrine therapy in a manner that is different from the predictive value of ER. Further studies are underway using tissue microarrays from other institutions to determine how tissue age affects this assay. 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 691. doi:1538-7445.AM2012-691
Abstract 4340: Sorafenib induces growth arrest and apoptosis in neuroblastoma cells via inhibition of JAK2/STAT3 and MEK1/2/MAPK (p44/42) signaling pathways
Authors: Fan Yang, Veronica Jove, Ralf Buettner, Hong Xin, Sangkil Nam, Tasnim Ara, Yves A. DeClerck, Robert C. Seeger, Hua Yu, Richard Jove
Journal: Cancer Research (2011)

Abstract Neuroblastoma is the most common extracranial solid tumor in the pediatric population. It accounts for 6-10% of all childhood cancers. Currently, there is a critical need to find new drugs that are less toxic and target cell signaling pathways implicated as key mediators in the formation of neuroblastoma. Sorafenib (Nexavar), a multikinase inhibitor, blocks cell proliferation and induces apoptosis in certain types of cancers. Here, we tested antitumor effects of sorafenib (≤ 10 µM) on three human neuroblastoma cell lines, CHLA255, CHLA171 and SK-N-AS. Sorafenib inhibited cell proliferation and induced apoptosis in these neuroblastoma tumor cells in a time- and dose-dependent manner. Sorafenib inhibited phosphorylation of Signal Transducer and Activator of Transcription 3 (STAT3) proteins at Tyr705 in these cells as early as 15 min after treatment, associated with inhibition of phosphorylated JAK2, an upstream kinase that mediates STAT3 phosphorylation. Expression of a constitutively-activated STAT3 mutant (pSTAT3-C) partially blocked the antitumor effects of sorafenib on neuroblastoma cells. Sorafenib also inhibited the phosphorylation of STAT3 induced by IL-6 in these tumor cells. Moreover, sorafenib downregulated phosphorylation of MAPK (p44/42) in these neuroblastoma cells after 5 min treatment, consistent with inhibition of their upstream regulators MEK1/2. Finally, sorafenib inhibited expression of cyclin E, cyclin D1, cyclin D2 and cyclin D3, key regulators for cell cycle, and the antiapoptotic protein Mcl-1, which was accompanied by induction of growth arrest and apoptosis in neuroblastoma cells. Taken together, these findings suggest the potential use of sorafenib for the treatment of pediatric neuroblastomas. 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 4340. doi:10.1158/1538-7445.AM2011-4340
Case Management and Quality of Care for Diabetic Patients
Authors: Allan M Korn
Journal: Diabetes Care (1992)

Increasing clinical demand for medical services in an environment of limited financial resources to reimburse for such services has lead to the evolution of case management processes. They may be defined as processes that help achieve the best possible clinical outcome for a patient at a cost that represents the best value to the patient and benefit plan. The most responsive and sensitive execution of a case management process is one that includes a high level of physician peer review. This type of case management may enhance the quality of care rendered to diabetic and other patients. Care that is neither necessary nor appropriate cannot be considered quality, no matter who renders it, nor how good the outcome. A case management process that focuses on medical necessity and seeks flexibility from patients, physicians, providers, and payors can help to maintain appropriate high-quality care with costs that, over time, deliver value to all participants in the process. The execution of, and the elements contained within, a clinically sensitive case management process is briefly discussed.
Abstract 1875: Lung cancer risk among hairdressers in SYNERGY – pooled analysis from case-control studies in Europe and Canada with detailed smoking data
Authors: Ann C. Olsson, Neela Guha, Thomas Brüning, Beate Pesch, Benjamin Kendzia, Heinz-Erich Wichmann, Irene Brüske, Dario Consonni, Maria Teresa Landi, Neil Caporaso, Jack Siemiatycki, Per Gustavsson, Nils Plato, Franco Merletti, Dario Mirabelli, Lorenzo Richiardi, Wolfgang Ahrens, Hermann Pohlabeln, Karl-Heinz Jöckel, David Zaridze, Adrian Cassidy, Jolanta Lissowska, Neonila Szeszenia-Dabrowska, Isabelle Stücker, Simone Benhamou, Vladimir Bencko, Lenka Foretova, Vladimir Janout, Peter Rudnai, Eleonora Fabianova, Rodica Stanescu Dumitru, Francesco Forastiere, Bas Bueno-de-Mesquita, Isabelle M. Gross, Veronique Benhaim-Luzon, Susan Peters, Roel Vermeulen, Paolo Boffetta, Hans Kromhout, Kurt Straif
Journal: Cancer Research (2011)

Abstract “Occupational exposure as a hairdresser or barber” was classified as probably carcinogenic to humans by the International Agency for Research on Cancer in volume 99 (2010). Small increases in lung cancer risk (20-40%) are found in most cohort studies but without adequate adjustment for smoking. Studies in Scandinavia and the USA show a higher prevalence of smokers among hairdressers than in the general population. The SYNERGY project has pooled information on lifetime work histories (ISCO-68) and tobacco smoking from 13479 cases and 16350 controls, including 20% women, from 11 case-control studies in 12 European countries and Canada. The original studies were conducted between 1985 and 2005. Odds ratios (OR) for lung cancer and 95% confidence intervals (CI) were estimated by unconditional logistic regression, adjusted for age, sex, study, cigarette pack-years and time since quitting smoking. Less than 1% of the study population had ever worked as hairdresser or barber (0.89% of cases and 0.74% of controls). Hairdressers and barbers experienced a slight increase in lung cancer risk OR 1.16 (95%CI 0.90-1.49), which disappeared after adjusting for smoking OR 0.97 (95%CI 0.73-1.30). Results by duration of employment showed highest risks in hairdressers with short employment. Results were similar by gender, histology of lung cancer, and for women hairdressers. We observed a slight and non-significant increase in risk for male barbers, particularly in barbers with the longest employment and after adjustment for smoking. We could not detect an association between having worked as hairdresser or barber and increased lung cancer risk overall after adjusting for smoking. However, among male barbers we observed an increasing risk with increasing duration, although non-significant, after adjusting for tobacco smoking. Final results will include several more studies, and thereby increase the precision of our effect estimates. 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 1875. doi:10.1158/1538-7445.AM2011-1875