tbuckley/cabot-search huggingface dataset:
Abstract 213: RNF126 E3 ubiquitin ligase targets p21cip for ubiquitin-mediated degradation
Authors: Xu Zhi, Dong Zhao, Zhongmei Zhou, Ceshi Chen
Journal: Cancer Research (2012)

Abstract Many E3 ubiquitin ligases, such as Mdm2 and Skp2, are potential therapeutic targets for cancers. To identify novel oncogenic E3 ubiquitin ligases as anti-cancer targets, we screened an E3 ubiquitin ligase siRNA library containing siRNA pools against 555 individual E3s using the SRB assay in the MDA-MB-231 breast cancer cell line and the PC3 prostate cancer cell line. RNF126 was identified and validated as a promising candidate from this screening. Depletion of RNF126 dramatically decreased cell viability in these cancer cell lines. Consistently, RNF126 depletion delayed cell cycle G1/S progression and decreased cell proliferation. By a protein array analysis, we found that RNF126 depletion increased the cell cycle dependent kinase inhibitor p21cip protein levels in both MDA-MB-231 and PC3. Knockdown of RNF126 stabilized the p21 protein rather than increased the p21 mRNA levels. We demonstrated that RNF126 interacts with p21 in cells and in vitro, and the protein-protein interaction depended on the N-terminal and middle parts of RNF126. RNF126 over-expression increased the p21 protein ubiquitination in an E3 ligase activity dependent manner. RNF126 knockdown induced loss of cell viability in MDA-MB-231 and PC-3 can be partially rescued by depletion of p21. RNF126 stable knockdown in SW527 inhibited tumor growth in SCID mice. Finally, we found that RNF126 is highly expressed in ER negative breast cancer cell lines and negatively correlated with the p21 expression levels. These findings suggest that RNF126 promotes cancer cell proliferation through targeting p21 for ubiquitin-mediated degradation. RNF126 could be a novel therapeutic target in breast and prostate cancers. This study was partially supported by a grant from the American Cancer Society (RSG-08-199-01), grants from National Nature Science Foundation of China (81072162, 81120108019, and U1132605), and a grant from Yunnan Province High-Profile Talents Program (2010CI114). 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 213. doi:1538-7445.AM2012-213
Relationship between Red Cell Distribution width and Stroke in Patients with Stable Chronic Heart Failure: A Propensity Score Matching Analysis
Authors: Ahmet Kaya, Turgay Isik, Yasemin Kaya, Özgür Enginyurt, Zeki Yüksel Günaydın, Murat Doğan İşcanlı, Mustafa Kurt, İbrahim Halil Tanboğa
Journal: Journal of the American College of Cardiology (2013)
OUTCOMES OF CONCOMITANT TRANSCATHETER AORTIC VALVE REPLACEMENT AND PERCUTANEOUS CORONARY INTERVENTION IN HIGH-RISK PATIENTS WITH SEVERE AORTIC STENOSIS AND OBSTRUCTIVE CORONARY ARTERY DISEASE
Authors: Eelin Wilson, Torsten Vahl, Hemal Gada, Isaac George, Omar Khalique, Rebecca Hahn, Martin Leon, Mathew Williams, Susheel Kodali
Journal: Journal of the American College of Cardiology (2015)
Abstract 4452: Controlled release complex of cisplatin for mesothelioma: gamma-PGA/Cisplatin complex formulation
Authors: Chunman Lee, Masao Sasai, Yoshiki Sawa
Journal: Cancer Research (2011)

Abstract Cisplatin is the standard anti-tumor drug for mesothelioma, and other malignant tumors, however acute renal failure due to renal tubule injury is often induced as its adverse event. Hence, the dose of cisplatin is limited by the patient's renal function. We developed the Cisplatin controlled release complex that released cisplatin steadily, and relieved the adverse event, and examined its characteristics. 1) Slow release of cisplatin from novel complex Concentration of cisplatin penetrated from the dialysis membrane was measured by ICP atomic emission spectrometer. - Approximately 4% of cisplatin was released by day1 (initial burst was very low), and 10% of cisplatin was released by day 15, while free cisplatin oozed out from dialysis membrane immediately. 2) Cytotoxicity of novel complex in vitro Cytotoxicity to murine mesothelioma cell line was measured by MTT assay. - Over 10 μg/mL of cisplatin, novel complex possessed cytotoxicity, but under 5 μg/mL of novel cisplatin complex did not inhibit the growth of the murine mesothelioma cell line. 3) Bio-distribution of novel cisplatin complex in mice Novel cisplatin complex was administrated intra-peritoneal cavity, and the cisplatin concentration of each organ was measured at 1, 3, 5, 7 days after the administration. - Cisplatin of the complex was kept the concentration in the blood after the initial peak concentration, while free cisplatin was disappeared immediately. Furthermore, cisplatin was found in the concentrated amount in the liver, since novel complex was accumulated in the liver at the early phase as a storage of cisplatin, and cisplatin was released steadily into the bloodstream. 4) Acute toxicity test for mouse 50 mg/kg of novel cisplatin complex was administrated into the peritoneal cavity, and mice were observed. - All mice were alive with 9 days after cisplatin complex administration. 5) The anti-tumor efficacy of novel cisplatin complex in mesothelioma bearing mice Each 10 mg/kg of cisplatin formulation was administrated into the peritoneal cavity at five days after subcutaneous inoculation of murine mesothelioma cells. - On 9 days after cisplatin formulation administration, novel cisplatin complex was more effective than free cisplatin. Conclusions; We have demonstrated that novel cisplatin complex that releases cisplatin steadily into the bloodstream can be successfully used for the chemotherapy without severe adverse event, despite high dose administration. Although much additional study of this complex is required, the results in this study warrant additional development of this complex for potential investigation into its use in clinical tumor chemotherapy for mesothelioma. 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 4452. doi:10.1158/1538-7445.AM2011-4452
Abstract 1387: WISP-1 increases MMP-2 expression and cell motility in human chondrosarcoma cells
Authors: Yi-Chun Chiang, Chih-Hsin Tang, Tzu-Wei Tan
Journal: Cancer Research (2011)

Abstract Chondrosarcoma is a type of highly malignant tumor with a potent capacity to invade locally and cause distant metastasis. Chondrosarcoma shows a predilection for metastasis to the lungs. WISP-1 is a cysteine-rich protein that belongs to the CCN (Cyr61, CTGF, Nov) family of matricellular proteins. However, the effect of WISP-1 on migration activity in human chondrosarcoma cells is mostly unknown. Here we found that WISP-1 increased the migration and expression of matrix metalloproteinase (MMP)-2 in human chondrosarcoma cells (JJ012 cells). We also found that human chondrosarcoma tissues had significant expression of the WISP-1 which was higher than that in normal cartilage. α5β1 monoclonal antibody and MAPK kinase (MEK) inhibitors (PD98059 and U0126) inhibited the WISP-1-induced increase of the migration and MMP-2 up-regulation of chondrosarcoma cells. WISP-1 stimulation increased the phosphorylation of focal adhesion kinase (FAK), MEK and extracellular signal-regulated kinase (ERK). In addition, NF-κB inhibitors also suppressed the cell migration and MMP-2 expression enhanced by WISP-1. Moreover, WISP-1 increased NF-κB luciferase activity and binding of p65 to the NF-κB element on the MMP-2 promoter. Taken together, our results indicated that WISP-1 enhances the migration of chondrosarcoma cells by increasing MMP-2 expression through the α5β1 integrin receptor, FAK, MEK, ERK, p65 and NF-κB signal transduction pathway. 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 1387. doi:10.1158/1538-7445.AM2011-1387
INCIDENCE AND DETERMINANTS OF LEFT VENTRICULAR REVERSE REMODELING AFTER MITRACLIP IMPLANTATION IN PATIENTS WITH MODERATE TO SEVERE OR SEVERE MITRAL REGURGITATION AND REDUCED EJECTION FRACTION
Authors: Sara Cimino, Manuela Reali, Elisa Silvetti, Tiziana Salatino, Massimo Mancone, Mauro Pennacchi, Gennaro Sardella, Arturo Giordano, Francesco Fedele, Luciano Agati
Journal: Journal of the American College of Cardiology (2016)
Abstract 1161: Detection and identification of a miRNA expression profile from cell-free urine: Potential utility in bladder cancer
Authors: Antonia H. Holway, Jessica DeLong, Niall Harty, Spencer Kozinn, Kelly Summerhayes, Ian C. Summerhayes, John A. Libertino, Kimberly M. Rieger-Christ
Journal: Cancer Research (2011)

Abstract Introduction/Objective: MicroRNAs are small, non-coding RNAs that have been shown to play an important role in tumorigenesis. There is differential expression of miRNA in cancer progression, and profiling of miRNA is promising for both diagnosis and treatment of malignant tumors. In this study we isolated RNA from cell-free urine in an attempt to characterize miRNA profiles indicating the presence of urothelial carcinoma and its potential use as a non-invasive assay to identify patients with cancer progression. Methods: Urine was collected from patients diagnosed with bladder cancer and control patients with no history of cancer under an IRB-approved protocol. Urine was centrifuged and total RNA was isolated from the supernatants using the mirVana Paris™ kit. A total of 178 samples were grouped according to grade and stage (healthy controls (35), TaG1 (19), T1G3 (16), ≥T2 (30), carcinoma in situ (CIS; 28) and no evidence of disease following therapy (50). Seven hundred and thirty miRNAs were profiled by qRT-PCR on pooled samples within each group. Validation of selected miRNAs was performed on individual samples using qRT-PCR. Results: Cell-free RNA was isolated from urine of 35 healthy controls and 143 patients with bladder cancer. Of the 730 miRNAs tested, 236 were detected in at least one of the pooled samples using a Ct cutoff of 35. The number of miRNAs detected in the pooled samples correlated with disease progression where the healthy control group and the ≥T2 group expressed 8 and 228 miRNAs, respectively. qRT-PCR of individual samples revealed a gradual increase of some miRNAs with disease progression. Statistical analysis adjusted for multiple comparisons demonstrated differences between groups based on miRNA expression levels. In addition, a panel of miRNAs was identified which discriminated between cancer and cancer-free patients. Conclusion: This study demonstrates the successful isolation of miRNAs from cell-free urine. Utilizing non-invasive urine based assays, we identified a miRNA panel that can discriminate between cancer-free patients and patients with urinary carcinoma of the bladder. These findings provide evidence that profiling of miRNAs from cell-free urine holds the promise for the development of valuable clinical tools. 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 1161. doi:10.1158/1538-7445.AM2011-1161
A phase II trial of induction and consolidation therapy of acute myeloid leukemia with weekly oral idarubicin alone in poor risk elderly patients
Authors: R Bouabdallah, F Lefrère, C Rose, P Chaïbi, J-L Harousseau, J-P Vernant, S Castaigne, F Bauduer, J-M Zini, D Coso, B Varet, J Robert, P Fenaux
Journal: Leukemia (1999)
AB0668 Use of Nonsteroidal Antiinflammatory Drugs in Patients with Axial Spondyloarthritis
Authors: M. Aparicio, M. Ricse, G. Albert, S. Heredia, A. Zacarias, H. Borrell, E. Armengol, J. Rodríguez-Moreno, J.M. Nolla, X. Juanola
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Objectives</h3> To assess the use of nonsteroidal antiinflammatory drugs (NSAIDs) in patients with axial spondyloarthritis (SpA) and their relationship with clinical, analytical and radiographic variables and biologic drugs (BD). <h3>Methods</h3> All patients with SpA axial ASAS criteria included in a prospectively designed database has been reviewed. To assess the use of NSAIDs, the information of the last visit included in the database has been collected. Patients have been categorized according to the NSAIDs dose administered in the last 3 months, in the following groups: 1) No NSAID: no intake, 2) NSAID minimum dose: &lt;25% optimal symptomatic dose, 3) NSAID medium dose: between 25-75% of optimal symptomatic dose and 4) NSAID high dose: &gt;75% of optimal symptomatic dose. We dichotomised patients into Group A (No NSAIDs or minimum dose) and Group B (medium or high dose). The following variables were recorded: filiation data, diagnosis, time of evolution, HLA B27, CRP, ESR, BASDAI, BASFI, ASDAS, BASRI, biological disease modifying drugs, history of hypertension, previous peptic ulcers, dose and type of NSAID. A descriptive analysis was developed using percentages, means and standard deviation. Statistical tests used were: Fisher test, independent Student T, Mantel-Haenszel and Mann-Whitney test. <h3>Results</h3> 294 patients with axial SpA were included: 74.8% male, mean age 53.8 (±14) years, age of onset 26.5 (±9) years, duration of the disease 27.3 (±14) years, 83.7% positive for HLA-B27 antigen, 89.8% did meet criteria for ankylosing spondylitis, CRP 5.9 (±8) mg/L, ESR 9.6 (±9.6), BASDAI 3.6 (±2.2), BASFI 3.6 (±2.5), ASDAS-CRP 2.1 (±1), ASDAS-ESR 2 (±0.9), sacroiliac BASRI 3.1, axial BASRI 6. 36.4% had history of hypertension and 4.6% previous peptic ulcers, 26.9% taking BD. The NSAID that was most frequently prescribed was etoricoxib (34.5%), followed by indomethacin (21.6%) and diclofenac/aceclofenac (18.7%). Of the total sample, 158 were Group A (54.5%) and 132 (45.5%) Group B. Group B has been associated with higher scores of BASDAI, ASDAS, CRP and ESR with a statistically significant difference (p&lt;0.01). The Group A has been associated with older age (p=0.01), longer history of the disease (p&lt;0.01) and previous peptic ulcers (p=0.02). <h3>Conclusions</h3> – Most patients with axial SpA do not take any NSAIDs or does it at low doses. – Older patients, with greater radiographic damage or longer history take less NSAIDs. – Taking NSAIDs has been associated with rates of activity. – Etoricoxib is the most currently used. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.4732
FRI0129 Pro-atherogenic chemokines and TNF-alpha family cytokines in rheumatoid arthritis patients treated with atorvastatin
Authors: R. Rupinski, Z. Lewandowski, E. Walewska, A. Filipowicz-Sosnowska, P. Gluszko
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Certain chemokines and TNF-α family cytokines participate in the development of atherosclerosis and in the pathogenesis of rheumatoid arthritis (RA). Early-onset and severe atherosclerosis is responsible for high incidence of cardiovascular diseases in RA patients. <h3>Objectives</h3> To investigate the impact of low-cholesterol diet and statin treatment on serum concentration of selected chemokines: CX<sub>3</sub>CL1 (Fraktalkine), CCL2 (MCP-1), CCL5 (RANTES) and TNF-α family cytokines: TNF-α, CD40-ligand, FAS-ligand, in patients with RA and hypercholesterolaemia. <h3>Methods</h3> 74 mostly female (93.2%) RA patients, age 59.4±7.3 years, disease duration 8.9±8.4 years, anti-CCP positive 69.8%, disease activity score (DAS28) 3.63±1.15, with serum total cholesterol (TCh) above 200 mg/dl (mean 246±33 mg/dl) were included in the study. All patients participated in a recommended low-cholesterol diet therapy and 36 patients (48.7%) received additional atorvastatin treatment (10 mg daily), according to the ATP III guidelines [1]. Atherogenicity index (AI = TCh/HDL-cholesterol) was calculated and serum concentration of CX<sub>3</sub>CL1, CCL2, CCL5, TNF-α, CD40-ligand, and FAS-ligand was measured using ELISA (R&amp;D Systems) before and after 4 months of treatment. Statistical analysis was performed using general linear models (SAS System v. 9.3). <h3>Results</h3> Statistically significant AI decrease after 4 months (4.70 vs 3.63) was observed in the group treated with atorvastatin, but not in the patients with dietary treatment only (3.32 vs 3.76, p&lt;0.001 for interaction effect). CCL5 concentration decreased similarly in both groups during the study (p&lt;0.0001 for time effect). CD40-ligand concentration increased significantly only in the diet group, but in the atorvastatin group it remained unchanged during the trial (p&lt;0.0001 for interaction effect). No differences were observed in the serum concentrations of CX<sub>3</sub>CL1, CCL2, TNF-α, FAS-ligand before and after the treatment in both groups. <h3>Conclusions</h3> Atorvastatin treatment influencing serum lipids and lowering atherogenicity index in patients with RA, simultaneously decreases serum level of pro-atherogenic chemokine CCL5 and prevents increase of CD40-ligand concentration. Diet treatment alone does not seem to influence pro-atherogenic factors in RA. <h3>References</h3> Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adults Treatment Panel III). Circulation 2002; 106: 3143. <h3>Disclosure of Interest</h3> None Declared
The Natural Occurrence of Venezuelan Equine Encephalitis in the United States
Authors: N. Joel Ehrenkranz, Michael C. Sinclair, Elsie Buff, Donald O. Lyman
Journal: New England Journal of Medicine (1970)

Naturally acquired Venezuelan equine encephalitis (VEE) has not been previously recognized in the United States, although VEE virus has been repeatedly isolated in Everglades National Park. In September, 1968, severe headache and feverishness suddenly developed in a 53-year-old woman living in Homestead, Florida. On admission the temperature was 105°F. Cerebrospinal-fluid findings indicated an aseptic-meningitis pattern. Electroencephalography showed diffuse disorganization. Hemagglutination-inhibition (HI) and complement-fixation antibodies to VEE virus rose in titer, but antibodies to other arboviruses or picornaviruses did not. A survey of 353 residents of the Homestead area revealed five to have VEE HI antibodies of 1:20 or higher and neutralizing antibodies of 2.0 logs or higher; one person had had recent illness. Since the Florida strain of VEE appears to be capable of causing disease in man, the occurrence of antibodies in persons living close to an urban area may have serious epidemiologic implications.
P144 TREM1-DEFICIENCY ACCELERATES VIRAL CLEARANCE IN A MOUSE MODEL OF LCMV-INDUCED ACUTE VIRAL HEPATITIS
Authors: J.-H. Kozik, T. Trautmann, A. Carambia, L. Eissing, A.W. Lohse, C. Wiegard, J. Heeren, J. Herkel
Journal: Journal of Hepatology (2014)
Abstract 106: Epigenetic regulation of snoRNAs in cancer
Authors: Humberto Ferreira, Holger Heyn, Balazs Balint, Jose Ignacio Martin-Subero, Manel Esteller
Journal: Cancer Research (2011)

Abstract Cancer has been associated with epigenetic abnormalities leading to deregulated expression of both coding and non-coding RNAs (ncRNAs) involved in oncogenesis. Among these ncRNAs, microRNAs (miRNAs) were identified acting as oncogenes or tumor suppressors by repressing the expression of cancer related genes. In addition, other studies suggest that other ncRNAs are similarly involved in tumorigenesis, including long non-coding RNAs (lncRNAs) and transcribed Ultraconserved Regions (t-UCRs) by different mechanisms. Recent studies have shown the impact of small nucleolar RNAs (snoRNAs) in the onset or progression of cancer. SnoRNAs encoded by the ncRNA GAS5 that is repressed in breast cancer or the snoRNA U50, which is mutated in breast and prostate cancer, are examples of the connection between snoRNAs and cancer. It is also known that some snoRNAs are differentially expressed in cancer in comparison with the correspondent matched tissue, indicating their possible role in this disease. This study focuses in the analysis of the DNA methylation profile associated with the differentially expression of snoRNAs in cancer considering a host gene dependent or independent regulation. To select snoRNAs regulated by DNA methylation we used two different epigenetic approaches: snoRNA expression arrays upon DNA methylation inhibition and global genomic DNA methylation arrays. Herein, we were able to indentify snoRNAs with different DNA methylation that might be involved in cancer. 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 106. doi:10.1158/1538-7445.AM2011-106
Burkitt lymphoma presenting as multifocal doughnut-shaped masses in the stomach of a patient with AIDS
Authors: Michael Sey, Magdalena Czader, John DeWitt
Journal: Endoscopy (2014)

A 46-year-old man presented with a 1-month history of epigastric pain. His medical history was significant for human immunodeficiency virus (HIV) infection but he was not on treatment for this. His physical examination and initial blood test results were unremarkable, other than the finding of a CD4 count of 198/μL and a viral load of 370 000 copies/mL.
S81 Gait Speed Is A Predictor Of Mortality Following Hospitalisation For Acute Exacerbations Of Copd
Authors: S. Kon, S. Jones, S. Schofield, J. Canavan, C. Nolan, M. Dickson, B. Haselden, M. Polkey, P. Cullinan, W.-C. Man
Journal: Thorax (2014)

<h3>Background</h3> Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are associated with significant morbidity, mortality, and high resource utilisation. More accurate prediction of prognosis following hospital discharge may help optimise clinical management and individualise post-discharge care. Physical performance is potentially amenable to treatment and may help stratify patients at risk of early mortality. In community-dwelling older adults, the 4-metre gait speed (4MGS) is a well-established physical performance measure and a consistent predictor of mortality. We hypothesised that 4MGS at discharge predicts 1 year mortality in patients hospitalised with AECOPD. <h3>Methods</h3> 213 patients admitted to one hospital with a primary diagnosis of AECOPD were recruited prospectively. 4MGS was measured on the day of hospital discharge. Data on all-cause mortality at one year were obtained from the patient care summary record, hospital and GP records, and corroborated by patients and their families. Logistic regression models were used to assess the association between 4MGS and death. <h3>Results</h3> Baseline characteristics: 111 males/102 females; mean (SD) age 72 (11) years, 4MGS 0.61 ms<sup>-1</sup> (0.26) and median (IQR) FEV<sub>1</sub>% predicted 35 (26, 49). 35 patients (16%) were not alive at 1 year. 4MGS at hospital discharge was significantly lower in these patients compared to survivors (mean (SD) 0.47 (0.24) vs 0.63 (0.26) ms<sup>-1</sup>; p &lt; 0.001). All-cause mortality at 1 year increased with decreasing quartiles of 4MGS (Q4 4%; Q3 9%; Q2 21%; Q1 32%; p &lt; 0.001). Multivariate logistic regression demonstrated a significant trend in the age adjusted odds of death with decreasing quartiles of gait speed (p &lt; 0.001) (see Table 1). Increased odds of death at 1 year were seen with each 0.1 ms<sup>-1</sup> decline in gait speed (OR 1.26 (1.06 to 1.49), p = 0.008). <h3>Conclusion</h3> The 4MGS measured at discharge predicts 1 year mortality in patients hospitalised with acute exacerbation of COPD. Given the simplicity of the 4MGS, it is a potentially useful tool to risk stratify patients with COPD in the acute setting and tailor post discharge care.