tbuckley/cabot-search huggingface dataset:
PMO-155 Low pre-treatment HBsAG plasma levels, on therapy HBsAG levels decline and IP-10 concentrations increase predict response to treatment in tolerant children with chronic hepatitis B
Authors: I Carey, M J Bruce, M Hussain, M Horner, S Bansal, D Vergani, G Mieli-Vergani
Journal: Gut (2012)

<h3>Introduction</h3> Changes in HBsAg plasma levels during antiviral therapy with pegylated interferon (IFN) predict response in chronic hepatitis B (CH-B). High baseline plasma levels of inducible interferon-γ protein 10 (IP-10) predicted HBsAg loss in CH-B adults patients on nucles(t)ide analogues (NA) therapy. No data are available on the relationship between IP-10 and HBsAg plasma levels in children with infancy-acquired CH-B on combination therapy. <h3>Aims</h3> To investigate whether baseline plasma IP-10 levels and their changes during therapy can help to predict HBsAg loss in children with infancy-acquired CH-B on combination therapy with lamivudine (LAM) and IFN-α. <h3>Methods</h3> <b>Patients:</b> 23 children (eight males, median age 10.2 yrs) with infancy-acquired CH-B (all HBeAg+), treated for 52 weeks [lead-in LAM (3 mg/kg/d) for 9 weeks; LAM plus IFN-α (5 MU/m<sup>2</sup> TIW) from week 9 for 44 weeks], were divided according to treatment response: five responders (R = anti-HBs seroconversion) and 18 non-responders (NR). <h3>Methods</h3> Plasma IP-10, HBsAg and AST levels were measured in serial samples before (treatment week 0, TW0), during (TW9, TW28, TW52) and after (follow-up week, FUW24) therapy by ELISA [pg/ml], Abbott ARCHITECT® assay [log<sub>10</sub> IU/ml] and AutoAnalyser [IU/l]. The results are presented median. <h3>Results</h3> Baseline IP-10 levels were similar in R and NR (123 vs 99, p=0.4), but increased significantly in R than NR at TW28 (220 vs 79, p=0.04). Baseline HBsAg levels were lower in R than NR (4.36 vs 4.74, p=0.02), but similar in R and NR at TW9 (4.34 vs 4.66, p=0.1) and markedly lower in R than NR during IFN add-on therapy and therapy follow-up (TW28: 2.34 vs 4.33; TW52: 0 vs 4.08 and FUW24: 0 vs 4.51; p&lt;0.01 for all). Baseline AST levels were similar in R and NR (29 vs 31, p=0.6) and tended to be higher in R than NR at TW28 (47 vs 32, p=0.07). At TW28, there was an inverse correlation between IP-10 and HBsAg levels (r=−0.45, p=0.03), but no correlation with AST. <h3>Conclusion</h3> Low baseline HBsAg levels, HBsAg plasma levels decline and IP-10 concentrations increase during interferon add-on at TW28 predict HBsAg loss and response to therapy in tolerant children with CH-B. <h3>Competing interests</h3> I Carey grant/research support from: BMS, Gilead, M Bruce: None declared, M Hussain: None declared, M Horner: None declared, S Bansal: None declared, D Vergani: None declared, G Mieli-Vergani: None declared.
ESTUDIO DE ADENOPATÍAS DE ORIGEN INCIERTO. PAPEL DE LA ECOENDOSCOPIA CON PAAF Y SU COMPARACIÓN CON EL PET-TAC
Authors: E Redondo Cerezo, C González-Artacho, JG Martínez Cara, C Alegria-Motte, J Esquivias López-Cuervo, V Martos Ruiz, P De La Torre Rubio, J De Teresa Galván
Journal: Endoscopy (2013)

Introducción: La PAAF de adenopatías sospechosas es una indicación habitual de la ecoendoscopia (USE). Numerosos estudios han analizando el papel de la USE en la PAAF de adenopatías relacionadas con diversas neoplasias, pero pocos lo comparan con métodos de imagen avanzada como el PET-TAC. Objetivo: Analizar el papel de la USE-PAAF en el estudio de adenopatías y compararlo con el PET-TAC. Material y Método: Estudio prospectivo, observacional que incluye 52 pacientes entre Enero/2010 y Junio/2012, a los que se realizó USE-PAAF por una adenopatía sospechosa. El diagnóstico inicial fue mediante TAC o ecografía abdominal. Posteriormente se indicó PET-TAC y USE-PAAF. El diagnóstico definitivo fue el de la pieza quirúrgica y, de no tenerla se estimó de la evolución. Resultados: Edad media: 62 años; un 70% varones. Indicaciones: Adenopatías mediastínicas 51%, hiliares 33%, tronco celíaco 6.3% y otras 9.7%. Citología: Insatisfactorio en 5 casos (10%), linfadenitis inespecífica 40%, linfoma 9%, carcinoma epidermoide de pulmón 8.4%, adenocarcinoma de páncreas 4.2%, hepatocarcinoma 2%, mesotelioma 2%, melanoma 2%, antracosis 2%, carcinoma anaplásico de células pequeñas de pulmón 2%, adenocarcinoma broncogénico de pulmón 2%, metástasis de liposarcoma 2%, otros tumores 15%. El 72% de las lesiones captaban en el PET-TAC. En la USE-PAAF obtuvimos VPP de 95%, VPN 81.4%, sensibilidad 95.4% y especificidad 81%. El coeficiente de correlación fue 0.75 (p < 0.0001). Para el PET, el VPP fue 65%, VPN 62.5%, sensibilidad 85% y especificidad 36%. La correlación entre ambas técnicas fue pobre (κ 0.17). Conclusiones: La USE-PAAF es más sensible y específica para el estudio de adenopatías sospechosas de origen incierto. El gran valor otorgado al PET-TAC no se confirma en nuestra experiencia, probablemente por la heterogeneidad de captación entre neoplasias. Así, en el estudio de estas lesiones, tras una primera aproximación por la técnica de imagen de diagnóstico resulta probablemente insustituible realizar una USE-PAAF.
Abstract 137: Molecular networks regulated by tumor suppressive microRNA-375 in head and neck squamous cell carcinoma
Authors: Takashi Kinoshita, Toyoyuki Hanazawa, Nijiro Nohata, Naoko Kikkawa, Miki Fuse, Takeshi Chiyomaru, Hirofumi Yoshino, Hideki Enokida, Masayuki Nakagawa, Yoshitaka Okamoto, Naohiko Seki
Journal: Cancer Research (2012)

Abstract BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) is the sixth most common malignancy worldwide. In spite of considerable advances in multimodality therapy including surgery, radiotherapy and chemotherapy, the overall five-year survival rate for patients with HNSCC is around 40%. Understanding of the molecular oncogenic pathway underlying HNSCC could significantly improve diagnosis, therapy, and disease prevention. Our microRNA (miRNA) expression signatures of hypopharyngeal squamous cell carcinoma (SCC), maxillary sinus SCC and esophageal SCC revealed that the expression of microRNA-375 (miR-375) was significantly reduced in cancer tissues. In this study, we investigated the functional significance of miR-375 and explored novel molecular networks regulated by miR-375 in HNSCC. METHODS: Cell proliferation assay was performed to investigate the functional significance of miR-375 and its target genes in HNSCC cell lines. Genome-wide gene expression analysis was performed to identify the molecular networks of miR-375 by microarray technique. The expression levels of miR-375 target genes were verified using quantitative real-time RT-PCR in HNSCC clinical specimens. A luciferase reporter assay was used to identify the actual binding site between miR-375 and its candidate target genes. RESULTS: Restoration of miR-375 significantly inhibited cancer cell proliferation in HNSCC cells. Genome-wide molecular targets search and TargetScan database indicated that homocysteine-inducible, endoplasmic reticulum stress-inducible, ubiquitin-like domain member 1 (HERPUD1), lactate dehydrogenase B (LDHB), PC4 and SFRS1 interacting protein 1 (PSIP1), metadherin (MTDH) and solute-carrier family 7, member 11 (SLC7A11) were the candidate genes of miR-375 target. Among them, the expression levels of LDHB and MTDH were significantly up-regulated in clinical HNSCC tumor specimens compared with adjacent normal epithelium. Luciferase reporter assay showed that LDHB and MTDH were directly regulated by miR-375. Silencing of these genes studies demonstrated significant inhibition of cell proliferation in HNSCC cells. CONCLUSIONS: miR-375 functions as a tumor suppressor in HNSCC. LDHB and MTDH are directly regulated by miR-375. These genes may function as oncogenes and contributed to cell proliferation in HNSCC. Tumor suppressive miR-375 and its target oncogenes may provide new insights into the molecular networks of HNSCC. 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 137. doi:1538-7445.AM2012-137
Abstract 2423: Acute <i>in vitro</i> exposure to cigarette smoke particulate matter does not induce epithelial-mesenchymal transition in lung epithelial cells
Authors: Damien M. Breheny
Journal: Cancer Research (2012)

Abstract The epithelial-mesenchymal transition (EMT) program was first identified from studies on embryogenesis and organ development, but has since been found to play vital roles in tissue remodelling and tumorigenesis. EMT is a biological process during which epithelial cells change their morphology to adopt fibroblast-like characteristics. During EMT, cell adhesion is lost while cells become more motile. A number of distinct molecular events are required for a cell to undergo EMT including transcription factor activation, cytoskeletal rearrangement, changes in cell adhesion molecule expression and increased production of extracellular matrix-degrading enzymes. EMT has recently been linked to chronic inflammation and cigarette smoke exposure in the lung and is believed to be involved in lung carcinogenesis. As the specific genes and proteins involved in EMT have been well defined, they can serve as markers to demonstrate the passage of cells through EMT in the context of cigarette smoking. The purpose of this study was to develop an in vitro model of EMT using immortalised human bronchial epithelial (BEAS-2B) cells. EMT was induced in BEAS-2B cells using a 72 hour treatment with 5 ng/mL TGF-β1. Expression of the following EMT markers were assessed at the transcript level using reverse transcription real time-polymerase chain reaction (RT-PCR): alpha smooth muscle actin (α-SMA), collagen 1, fibronectin, vimentin, e-cadherin, slug and snail. Protein levels of α-SMA, fibronectin, β-catenin, e-cadherin and zonular occludin-1 were evaluated using immunocytochemistry techniques. This model was then used to determine the effects of acute (72 hour) cigarette smoke particulate matter treatment on EMT in BEAS-2B cells. Cells were treated with particulate matter alone, and in combination with TGF-β1. Particulate matter did not induce EMT directly, nor did it influence EMT induced by TGF-β1 under the treatment conditions used in this study, based on marker expression. It is possible that a more prolonged exposure to particulate matter is required for EMT induction in BEAS-2B cells. 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 2423. doi:1538-7445.AM2012-2423
Hospital ownership of doctors' practices is linked to higher prices and spending, US study finds
Authors: M. McCarthy
Journal: BMJ (2014)

When hospitals that own doctors’ practices gain market share, healthcare prices and spending tend to rise, a new US study has found.1

In the study researchers at Stanford University in California looked at how various forms of contractual relationships between hospitals and doctors—including hospital ownership of practices—affected prices, spending, and admissions.

Such contractual relationships can help to vertically integrate the supply of healthcare services from primary to specialty and surgical care, but whether such arrangements benefit consumers is open to debate.

Vertical integration, for example, can improve quality and efficiency by enhancing communications between doctors, streamlining service provision, and reducing duplication of services, the researchers noted.

But it …
Abstract 2314: Dovitinib demonstrates antitumor and anti-metastatic activities in xenograft models of hepatocellular carcinoma
Authors: Huynh T. Hung, Su Pin Choo, Khee Chee Soo, Richard Ong, Ronald Linnartz, Michael Ming Shi
Journal: Cancer Research (2012)

Abstract Background and aims: Hepatocellular carcinoma (HCC) is the third leading cause of cancer death. Although sorafenib has been shown to improve survival of patients with advanced HCC, this improvement is modest and patients eventually have refractory disease. This study aims to investigate the antitumor, antiangiogenesis and antimetastatic activities of dovitinib in preclinical models of HCC. Methods: 21-0208 and SK-HEP1 cells as well as patient-derived HCC models were employed to study of the antitumor effect of dovitinib. Changes of biomarkers relevant to FGFR/VEGFR/PDGFR pathways were determined by Western blotting. Microvessel density, apoptosis and cell proliferation were analyzed by immunohistochemistry. Results: Treatment of SK-HEP1 cells with dovitinib resulted in G2/M cell cycle arrest, inhibition of colony formation in soft agar and blockade of bFGF-induced cell migration. Dovitinib inhibited basal expression and FGF-induced phosphorylation of FGFR-1, FRS2-α and ERK1/2. In vivo, dovitinib potently inhibited tumor growth of six HCC lines. Inhibition of angiogenesis correlated with inactivation of FGFR/PDGFR-α/VEGFR-2 signaling pathways. Dovitinib also caused dephosphorylation of retinoblastoma, upregulation of p-histone H2A-X and p27, and downregulation of p-cdk-2 and cyclin B1, which resulted in a reduction in cellular proliferation and the induction of tumor cell apoptosis. In an orthotopic model, dovitinib potently inhibited primary tumor growth and lung metastasis and significantly prolonged mouse survival. Conclusion: Dovitinib demonstrated significant antitumor and antimetastatic activities in HCC xenograft models. This study provides a compelling rationale for clinical investigation in patients with advanced 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 2314. doi:1538-7445.AM2012-2314
Fetal Echocardiography for Evaluation of in Utero Congestive Heart Failure
Authors: Charles S. Kleinman, Richard L. Donnerstein, Greggory R. DeVore, C. Carl Jaffe, Diana C. Lynch, Richard L. Berkowitz, Norman S. Talner, John C. Hobbins
Journal: New England Journal of Medicine (1982)

Thirteen fetuses with nonimmune hydrops (22 to 39 weeks of gestation) were evaluated with two-dimensional and M-mode echocardiography. Ten fetuses had cardiovascular abnormalities resulting in heart failure, and three had noncardiac causes of hydrops. In three cases, hydrops was caused by supraventricular tachycardia. One of these fetuses responded to cardioversion at birth, another responded to transplacental digoxin therapy, and the third died with atrial flutter and high-grade atrioventricular block before delivery. There were no cases of "idiopathic" hydrops. Our results show that fetal echocardiography is useful in determining cardiac causes of in utero heart failure resulting in hydrops fetalis. The fetal echocardiogram may also be used in monitoring transplacental therapy of heart failure. (N Engl J Med. 1982; 306:568–75.)
Fluorine-18 Fluorodeoxyglucose Uptake in Tubovillous Adenoma of the Colon
Authors: HALUK ALIBAZOGLU, BUKET ALIBAZOGLU, EDWARD F. HOLLINGER, AMJAD ALI, GREGORY LAMONICA
Journal: Clinical Nuclear Medicine (1999)

The authors report intense uptake of fluorine-18 fluorodeoxygluclose in benign tubovillous adenoma of the sigmoid colon in a patient with a history of renal cell cancer who was being evaluated for metastatic disease.
Westermark Sign in Pulmonary Embolism
Authors: Anant Subramanian Krishnan, Tristan Barrett
Journal: New England Journal of Medicine (2012)

A 47-year-old woman presented to the emergency department with acute shortness of breath and hypoxia. Her medical history included sex reassignment, for which she was taking estrogen, and a deep-vein thrombosis on the left side, for which she had required warfarin.
A Novel Pattern of Abnormal Spinal Uptake on Tc-99m MDP Skeletal Scintigraphy in Ankylosing Spondylitis
Authors: Helen M. Branson, Les Barnsley, Joshua E. Duggan, Kevin C. Allman
Journal: Clinical Nuclear Medicine (2001)

Branson, Helen M. M.B.B.S.; Barnsley, Les B.med., Ph.D.; Duggan, Joshua E. C.N.M.T.; Allman, Kevin C. M.B.B.S. Author Information
Primary syphilitic chancre in the rectum
Authors: Israel Grilo Bensusan, Leonor Gómez-Regife
Journal: Endoscopy (2014)

A 50-year-old homosexual man was referred for rectal bleeding with the passage of red blood, increased bowel habit, and rectal discomfort for 15 days, without constitutional or febrile symptoms. A colonoscopy performed 6 years previously had been normal. Examination revealed a soft nipple-shaped papillary lesion with traces of blood on rectal palpation. The results of his blood count and tests for liver and renal function, ferritin, human immunodeficiency virus (HIV), and carcinoembryonic antigen (CEA) were all normal, but he had an elevated C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). A thoracoabdominal computed tomography (CT) scan showed a reduction in the caliber of the rectum, with locoregional, abdominal, and inguinal lymphadenopathy ([Fig. 1]).
Differential Contributions of<i>BRCA1</i>and<i>BRCA2</i>to Early-Onset Breast Cancer
Authors: Michael Krainer, Sandra Silva-Arrieta, Michael G. FitzGerald, Akira Shimada, Chikashi Ishioka, Ryunosuke Kanamaru, Deborah J. MacDonald, Hilal Unsal, Dianne M. Finkelstein, Anne Bowcock, Kurt J. Isselbacher, Daniel A. Haber
Journal: New England Journal of Medicine (1997)

Germ-line mutations in the BRCA1 and BRCA2 genes predispose women to breast cancer. BRCA1 mutations are found in approximately 12 percent of women with breast cancer of early onset, and the specific mutation causing a deletion of adenine and guanine (185delAG), which is present in 1 percent of the Ashkenazi Jewish population, contributes to 21 percent of breast cancers among young Jewish women. The contribution of BRCA2 mutations to breast cancer of early onset is unknown.
Controversial Smoking Ad Posted in NYC
Authors: F. X. Mahaney
Journal: JNCI Journal of the National Cancer Institute (1992)

Journal Article Controversial Smoking Ad Posted in NYC Get access Francis X. Mahaney, Jr. Francis X. Mahaney, Jr. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 84, Issue 17, 2 September 1992, Page 1315, https://doi.org/10.1093/jnci/84.17.1315-a Published: 02 September 1992
Abstract SY07-01: Functions of ubiquitin and SUMO in DNA damage bypass
Authors: Helle D. Ulrich
Journal: Cancer Research (2012)

Abstract Ubiquitin and SUMO are members of a conserved family of proteins that exert their functions by being covalently attached to intracellular substrate proteins. Ubiquitin is best known for targeting its substrates to the 26S proteasome, but it mediates many non-proteolytic functions, mainly by modulating protein-protein interactions. Similarly, SUMO controls a variety of biological processes by changing the properties of its substrates. Both ubiquitin and SUMO play a prominent role in the maintenance of genome stability, and our lab is interested in elucidating the mechanisms by which the two modifiers affect DNA replication, repair and mutagenesis. An important focus of our research is the investigation of DNA damage tolerance, a highly conserved mechanism that protects cells from the harmful effects of genotoxic agents by allowing the replication machinery to pass over DNA lesions. Although beneficial in terms of promoting cell survival, bypass of DNA damage can result in unwanted mutations that may ultimately lead to genetic instability and cancer. The activity of lesion bypass is carefully controlled through posttranslational modifications of PCNA, an essential processivity factor for DNA polymerases, by monoubiquitin, polyubiquitin chains and SUMO. Here I will discuss the effects of these modifications on the replication of damaged DNA, the interplay between the different conjugation systems and the mechanisms by which the relevant modifying enzymes are activated in response to the appropriate cellular signals. 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 SY07-01. doi:1538-7445.AM2012-SY07-01
DIAGNOSTIC COMPARISON OF CARDIAC MAGNETIC RESONANCE WITH MYOCARDIAL BIOPSY IN SUBJECTS WITH MYOCARDIAL DISEASES: A SEGMENT-BY-SEGMENT ANALYSIS
Authors: Hiroyuki Takaoka, Nobusada Funabashi, Koya Ozawa, Keishi Ishikawa, Takashi Nakayama, Yoshihide Fujimoto, Michiko Daimon, Kazuo Miyazawa, Marehiko Ueda, Goro Matsumiya, Yoshio Kobayashi
Journal: Journal of the American College of Cardiology (2015)
P56 Use of the Tuberculin Skin Test and Tspot For Screening Prior to TNF Antagonist Therapy Identifies Additional Patients Eligible For Chemoprophylaxis Compared to Use of Risk Assessment Strategies Alone
Authors: K Manalan, A Singanayagam, PL Molyneaux, PM George, DW Connell, A Lalvani, M Wickremasinghe, OM Kon
Journal: Thorax (2012)

<h3>Patients</h3> with rheumatological disease who are treated with TNF antagonist therapy are at increased risk of reactivating latent tuberculosis infection (LTBI). It is believed that immunosuppressant therapy in this group may reduce the reliability of the tuberculin skin test (TST) due to a high incidence of anergy. The value of interferon gamma release assays in this setting is also unclear. The aim of this study was to assess the value of a combination of the TST and <i>Tspot</i> for screening in patients on immunosuppressants and compare to the BTS-recommended approach, which advocates treatment decisions based on risk stratification. <h3>Methods</h3> Adult patients referred for TB screening to a tertiary centre prior to commencement of Anti-TNF therapy were included in the study. All patients received a uniform screening protocol of clinical history, chest radiograph, stratification of TB risk (by ethnicity and age according to BTS guideline risk-tables), TST and <i>Tspot</i>. <h3>Results</h3> There were 137 patients included with 116 (84.7%) taking immunosuppressant medication at the time of screening. Of the sub-group on immunosuppressants, 17 patients (14.7%) had positive TST results (5 patients with result &gt;15mm in presence of BCG, 12 patients with result &gt;5mm in absence of previous BCG). Of this sub-group with positive TST results, 12 patients (70.6%) would not have been treated according to risk-stratification tables. Of the sub-group on immunosuppressants, 25 patients (21.6%) had positive <i>Tspot</i> results and 1 patient had an indeterminate result. Of this subgroup with positive <i>Tspot</i> results, 17 patients (68%) would not have been treated according to risk-stratification tables. When comparing strategies, use of risk-stratification tables alone would lead to 26 patients being treated with chemoprophylaxis. Addition of either positive TST and/or positive <i>Tspot</i> in patients not identified by risk stratification method led to an additional 22 patients eligible for treatment (9 patients <i>Tspot</i> positive alone; 7 patients TST positive alone; 6 patients double positive). <h3>Conclusion</h3> Performing both a TST and <i>Tspot</i> in patients on immunosuppressants prior to commencement of Anti-TNF screening gives an additional yield of potential LTBI when risk assessment strategies alone would not have identified these.