tbuckley/cabot-search huggingface dataset:
Abstract 5442: The role of ATF3 in arsenic-induced GADD45 expression.
Authors: Qiwen Shi, Deepak Bhatia, Vijaykumar B. Sutariya
Journal: Cancer Research (2013)

Abstract GADD45 (growth arrest and DNA damage inducible gene 45), an effector of G2/M checkpoint, is induced by trivalent arsenic (As3+) in human bronchial epithelial cell line, BEAS-2B. In the present study, we investigated the regulation of ATF3 (activating transcription factor 3) on GADD45 with As 3+ treatment. We demonstrated that As3+ induced ATF3 expression, at both mRNA and protein level, and the induction was reduced by p38 and JNK inhibition, but not affected by PI3K and ERK inhibition. Luciferase assay also confirmed As3+ involvement in ATF3 transcriptional regulation. Moreover, silencing of ATF3 downregulated As3+-induced expression of GADD45 and chromatin immunoprecipitation suggested that ATF3 acted as an activator of GADD45 transcription in the presence of As3+. Taken together, our data indicated that the increase of GADD45 in response to As3+ was mediated by ATF3. Citation Format: Qiwen Shi, Deepak Bhatia, Vijaykumar B. Sutariya. The role of ATF3 in arsenic-induced GADD45 expression. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 5442. doi:10.1158/1538-7445.AM2013-5442
Abstract 2698: The parametric response map as an imaging biomarker for identifying progression from pseudoprogression in glioma patients
Authors: Christina Tsien, Craig J. Galban, Thomas L. Chenevert, Timothy D. Johnson, Daniel A. Hamstra, Pia C. Sundgren, Larry Junck, Charles R. Meyer, Alnawaz Rehemtulla, Theodore S. Lawrence, Brian D. Ross
Journal: Cancer Research (2010)

Abstract We assessed whether a new method of quantifying therapeutic-associated hemodynamic alterations may help to distinguish pseudoprogression from true progression in patients with high grade glioma. Patients from a prospective IRB-approved trial with high grade glioma received concurrent chemoradiation. Relative cerebral blood volume (rCBV) and blood flow (rCBF) maps were acquired prior and at week 3 mid-treatment. Pseudoprogression was defined as imaging changes 1-3 months after chemoradiation that mimic tumor progression but stabilized or improved without change in treatment or for which resection revealed radiation effects only. Clinical and conventional MR parameters, including average percent change of rCBV and CBF, were evaluated as potential predictors of pseudoprogression. Parametric response map (PRM), an innovative, voxel-by-voxel method of image analysis, was also performed. Median radiation dose was 72 Gy (range: 60-81). Of 27 patients, stable disease/partial response was noted in 13 and apparent progression in 14. Adjuvant temozolomide was continued in all patients. Pseudoprogression occurred in 6 patients. Based upon PRM analysis, a significant portion of the tumor volume had reduced rCBV (PRMrCBV) at week 3 in patients with progressive disease compared to those with pseudoprogression (p&amp;lt;0.01). In contrast, change in average percent rCBV or rCBF, MR tumor volume changes, age, extent of resection, and RTOG RPA classification did not distinguish progression from pseudoprogression. PRMrCBV at week 3 during chemoradiation is a potential early imaging biomarker of response that may be helpful in distinguishing pseudoprogression from true progression in glioma patients. 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 2698.
1234 PRO-APOPTOTIC MIR-34A/SIRT1/P53 PATHWAY IN NAFLD PATIENTS AND TARGETING BY URSODEOXYCHOLIC ACID IN RAT LIVER
Authors: D.M.S. Ferreira, P.M. Borralho, M.V. Machado, H. Cortez-Pinto, C.M.P. Rodrigues, R.E. Castro
Journal: Journal of Hepatology (2012)
A Student's View of a Medical Teaching Exercise
Authors: Abenaa Brewster
Journal: New England Journal of Medicine (1993)

Physicians are usually careful to explain the purpose and format of a teaching session when asking a patient to take part. Failure to do so when the patient is poorly educated or of a different cultural background may seriously disturb the patient and mislead the other participants. Consider the events at a recent neurology conference at a Boston teaching hospital.The resident began by describing the case of “a 52-year-old postmenopausal black woman with a history of breast cancer at age 46 treated by mastectomy and radiation.” She went on to say:A year ago the patient had back, leg . . .
An Avascular Crisis in Gaucher’s Disease
Authors: ROBERT MANSBERG, ROGER UREN, ROBERT HOWMAN-GILES
Journal: Clinical Nuclear Medicine (2000)

Avascular necrosis is frequently associated with sickle cell disease and other hemoglobin disorders. It is less commonly associated with Gaucher’s disease, which is a metabolic disorder caused by a deficiency of glucosylceramidase. A severe avascular episode in a young man with Gaucher’s disease is presented.
Abstract 4788: Modulation of T lymphocytes by tumor-released survivin
Authors: Jessica M. Slater, Salma Khan, Nathan R. Wall
Journal: Cancer Research (2010)

Abstract Introduction: The role of tumor infiltrating lymphocytes (TILs) in the progression of cancer has become an important area of research. Recent studies have shown that T lymphocytes within the tumor microenvironment have decreased activation and proliferation. Our lab has shown survivin is released from tumor cells within exosomes, and is capable of altering the phenotype of malignant cells. We hypothesize that this exosomally-released survivin prevent TIL activation and proliferation in T cell subsets and that Th2 type cytokines will be released in higher levels than Th1 cytokines. Methods: HeLa-S-WT cells that produce Flag-HA tagged survivin were growth in a bioreactor and survivin isolated from the media using Flag-HA tandem affinity purification. T lymphocytes from normal donors were cultured in control or survivin-containing media and activated with anti-CD28-anti-CD3 microbeads (32 ul/ml). Flow cytometric analysis of activation marker CD69 and the proliferation marker Ki-67 were performed at 24h and 6 days, respectively. Cytokine release was evaluated using a Cytokine Bead Array (BD Bioscience) for IFN-gamma, IL-2, IL-4 and IL-10. Results: CD69 expression was decreased significantly in CD8+ T cells after incubation with survivin (Control = 72 MFU, Treated = 57 MFU; p&amp;lt;0.05) while no significant change was seen in CD4+ T cells (Control = 65 MFU, Treated = 68 MFU). CD8+ T cells showed a significant reduction in Ki-67 expression after incubation with survivin when compared to controls (Control = 218 MFU, Treated = 139 MFU; p &amp;lt; 0.001), while CD4+ T cells showed little difference between control and treated groups (Control = 74 MFU, Treated = 81 MFU). Cells treated with survivin in activating conditions released higher amounts of IL-4 (Control = 4.8 pg/ml, Treated = 28.3 pg/ml) and decreased amounts of IFN-gamma (Control = 32.4 pg/ml, Treated = 16.9 pg/ml) compared to control activating conditions. IL-2 and IL-10 showed little difference between treatment groups. Conclusions: This data suggests that survivin in the tumor microenvironment is capable of negatively affecting cytotoxic T cell activation and proliferation. While survivin treatment does not affect the activation or proliferation of CD4+ subsets, the Th1: Th2 cytokine balance is altered when survivin is present. Thus, survivin in the tumor microenvironment could play a role in the suppression of immune surveillance by inhibiting the cytotoxic T cell response and preventing tumor death by increasing levels of Th2 cytokines and decreasing levels of Th1 cytokines. 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 4788.
Abstract 5222: Identification of cell signaling pathway associated miRNAs in cancer cells using a systems biological approach.
Authors: Sangbae Kim, Bo Hwa Sohn, Yun-Yong Park, Ji-Hoon Kim, Sung Sook Lee, Micheal A. Davies, Gordon B. Mills, Ju-Seog Lee
Journal: Cancer Research (2013)

Abstract MicroRNAs(miRNAs) are single-stranded, non-coding RNA molecules and on average only 22 nucleotides long that regulate gene expression at the post-transcriptional level. Target predictions of miRNA based on sequence are limited due to too many candidates resulting in high false positives. To overcome this limitation functional target prediction approaches have been investigated with mRNA and miRNA expression data. These approaches can be used in the computational assessment of functional miRNA-target association. However, these approaches with miRNA-mRNA association were not enough to verify real functional targets at protein level, which could affect on cell signaling pathway. Therefore, in the present study to compensate this limitation, we developed a novel correlation based approach (sequence-independence) to predict potential miRNA targets with genomic and proteomic data, protein, miRNA and mRNA array data, in NCI-60 cells. To establish a prediction model for identifying the association of miRNA-cell signaling pathways by analyzing genomic and proteomic data, we performed a correlation based method among miRNA, mRNA and protein expression profile. Using this approach, we generated the Association score matrix (ASM) between miRNA and protein probes. Based on ASM, we finally generated the highly associated miRNAs with cell signaling pathways called miRNA-pathway association map (miRPM). To validate our approach, we used miR-500 as an example to investigate the hypothetical target regulation mechanisms predicted by miRPM. We confirmed in-vitro that mir-500 highly is associated with ERK/MAPK signaling pathway in melanoma and breast cancer cells. Furthermore, we found PP1/PP2 might be a direct target of miR-500 to regulate activating the ERK/MAPK pathway. In conclusion, we developed a novel expression profile based approach to systematically predict potential miRNA functional targets which play critical roles in cell signaling pathways from the NCI-60 genomic and proteomic data at whole genomic scale. Our approach might be applied to investigate the unknown regulatory role of miRNAs in signaling pathways and gene regulatory networks. Citation Format: Sangbae Kim, Bo Hwa Sohn, Yun-Yong Park, Ji-Hoon Kim, Sung Sook Lee, Micheal A. Davies, Gordon B. Mills, Ju-Seog Lee. Identification of cell signaling pathway associated miRNAs in cancer cells using a systems biological approach. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 5222. doi:10.1158/1538-7445.AM2013-5222
PMO-087 Laparoscopic insertion of freka feeding jejunostomy as a part of laparoscopic thoracoscopic cardio-osophagectomy—a review of our outcome
Authors: V Daya Shetty, K Akhtar
Journal: Gut (2012)

<h3>Introduction</h3> A retrospective review of outcomes of laparoscopic insertion of feeding jejunostomy as a part of laparoscopic thoracoscopic cardio-oesophagectomy. <h3>Methods</h3> From October 2010 to January 2012 (15 months) 18patients underwent laparoscopic thoracoscopic cardio-oesophagectomy. All 18 patients (12 male, 6 female) had laparoscopic insertion of Freka feeding jejunostomy are included in the study. The feeding jejunostomy was used for feeding from first postoperative day. The standard regime was water at 20 mls/h on day 1 followed by feed (jevity/osmolyte) at 30 mls/h on day 2. The rate of feed was increased at daily increments of 10 mls/h/day to achieve target rate to meet patient9s nutritional requirements. Patients were discharged with feeding jejunostomy in situ, removed at follow-up if nutritionally stable. <h3>Results</h3> The average procedure time was 20 min. Median duration of feeding jejunostomy in situ was 3 weeks (range 8 days–6 weeks). Tube related complications, n=3 patients (tube fallout-1, leak-2). Only one of these three patients needed additional parenteral nutrition. There were no procedure or feed related complications. The overall length of stay was not affected by this procedure. The availability of enteral route was useful in n=2 patients (chest infection-1, gastric stasis-1) for nutrition longer than the anticipated period. <h3>Conclusion</h3> Laparoscopic insertion of feeding jejunostomy is safe, aids early establishment of enteral route for nutrition in patients undergoing cardio-oesophagectomy and useful in providing prolonged nutritional support in patients who develop complications were oral route is not possible. <h3>Competing interests</h3> None declared.
PARE0013 Financial crisis in europe affecting national health policies and patients
Authors: I.I. Stylianou
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> In USA a property bubble has burst in 2007-8, causing a financial crash. Banks worldwide, including Europe, had to write off lots of assets so had much less money than they thought. This had two effects, (a) it caused interest rates to rise a lot, as banks couldn't lend money and (b) governments took on lots of debt bailing out banks. European countries having high national debts, either from overspending pre-crash or from bailing out their collapsing banks, plus the high interest rates for borrowing, brought them a step before bankruptcy. <h3>Objectives</h3> European Region countries are employing a mix of policy tools in response to the financial crisis. Many of them are affecting National Health policies and by extension quality of life of patients with Rheumatic diseases. Status of life for patients with chronic diseases is changing as countries are shrinking the budget supporting those groups. Patients with Rheumatic diseases are facing problems in many different levels; finding and keeping a job, getting proper medical care regardless of cost, having enough money to support their families, keeping a good quality of life. <h3>Results</h3> Policy-makers are facing three main challenges: –Health systems require predictable sources of revenue. Sudden interruptions to public revenue streams can make it difficult to maintain necessary levels of health care. –Cuts to public spending on health made in response to an economic shock typically come at a time when health systems may require more, not fewer, resources. –Arbitrary cuts to essential services may further destabilize the health system if they erode equitable access to care and the quality of care provided, increasing costs in the longer term. <h3>Conclusions</h3> Where the short-term situation compels governments to cut public spending on health, the policy emphasis should be on cutting wisely so to minimize adverse effects on health system performance, enhancing value and facilitating efficiency. <h3>Disclosure of Interest</h3> None Declared
Dipyridamole Modulated Tc-99m Sestamibi Lung SPECT in Small Cell Lung Cancer
Authors: H S Bom, S C Lim, Y C Kim, H C Song, J J Min, H J Jeong, J Y Kim, J Lee, K O Park
Journal: Clinical Nuclear Medicine (1999)

Purpose: In this study, the authors wanted to determine whether dipyridamole-modulated MIBI (dipyridamole-MIBI) could enhance the prediction of the response to chemotherapy in patients with small cell lung cancer. Methods: Twenty-seven patients with biopsy-proved small cell lung cancer (25 men, 2 women; mean age, 61 ± 7 years) underwent dipyridamole-MIBI SPECT 3 to 7 days before starting chemotherapy (80 mg/m2 etoposide and 80 mg/m2 cisplatin every 3 or 4 weeks for at least two cycles). Tomographic images before and after dipyridamole (0.84 mg/kg) were acquired 1 hour after injection of 370 (10 mCi) and 1,110 (30 mCi) MBq MIBI, respectively. The response to chemotherapy was grouped as specified as complete response (CR), partial (PR), no change (NC), or progressive disease (PD), according to the change in tumor size on chest roentgenography and CT. Patients showing CR and PR were classified as responders, and those who showed NC and PD were considered nonresponders. Results: Among the 27 patients, 22 were responders (3 CR, 19 PR) and 5 were nonresponders (3 NC, 2 PD). The tumor-to-normal lung ratio (T:NL) of responders was significantly higher than that of nonresponders. The diagnostic accuracy of the T:NL ratio to differentiate responders and nonresponders was 33.3%, with a cutoff value of 2.5, which was significantly improved to 77.8% when an increased T:NL ratio after dipyridamole was assigned to a nonresponder. Furthermore, all patients with CR showed diminished T:NL ratios after dipyridamole, and all patients with NR showed an increased T:NL ratio after dipyridamole. Conclusion: Dipyridamole-MIBI SPECT could enhance the prediction of response to chemotherapy in patients with small cell lung cancer.
Case 34-1989
Authors: Richard C. Cabot, Robert E. Scully, Eugene J. Mark, William F. McNeely, Betty U. McNeely, W.J. Koroshetz, J.C. Sullinger
Journal: New England Journal of Medicine (1989)

Presentation of CaseA 74-year-old woman was admitted to the hospital because of vertigo, anorexia, and weight loss.She was well until about two months earlier, when vertigo developed. One month before entry she was examined before a scheduled cataract extraction. It was noted that she had lost 5 kg in weight during the previous year. Examination revealed that the blood pressure was 170/80 mm Hg and the weight 73.6 kg. Mild vertigo was noted on movement of her head to the left; no other abnormalities were found. Laboratory studies included a normal blood count; the cholesterol was 6.26 mmol . . .
Abstract 1378: Concurrent inhibition of c-Met and VEGF signaling suppresses tumor invasion in orthotopic Panc-1 pancreatic carcinomas in mice
Authors: Barbara Sennino, Casey W. Williamson, Vikash Bhagwandin, James G. Christensen, Donald M. McDonald
Journal: Cancer Research (2012)

Abstract Multiple factors can contribute to evasive resistance that develops during treatment with angiogenesis inhibitors that target the vascular endothelial growth factor (VEGF) pathway. Evidence from studies of neuroendocrine tumors in RIP-Tag2 transgenic mice indicates that hypoxia-induced activation of pro-invasive pathways involving the receptor for hepatocyte growth factor, c-Met, can participate. The present study sought to determine whether this mechanism also applies to other types of tumors. Our approach was to ask whether growth and invasiveness of Panc-1 pancreatic adenocarcinomas implanted orthotopically in nude mice were reduced by inhibition of c-Met during concurrent treatment with an angiogenesis inhibitor for 3 weeks. Panc-1 tumors in mice treated with the angiogenesis inhibitor sunitinib, a tyrosine kinase inhibitor that blocks VEGFR and related receptors, had a 75% reduction in vascularity and grew more slowly than controls but had twice as much of intratumoral hypoxia, assessed by pimonidazole staining. Unlike the faint c-Met immunoreactivity in most tumor cells of vehicle-treated Panc-1 tumors, c-Met staining was stronger in tumor cells after treatment with sunitinib. Tumors in mice treated with the selective c-Met inhibitor PF-04217903 alone had little change in tumor vascularity or intratumoral hypoxia and grew faster than those treated with sunitinib. However, tumors treated with sunitinib plus PF-04217903 together grew more slowly than after sunitinib alone but had similar amounts of vascular pruning and hypoxia. Tumor invasiveness, reflected by amylase-positive acinar cells of the exocrine pancreas located within tumors, was exaggerated after sunitinib treatment but, importantly, was significantly less in tumors treated with sunitinib plus PF-04217903. These findings indicate that sunitinib used alone reduced the growth of Panc-1 tumors but increased intratumoral hypoxia, c-Met expression, and local invasion into the surrounding normal pancreas. By comparison, sunitinib administered concurrently with the c-Met inhibitor PF-04217903 resulted in further slowing of tumor growth and less tumor invasiveness. 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 1378. doi:1538-7445.AM2012-1378
INHIBITION OF AORTIC VALVE CALCIFICATION IN AN EXPERIMENTAL MODEL OF AORTIC VALVE STENOSIS
Authors: Andreas Synetos, Konstantinos Toutouzas, Maria Drakopoulou, Odysseas Kaitozis, George Latsios, Apostolos Papalois, Georgios Benetos, Eleftherios Tsiamis, George Agrogiannis, Angelos Papanikolaou, Eustratios Patsouris, Dimitris Tousoulis
Journal: Journal of the American College of Cardiology (2016)
O113 COMBINATION THERAPY WITH PEGINTERFERON ALFA-2a AND A NUCLEOS(T)IDE ANALOGUE FOR HBeAg-POSITIVE CHRONIC HEPATITIS B PATIENTS: RESULTS OF A LARGE, RANDOMISED, MULTICENTRE, DOUBLE-BLIND, PLACEBO-CONTROLLED STUDY
Authors: W.-W. Su, C.-W. Hsu, C.-M. Lee, C.-Y. Peng, W.-L. Chuang, J.-H. Kao, R.-N. Chien, H.-C. Chu, Y.-H. Huang, Y.-F. Liaw
Journal: Journal of Hepatology (2014)
Abstract SY13-01: Reporter imaging in cancer biology and therapy
Authors: David Piwnica-Worms
Journal: Cancer Research (2012)

Abstract The tools of molecular imaging can provide spatially- and temporally-resolved information on biological structures and functions. Because researchers have increasingly recognized the importance of context for understanding gene expression and protein function as well as regulatory mechanisms within cellular micro-environments, they have turned to non-invasive imaging technologies to advance research on human health and disease. These non-invasive imaging data can interrogate protein processing, protein-protein interactions, gene expression and flux through metabolic pathways in real-time in cells and live animals, and are increasingly useful in understanding signal transduction and the pathobiology of cancer, which can facilitate development of effective therapies. 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 SY13-01. doi:1538-7445.AM2012-SY13-01