tbuckley/cabot-search huggingface dataset:
Abstract 3917: Molecular mechanisms underlying hedgehog-GLI oncogenic function via interaction with the TGF-beta-SMAD4 axis
Authors: Monica D. Nye, Aishah Cross, Lucianna L. Almada, Sherine F. Elsawa, Martin E. Fernandez-Zapico
Journal: Cancer Research (2010)

Abstract Crosstalk between signaling pathways is crucial to the initiation, progression and maintenance of the transformed phenotype. Therefore, characterization of these signaling interactions is fundamental for the understanding of the complex and varied network of events that leads to the development and spread of tumors. The Hedgehog (HH)-GLI pathway, an important carcinogenic cascade, is required for the growth and survival of tumors of diverse origin. Recent reports, mainly from animal models, suggest that key signaling interactions are required by HH-GLI signaling to modulate cancer-associated cellular functions. However, the molecular mechanisms underlying this phenomenon in cancer and non-cancer cells remain elusive. Our preliminary data show a crosstalk between the HH-GLI axis and TGF-beta pathway, a well-characterized tumor suppressor/oncogenic signaling pathway. Luciferase reporter and expression assays in combination with genetic and pharmacological manipulations of the TGFbeta pathway show that this cascade is able to activate GLI transcriptional activity, even in the absence of an active HH signaling. The TGFbeta pathway is required to maintain active GLI transcriptional complexes at GLI target genes. Further analysis of this molecular interaction suggests that TGFbeta pathway-mediated activation of GLI transcription factors requires an intact SMAD4, thus suggesting a potential mechanism mediating this functional interaction. The knowledge derived from this study provides both mechanistic insight into the contribution of this HH-GLI/TGF-beta pathway interaction to carcinogenesis and could serve as a foundation for development of new therapeutic approaches for tumors with active HH-GLI and TGF cascades. 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 3917.
THU0228 Serum IL-33 level in behçet’s disease and rheumatoid arthritis:
Authors: S.S. Koca, E. Donder, F. Deniz, M. Ozgen, N. Ilhan, A. Isik
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Behçet’s disease (BD) is a systemic vasculitis characterized by a triad of recurrent oral and genital ulcers and uveitis. Although the pathogenesis of BD remains uncertain, immunological abnormalities is mediated by Th1 type derived cytokines in BD. IL-33, from the IL-1 cytokine family, is reported to be increased in various inflammatory diseases including rheumatoid arthritis (RA). <h3>Objectives</h3> To assess the serum levels of IL-33 in BD, RA and healthy controls (HC). <h3>Methods</h3> Fasting blood samples were obtained from 85 patients with BD, 87 patients with RA and 88 HC. Serum IL-33 levels were measured using commercially available ELISA kit.Appropriate statisticaltests were used to analyze the data. <h3>Results</h3> There was no significant difference between the BD and HC groups in terms of serum IL-33 level (p&gt;0.05), while it was lower in the RA group compared to the BD and HC groups (Table, p&lt;0.001 for both). The level of IL-33 was significantly lower in the active BD (n=39) subgroup than inactive BD (n=46) subgroup (11.3±9.3 vs. 13.7±.2 pg/ml, p=0.02). <h3>Conclusions</h3> IL-33, also called IL-1F11, induces Th2 responses and exerts anti-inflammatory effects. BD and RA are characterized by a marked shift toward Th1 type phenotype. The serum levels of IL-33, the recently identified cytokine, were decreased in active BD and RA in the present study. These results may suggest the Th1/Th2 imbalance in BD and RA. <h3>References</h3> Zhou ZY, et al. Cytokines and Behcet’s Disease. Autoimmun Rev. 2012. Boissier MC. Cell and cytokine imbalances in rheumatoid synovitis. Joint Bone Spine. 2011. Miller AM. Role of IL-33 in inflammation and disease. J Inflamm (Lond). 2011. <h3>Disclosure of Interest</h3> None Declared
REVERSIBLE SCHIZOPHRENIA
Authors: Karl A. Menninger
Journal: American Journal of Psychiatry (1922)

Data.—Type cases of post-influenzal schizophrenia arranged in ascending order of severity from delirium to dementia præcox. Pertinent literature. Deductions.—Dementia præcox is apparently sometimes a chronic delirium (schizophrenia deliriosa). Delirium is apparently sometimes an acute dementia praæcox (delirium schizophrenoides). Both forms are (sometimes) reversible. Inductions.—These two forms may represent an identical process manifested by varying degrees of reversibility of the schizophrenia. The concept "Reversible Schizophrenia" (cf. the term "delirium schizophrenoides") is not a mere nosological quibble, since it may affect our conception of the nature of dementia præcox. It implies conditions of reversibility which we may discover to be under our control!
FRI0566-PC Prevalence of arterial hypertension in outpatients with rheumatoid arthritis
Authors: M. C. De La Vega, F. Eraña, C. Fecchio, N. Villa, E. Chiuzzi, C. Uña, D. Mata, A. Russo, G. Redondo, J. Gamba, M. Girard Bosch, A. Villamil, G. Gomez, O. Rillo, O. Messina, A. Riopedre
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Rheumatoid arthritis (RA) is associated with increased cardiovascular mortality due to myocardial infarction, stroke and heart failure. Both, chronic inflammation leading to arterial stiffness, and some of the drugs used to treat RA, such as corticosteroids and leflunomide, are risk factors for developing arterial hypertension (HT). <h3>Objectives</h3> The aim of this study is to determine the prevalence of HT in outpatients with RA at a rheumatology office in Buenos Aires, and describe their relationship with clinical, laboratory and disease activity <h3>Methods</h3> We evaluated consecutive outpatients with a diagnosis of RA according ACR 90 criteria that attend to the Rheumatology office of a public hospital in Buenos Aires. Blood pressure (BP) was assessed by 3 protocolized measurements, clinical data was collected and disease activity was evaluated by DAS28-ESD. Statistical analysis was performed to establish prevalence of hypertension and to establish association with clinical and laboratory variables using Mann Whitney and Chi Square test. Significance was p≤0.05. <h3>Results</h3> We analyzed 99 patients (85.9% female and 14.1% male) with a mean age of 51.3 years old (range 26-80). 79.8% had Functional Class I and II. The prevalence of hypertension in our population was 50.5%. The median time to progression of RA: 9.57 years, DAS 28: 4.06 (range: 1.54 to 7.55), 65.7% of individuals take corticosteroids. HT was associated with age (56.16 years (26-80) the HT patients versus 46.35 years (26-81) for non HT patients(p &lt;0.0001). The abdominal diameter was greater for the HT group (95.74 cm (92.31- 99.17) versus 90.59 cm (86.67 - 94.51) (p=0.035). The other analyzed variables don´t show statistical significance <h3>Conclusions</h3> Almost a half of RA patients had blood hypertension at the medical office during a standard control. It was significantly related to age and abdominal diameter. It was higher than the prevalence for the general population of Buenos Aires <h3>References</h3> Solomon D, Karlson E, Rimm E, Cannuscio C, Mandl M. Cardiovascular morbidity and mortality in women diagnosed with Rheumatoid arthritis. Circulation 2003;107:1303–7. Ferrante D, Virgolini M. Encuesta Nacional de Factores de Riesgo 2005: resultados prinicpales. Prevalencia de factores de riesgo de enfermedades cardiovasculares en la Argentina. Rev. Argent Cardiol. 2007; 75; 20-29. Hernandez- Hernandez R, Silva H, Velasco M, et al. Hypertension in seven Latin American cities: the cardiovascular Risk Factor Multiple Evaluation in Latin America (CARMELA) study. J. Hypertens 2010; 28; 24-34. Panoulas V, et. al. Prevalence and associations of hypertension and its control in patients with rheumatoid arthritis. Rheumatology 2007;46:1477–1482 <h3>Disclosure of Interest</h3> None Declared
52 INTRAHEPATIC CHOLESTASIS OF PREGNANCY AND PREEXISTING OR FUTURE HEPATOBILIARY DISEASES: A POPULATION-BASED COHORT STUDY OF 125,281 SWEDISH WOMEN SHOWS STRONG ASSOCIATIONS WITH HEPATITIS C
Authors: H.-U. Marschall, E. Wikström Shemer, J.F. Ludvigsson, O. Stephansson
Journal: Journal of Hepatology (2013)
Clinical, Laboratory and Echocardiographic Features of Patients with Pericardial Effusion in Gaziantep Regions
Authors: Süleyman Ercan, Orhan Özer, Fethi Yavuz, Mehmet Kaplan, Hayri Alıcı, Burcu Günsoy, Gökhan Altunbaş, Fuat Başanalan, Vedat Davutoğlu
Journal: Journal of the American College of Cardiology (2013)
Interim analysis of a phase II study of the safety and efficacy of gemtuzumab ozogamicin (Mylotarg (R)) given in combination with cytarabine and daunorubicin to patients < 60 years old with untreated acute myeloid leukemia.
Authors: DJ De Angelo, C Schiffer, R Stone, P Amrein, H Fernandez, K Bradstock, M Tallman, J Foran, Gunnar Juliusson, D Liu, C Paul, D Russo, L Stenke, L Leopold, D Stevenson, M Richie, M Berger
Journal: Blood (2002)
Abstract 5326: ID3 contributes to cerebrospinal fluid seeding and poor prognosis of medulloblastoma
Authors: Ji Hoon Phi, Seung Ah Choi, Sang-Hee Lim, Kyu-Chang Wang, Byung-Kyu Cho, Sung-Hye Park, Chul-Kee Park, Ji Yeoun Lee, Seung-Ki Kim
Journal: Cancer Research (2012)

Abstract Seeding of medulloblastoma is the most influential prognostic factor for survival, but little has been known about the molecular mechanism of seeding in medulloblastoma. Inhibitor of differentiation (ID) genes are implicated as promoter of tumor progression and metastasis in many human cancers. We investigated the expression and functional roles of ID genes in terms of seeding and prognosis of medulloblastoma. Significantly higher ID3 expression was observed in medulloblastoma with seeding than in tumors without seeding. In vitro studies using D283 medulloblastoma cells and ID3-siRNA showed that ID3 knockdown resulted in decreased proliferation, enhanced apoptosis, and suppressed migration. We made a seeding model of medulloblastoma in mice and injected a stable cell line with ID3 knockdown with shRNA. ID3 knockdown in vivo inhibited growth of primary tumor and development of leptomeningeal seeding and prolonged survival of animals compared with controls. A mRNA mini-array revealed that ID3 knockdown leads to up-regulation (TIMP3, ITGB4, COL12A1, ADAMTS8) and down-regulation (TNC, CTGF, ICAM1) of several genes related to cellular invasion and migration. High ID3 expression was associated with poor survival of patients with medulloblastoma as with seeding at presentation. These findings indicated that ID3 plays an important role in seeding of medulloblastoma and may be a target of therapeutic intervention for enhancing survival of the patients in the poor-prognostic group. 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 5326. doi:1538-7445.AM2012-5326
Abstract 3064: HPP1 tumor suppression and JAK-STAT signaling
Authors: Abul Elahi, Jonathan M. Hernandez, David Shibata
Journal: Cancer Research (2010)

Abstract Introduction: HPP1 is a putative tumor suppressor gene that is epigenetically silenced in various tumor types including colorectal cancer. We have previously reported that the ectopic expression of HPP1 results in the upregulation of STAT1, STAT2 and a number of interferon-inducible genes, and that activation of STAT1 is critical for HPP1's growth suppressive functions. We have sought to comprehensively evaluate alterations and the importance of the JAK-STAT signaling axis as they relate to HPP1 overexpression. Methods: Full-length HPP1 was amplified and cloned into the pcDNA3.1 expression vector which was then stably transfected into the HCT116 colon cancer cell line. Western Blot analyses were performed to assess both expression and activation for STAT1, STAT2, STAT3, JAK1, JAK2, JAK3 and TYK2 in HPP1 transfectants and empty vector controls. Functional STAT1 and STAT2 promoter binding were quantified using luciferase reporter plasmids containing ISRE-(Interferon Stimulated Regulatory Element) and GAS-(Gamma Activated Site) promoter elements. Results: The overexpression of HPP1 resulted in increased expression and activation of STAT1 and STAT2. Overexpression of HPP1 was associated with significant increases in both STAT1:STAT1 (p=0.007) and STAT1:STAT2 (p=0.036) binding, suggesting HPP1 mediates tumor suppression via association with Type II-like (gamma) and Type I-like (alpha) interferon pathways. Furthermore, additional corresponding dose-dependent inductions of STAT1 and STAT2 activation were achieved by treatment of HPP1 transfectants with interferon gamma and alpha. In contrast to STAT1 and 2, forced expression of HPP1 resulted in a downregulation of both STAT3 total expression and activation. HPP1 transfectants demonstrated increases in expression and activation of JAK1, JAK2 and JAK3, as well as a reduction in levels of TYK2 and phosphoTYK2. Conclusion: Activation of JAK1, 2 and 3 likely contribute to the upregulation and phosphorylation of STAT1 and STAT2 which in turn, result in the activation of Type I- and Type II-like interferon-inducible elements and their growth suppressive effects. Moreover, we demonstrate a reciprocal abrogation of the oncogenic STAT3 and its associated dominant kinase TYK2. HPP1 appears to mediate tumor suppression via modulation of JAK-STAT-interferon pathways. 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 3064.
Government and Industry Collaboration: Formal or Informal?
Authors: K. Smigel
Journal: JNCI Journal of the National Cancer Institute (1989)

Journal Article Government and Industry Collaboration: Formal or Informal? Get access Kara Smigel Kara Smigel Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 22, 15 November 1989, Pages 1689–1690, https://doi.org/10.1093/jnci/81.22.1689 Published: 15 November 1989
New NIH Director Holds Town Meeting
Authors: S. Jenks
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article New NIH Director Holds Town Meeting Get access Susan Jenks Susan Jenks Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 20, 16 October 1991, Page 1446, https://doi.org/10.1093/jnci/83.20.1446 Published: 16 October 1991
Hepatocelluar Carcinoma in an Accessory Lobe of the Liver Revealed by 11C-Acetate PET With a Negative Finding on FDG Imaging
Authors: Li Huo, Yonghong Dang, Ruie Feng, Hongming Zhuang, Fang Li
Journal: Clinical Nuclear Medicine (2012)

An accessory lobe of the liver is a rare congenital anomaly, which is very difficult to diagnose preoperatively. Hepatocellular carcinoma in an accessory lobe of the liver is much rarer. We report here our findings of hepatocellular carcinoma in an accessory left lobe on 11C-acetate PET/CT images in a 67-year-old man who had both an unremarkable diagnostic contrast abdominal CT and a negative FDG PET/CT scan before the 11C-acetate PET/CT study.
991 ACUTE LIVER FAILURE IN HIV INFECTED PATIENTS: A SINGLE CENTER EXPERIENCE
Authors: T.M. Antonini, C. Vinaixa, P. Ichai, M. Sebagh, S. Haim- Boukobza, E. Teicher, A. Coilly, A.-M. Roque-Afonso, B. Roche, E. Vibert, R. Adam, D. Castaing, J.-C. Duclos-Vallee, D. Samuel
Journal: Journal of Hepatology (2013)
Optimism Expressed Over Prostate Drug
Authors: S. Jenks
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Optimism Expressed Over Prostate Drug Get access Susan Jenks Susan Jenks Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 23, 4 December 1991, Pages 1712–1713, https://doi.org/10.1093/jnci/83.23.1712 Published: 04 December 1991
CAPSULA ENDOSCÓPICA EN EL ESTUDIO DE HIPERTENSIÓN PORTAL Y ANEMIA
Authors: J De la Peña, MT Arias, P Fernández Gil, A Terán, A Puente, F Pons Romero
Journal: Endoscopy (2010)

Introducción: La anemia es un problema frecuente en el paciente con hipertensión portal. Existen pocos datos acerca de la rentabilidad diagnóstica del empleo de cápsula endoscópica en estos casos, así como su utilidad en la toma posterior de decisiones terapéuticas.
TCTAP C-076 Percutaneous Coronary Intervention of Left Anterior Descending Artery Chronic Total Occlusion Using Septal-Septal Collateral Channel
Authors: Ying-Hsien Chen, Jiun-Yang Chiang, Ching-Chang Huang, Mao-Shin Lin, Paul Hsien-Li Kao
Journal: Journal of the American College of Cardiology (2015)
VASCULAR RESPONSE TO LIPID-LOWERING THERAPY IN DIABETES VERSUS NON-DIABETES PATIENTS: SERIAL OPTICAL COHERENCE TOMOGRAPHY AND INTRAVASCULAR ULTRASOUND STUDY
Authors: Yoshiyasu Minami, Jingbo Hou, Haibo Jia, Sining Hu, Rocco Vergallo, Tsunenari Soeda, Shaosong Zhang, Bo Yu, Ik-Kyung Jang
Journal: Journal of the American College of Cardiology (2015)
Abstract 533: Dendritic cells are professional educators of Natural Killer cells
Authors: Andres Wiernik, Jeffrey S. Miller
Journal: Cancer Research (2012)

Abstract Dendritic cells (DCs) and Natural Killer (NK) cells are important components of innate immunity. NK cells are the principal effectors of the innate immune system and play an important role in tumor surveillance and anti-viral immunity. It has been commonly accepted that CD56bright NK cells are the main source of cytokine production while CD56dim are mostly responsible for cytolytic activity and target cell killing. CD56dim NK cells acquire KIR (Killer cell Immunoglobulin-like Receptors or KIR) receptors by a process called NK cell education or licensing. NK cell education has been defined as the mechanism by which NK cell acquire inhibitory KIR and how signaling by specific cognate ligands leads to gain of NK cell function. DCs are antigen presenting cells which act as sentinels for the immune system by engulfing pathogens, processing and presenting them to CD4 and CD8 T cells. Interactions between dendritic cells and natural killer cells have been extensively studied but the role that DCs might play in NK cell education remains elusive and poorly understood. We evaluated the in-vitro interaction between adult monocyte-derived dendritic cells and natural killers cells from healthy donors. Mature monocyte-derived dendritic cells (mdDCs) were co-cultured with KIR negative and KIR positive NK cells in addition to different concentrations of IL-15. After 5 days of co-culture; the KIR negative population (0.8% KIR positive after 5 days of co-cultured) acquired up to 3.8% KIR expression when co-cultured with mdDCs (1:1 ratio) and 0.5 ng/mL of IL-15. In addition, a population of NK cells which expressed 28% KIR after 5 days of culture expressed up to 38% KIR when mdDCs and 0.5 ng/mL of IL-15 were added to the culture. Of note, enhanced KIR expression (as a marker of maturation) required both IL-15 and mdDcs as no effect was seen when mdDcs or IL-15 were added alone. Aside from the differences noted in KIR expression, a population of CD56dim NK cells became CD56bright when both KIR negative (8.44% to 23.6%) and KIR positive (0.8% to 24.9%) NK cells were co-cultured with mdDCs and IL-15. In conclusion, our studies suggest that dendritic cells have the ability to educate NK cells and that this process is dependent on IL-15, which can be trans-presented through IL-15Rα on DCs. Dendritic cells in addition to IL-15 may also revert a population of mature CD56dim NK cells to a CD56bright NK cells, which are considered less differentiated, suggesting that NK maturation can be bidirectional and may exhibit more plasticity than previously recognized. 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 533. doi:1538-7445.AM2012-533
Abstract 830: Clinical significance of measuring serum p53 antibodies in synchronous multiple colorectal cancer and double cancer patients
Authors: Mayumi Kawamata, Mitsuyoshi Ota, Shoichi Fujii, Yasushi Ichikawa, Hirokazu Suwa, Kenji Tatsumi, Kazuteru Watanabe, Shigeru Yamagishi, Hirotoshi Akiyama,, Takashi Ishikawa, Takashi Chishima, Daisuke Shimizu, Satoshi Hasegawa, Itaru Endo
Journal: Cancer Research (2010)

Abstract Aims: The clinical significance of measuring serum p53 antibodies in colorectal cancer patients was evaluated. Patients and Methods: Preoperative serum tumor markers including CEA, CA19-9 and p53 antibody were examined in 264 patients (stage I: 68, II: 73, III; 81) who were given diagnoses of colon and/or rectal cancer in Yokohama City University Hospital from 2007 to 2008. Correlativity of tumor markers to clinical findings was investigated. Results: In the overall patients, range, median and positive ratio of each tumor marker are shown in Table 1. Positive ratio of CEA and CA19-9 gradually increased according to clinical stage of the tumor, however, those of p53 showed almost the same concentration in any stage. Then, in stage I patients, positive ratio of p53 was higher than CEA and CA19-9 (p=0.0005). Thirty five cases (13.3%) of patients had synchronous or metachronous double or triple colorectal cancers. In that group, positive ratio of p53 was 48.3%, and median serum concentration of p53 was 0.915U/ml (0.15-295). Positive ratio and serum concentration of p53 of double or triple colorectal cancer patients were significantly higher than that of single cancer patients (p=0.0375). Conclusions: Serum concentration of p53 is sensitive, especially in early stage of colorectal cancer compared with other tumor markers. Colorectal cancer patients who showed high concentration of p53 have to be carefully checked for occult 2nd gastrointestinal tumor.1 nnCEA(ng/ml)CA19-9(ng/ml)p53 antibody(U/ml)Range (median)overall2640.3-3371(2.95)1-18927(12)0.15-443(0.53) Stage0180.3-5.7(1.45)1-44(9)0.15-2.36(0.28) StageI680.3-18.3(1.7)1-161(10)0.15-233(0.45) StageII730.5-148.1(3.9)1-1353(13)0.15-435.5(0.775) StageIII810.7-124.4(3.5)1-345(14)0.15-136.2(0.645) StageIV251.8-3371(23.9)1-18927(31)0.15-443(0.58) nCEA(%)CA19-9(%)p53 antibody(%)Positive ratiooverall26432.214.835.2 Stage0185.65.616.7 StageI687.45.929.4 StageII7337.012.341.1 StageIII8137.016.038.3 StaIV2588.048.036.0 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 830.