tbuckley/cabot-search huggingface dataset:
Abstract 136: Suppression of the uPA/uPAR system causes the overexpression of miR124 and suppresses stemness in glioma stem cells
Authors: Swapna Asuthkar, Bharathi Gorantla, Jasti S. Rao, Christopher S. Gondi
Journal: Cancer Research (2012)

Abstract The invasiveness and destructiveness of malignant neoplasms in the central nervous system are of great clinical importance. Higher-grade tumors, such as glioblastomas, are associated with poor prognosis, and patients’ average survival is only 8 to 12 months after chemotherapy and/or radiotherapy. This poor prognosis reflects the resistance of tumor cells to radiation and cytotoxic agents as well as the difficulty in achieving total tumor resection. Highly infiltrative gliomas are known to overexpress both uPA and uPAR. MicroRNAs (miRNAs) are essential post-transcriptional regulators known to determine cell identity and fate and are also known to be involved not only in development and differentiation but also in glioma progression. Acquisition of EMT has also recently been linked to stem cell phenotypes which is mediated by microRNAs. However, the molecular mechanism underlying EMT regulation still remains elusive. In the present study, we used glioma initiating cells (GICs), which show stem cell-like character, and determined whether their stemness can be suppressed by targeting the uPA/uPAR system. We raised glioma GICs from U87MG and 4910 glioma xenograft cells and observed that GICs expressed 2- to 3-fold increased levels of uPA and uPAR when compared to non-GIC. Further, the simultaneous downregulation of both uPA and uPAR suppressed GIC from establishing intracranial tumors in nude mice. Further, to understand whether this suppression of GIC involved microRNAs, we profiled miR expression in U87 cells and observed that miR124 and miR200a were significantly overexpressed. Using miRanda analysis, we determined that miR124 targets the regulation of Lhx-2 and Lhx-2 is over expressed (3- to 4-fold) in GIC when compared to non-GIC. To determine whether this suppression of Lhx-2 by downregulation of uPA and uPAR is mediated via miR124, we overexpressed miR124 in U87MG and 4910 glioma xenograft GICs and observed that miR124-overexpressed cells failed to establish intracranial tumors in nude mice. Our results demonstrate that the uPA/uPAR system may be involved in GIC maintenance via suppression of miR124. 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 136. doi:1538-7445.AM2012-136
C7
Authors: Robert D. Karl, Michael F. Hartshorne, Stephen R. Bunker, Michael A. Cawthon, William H. Howard, John M. Bauman
Journal: Clinical Nuclear Medicine (1984)

Karl, Robert D. Jr.; Hartshorne, Michael F.; Bunker, Stephen R.; Cawthon, Michael A.; Howard, William H. III; Bauman, John M. Author Information
INITIAL RESULTS OF THE FANTOM 1 TRIAL: A FIRST-IN-MAN EVALUATION OF A NOVEL, RADIOPAQUE SIROLIMUS-ELUTING BIORESORBABLE VASCULAR SCAFFOLD
Authors: Jose de Ribamar Costa, Alexandre Abizaid, Daniel Chamie, Alexandra Lansky, Janusz Kochman, Lukasz Koltowski
Journal: Journal of the American College of Cardiology (2016)
Abstract P4-06-23: KLF8 Is Regulated by Its Novel Interacting Protein PARP-1
Authors: H Lu, X Wang, AM Urvalek, T Li, L Yu, J Zhu, Q Lin, J. Zhao
Journal: Cancer Research (2010)

Abstract Krüppel-like factor 8 (KLF8) plays an important role in the progression of breast cancer invasion and metastasis. Using mass spectrometry and co-immunoprecipitation, we identified PARP-1, a chromatin-associated enzyme that catalyzes protein poly(ADP-ribosyl)ation (PARylation), as a novel KLF8 interacting protein. Co-IP and western blotting indicated that KLF8 is a PARylation substrate. Mutation of the cystein residues in the first and second zinc-finger motifs of KLF8 abolishes its interaction with PARP-1. Luciferase assays showed KLF8 activation on the cyclin D1 promoter was significantly reduced when PARP-1 was physically deleted or functionally inhibited or when KLF8-PARP-1 interaction was disrupted. Surprisingly, immunofluorescent staining demonstrated that KLF8 was localized in the nuclei of wide type MEFs, but was mislocalized in the perinuclear cytoplasm of the PARP-1-/- cells, which could be rescued by re-expression of PARP-1. The detection of γH2A.X, comet assay and clonogenic assay indicated KLF8 play a DNA repair role in a PARP-1- dependent matter. Cychloheximade-chase assay revealed the stability of KLF8 dramatically reduced by loss of PARP-1 or when KLF8-PARP-1 interaction was disrupted, meanwhile ubiquitination assay showed heavier ubiquitin chains of KLF8. This work has identified PARP-1 as a novel binding partner and post-translational modifier of KLF8 and a critical regulator of KLF8 localization, functions and stability in the cells and suggested a critical role of the interaction between KLF8 and PARP1 during metastatic progression of breast cancer. Support by: NIH, ACS and Komen grants to J.Z. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P4-06-23.
Abstract P3-07-03: The impact of Carcinoma <i>in situ</i> of the breast and family history on risk of subsequent breast cancer events and mortality - a population based study from Sweden
Authors: H Sackey, M Hui, K Czene, G Edgren, J Frisell, M Hartman
Journal: Cancer Research (2012)

Abstract Purpose: To evaluate the long-term risk of subsequent breast cancer and mortality among women diagnosed with carcinoma in situ of the breast. Patients and Methods: Using the population-based Swedish Multi-Generation and Cancer Registers we selected 8,111 women diagnosed with in situ breast cancer between 1980 and 2004. We estimated the relative risks of subsequent ipsi- and contralateral invasive breast cancer or a contalateral in situ expressed as standardized incidence ratios (SIRs), in relation to age, year, time since diagnosis and family history (1st degree relative) for breast cancer. The relative risk of death was expressed as standardized mortality ratio, (SMR). Results: Of 8,111 women identified with first in situ, 859 had a family history for breast cancer. The overall risk of a subsequent invasive breast cancer is over four fold and the risk for contralateral in situ breasts cancer was almost seven fold, compared with the risk in healthy women. Women with a family history had almost a 50% increased risk for a contralateral invasive breast cancer, IRR 1.49 (95% CI 1.06–2.09) compared to women without, but had no increased risk for a contralateral in situ cancer or ipsilateral invasive breast cancer. The risk for subsequent breast cancer decreased over time after diagnosis, but still 15 years after first in situ diagnosis the risk was over three times higher compared to the general population. Women below 40 years at diagnosis had the highest risk for a subsequent breast event, SIR 8.54 (95% CI 6.07–11.67). The overall mortality for women with no second invasive event was the same as for women in the general population, SIR 1.01 (95% CI 0.95–1.08). Women below 50 years at first in situ diagnosis, with a second invasive cancer, had a higher mortality compare to women above 50 years, SIR 8.3 (95% CI 5.38–11.54) and SIR 1.70 (95% CI 1.39–2.06) respectively. Conclusion: The risk for a subsequent invasive breast cancer, as well as mortality was substantially higher in younger women, which should be taken into account when planning their treatment and follow-up. Family history did not increase the risk for a subsequent ipsilateral invasive cancer. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P3-07-03.
Reflux and Barrett's disease. Can we stop surveillance after 2011?
Authors: R. Bisschops
Journal: Endoscopy (2012)

Hvid-Jensen et al. reported on a large population-based cohort study involving mostly Danish patients with Barrett’s esophagus between 1992 and 2009 [1]. Data on 11 028 patients were collected with a median follow-up period of 5.2 years. In total, 131 cases of adenocarcinoma were newly diagnosed within 1 year of the index endoscopy and were regarded as missed cases and not incorporated in the incidence calculation. During the subsequent years, an additional 66 new cases of adenocarcinoma were registered, yielding an incidence rate of 0.12 %. This is much lower than the assumed and previously reported risk of 0.5 %, the latter being used to substantiate surveillance guidelines. Notwithstanding this low incidence, the relative risk of developing cancer was 11.3 for Barrett’s esophagus – significantly elevated compared with the general population. However, in view of their findings the authors wonder whether surveillance of patients with Barrett’s esophagus is still warranted.
SAT0410 Long Term Effect of MBT Unstable Shoes on Low Back Pain. Follow-Up of a Randomized Controlled Trial
Authors: S. Genevay, Z. Tavcar, S. Armand
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Wearing unstable shoes at work was found to induce a significant reduction of several dimensions of pain, in a randomized controlled trial conducted among employees of a university hospital who were complaining of chronic low back pain.<sup>1</sup> Employees randomized to the intervention group (MBT unstable shoes) had a significant effect on pain but not on function at 6 weeks compared to the group wearing control shoes (Adidas). <h3>Objectives</h3> The goal of the present study is to evaluate long term clinical effect on pain and function. <h3>Methods</h3> At the end of the 6-weeks trials, all 35 participants who were still included in the trial were offered a pair of shoes. 34/35 selected MBT shoes (one in the MBT group declined) and were followed-up at 18 months. All dimensions (pain, function, and quality of life) were evaluated through an interview using previously validated questionnaires <h3>Results</h3> Subjects were contacted after a mean time of 19 months. The follow-up rate was 100% (35/35). Low back pain was significantly reduced (4.2 (1.8) to 2.0 (2.4), p &lt; 0.001) and function was increased (Roland and Morris back specific questionnaire decreased from 4.7 (5.2) to 1.8 (5.0), p = 0.01). On a 5-point scale, 14/35 (40%) reported an important or very important effect related to unstable shoes. The health related quality of life was not modified (EQ-5D). Duration of the current episode of pain was reduced (p&lt;0.01) as was the consumption of pain medication (p&lt;0.01). The effect on pain was higher among those (16/35) who continued to wear unstable shoes at least one weakly, but the difference was not statistically significant (-2.9 (2.7) vs. -1.6 (3.1), p=0.2). Eight subjects dropped the unstable shoes because of side effect: 6 because of musculoskeletal pain, 1 because shoes were too warm and 1 because of instability. <h3>Conclusions</h3> Regularly wearing unstable shoes over a long period of time appear to decrease low back pain and pain medication consumption while increasing back related physical function in an important subset of persons. As this simple method could have an important societal impact, larger trials are needed. <h3>References</h3> Armand S, Tavcar Z, Turcot K, Allet L, Hoffmeyer P, Genevay S. Effects of unstable shoes on chronic low back pain in health professionals: a randomized clinical trial. SpineWeek 2012; Amsterdam (Netherlands) <h3>Acknowledgements</h3> We thank the University Hospitals of Geneva for their financial support, allowing us to conduct an indepedant study and MBT for providing the shoes. <h3>Disclosure of Interest</h3> S. Genevay Grant/research support from: MBT, Z. Tavcar: None Declared, S. Armand Grant/research support from: MBT
Hemolytic–Uremic Syndrome in a Six-Year-Old Girl after a Urinary Tract Infection with Shiga-Toxin–Producing<i>Escherichia coli</i>O103:H2
Authors: Phillip I. Tarr, Laurie S. Fouser, Ann E. Stapleton, Richard A. Wilson, Harold H. Kim, James C. Vary, Carla R. Clausen
Journal: New England Journal of Medicine (1996)

In the United States, the hemolytic–uremic syndrome of childhood typically follows gastrointestinal infection with Escherichia coli O157:H7.1–3 It is presumed that the absorption from the gastrointestinal tract of Shiga toxins 1, 2, or both (formerly called Shiga-like toxins4) produced by E. coli O157:H7 causes microangiopathic hemolytic anemia as a result of endothelial-cell injury.5 Shiga-toxin–producing E. coli belonging to serotypes other than O157:H7 can also cause the hemolytic–uremic syndrome.5,6 However, even though such organisms have been implicated as causes of sporadic cases7 or outbreaks8 of gastroenteritis, they are not believed to be important causes of the hemolytic–uremic syndrome . . .
Abstract 851: Epidermal growth factor receptor inhibitor erlotinib prolongs survival in <i>Kras</i>-mutant pancreatic ductal adenocarcinoma by inhibiting gemcitabine-induced mitogen activated protein kinase signaling activation
Authors: Koji Miyabayashi, Hideaki Ijichi, Dai Mohri, Motohisa Tada, Keisuke Yamamoto, Yoshinari Asaoka, Tsuneo Ikenoue, Yousuke Nakai, Hiroyuki Isayama, Masao Omata, Harold Moses, Kazuhiko Koike
Journal: Cancer Research (2012)

Abstract Pancreatic ductal adenocarcinoma (PDAC) is one of the most deadly cancers. New therapeutic approaches to improve the prognosis are highly required. We generated pancreas-specific TGF-beta receptor II (Tgfbr2) knockout mice in the context of Kras activation, which recapitulated clinical and histopathological manifestations of human PDAC, indicating that an impact of blockade of TGF-beta signaling in PDAC progression. An EGFR inhibitor erlotinib showed a superior survival effect in combination with gemictabine, however, the mechanism by which PDAC with extremely frequent KRAS-mutation benefits from EGFR inhibition remains largely unkown. Using the model we investigated the anti-tumor impact and mechanisms of erlotinib in combination with gemcitabine. We treated the mice with elrotinib and gemcitabine. Median survival times were 52.5, 69, and 74 days for control, gemcitabine alone, and gemcitabine + erlotinib, respectively. Gemcitabine alone significantly extended the survival compared to the control. Further, adding erlotinib to gemcitabine prolonged the survival significantly compared to gemcitabine alone. Interestingly, treatment with gemcitabine enhanced the activation of MAPK signaling, which was inhibited by adding erlotinib, even in the KRAS-mutant PDAC in vivo and in vitro. We observed that the gemcitabine-induced MAPK signaling activation was due to induction of EGFR ligands expression and also due to ERBB2 activation in PDAC cells. Erlotinib inhibited the ERBB2 activation, partly by inhibiting heterodimer formation with EGFR and also decreasing ERBB2 protein expression in PDAC cells. This mouse model appears recapitulating chemosensitivity of human PDAC and indicates the significance of ERBBs in PDAC treatment. This model also might provide important insights into the beneficial patient subpopulation and the mechanism of the action of drugs and chemoresistance, in which TGF-beta signaling might be highly involved. 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 851. doi:1538-7445.AM2012-851
Abstract 766: Phenformin is a MYCN/MYC destabilizer that can specifically target neural crest derived tumors.
Authors: Naohiko Ikegaki, Srah Lomahan, Xao X. Tang
Journal: Cancer Research (2013)

Abstract We have been interested in identifying MYCN/MYC destabilizers that can specifically target neural crest derived tumors (neuroblastoma, melanoma, and malignant pheochromocytoma). MYCN amplification and its over-expression are associated with the worst neuroblastoma disease outcome. Non-MYCN amplified neuroblastomas express high-levels of MYC, and prognosis of these neuroblastomas is very poor. Melanoma and malignant pheochromocytoma are also known for high MYC expression. Interestingly, these neural crest derived tumors characteristically express the norepinephrine transporter (NET). This feature can be used to specifically target the tumor cells with agonists of NET, such as Meta-Iodo-BenzylGuanidine (MIBG). In the previous AACR meeting, we presented our finding that non-radio-labeled MIBG can suppress growth of neuroblastoma cells in vitro, and this effect is in part related to its ability to destabilize MYC and MYCN. We have also shown that FCCP, a well-known mitochondrial respiration inhibitor, destabilized MYCN and MYC in neuroblastoma cells and caused growth suppression. Recently, it has been reported that Phenformin, a Type II diabetic drug, binds NET, suggesting that NET positive cells preferentially uptake Phenformin. It is also known that Phenformin inhibits the mitochondrial electron transfer system. In this study, we have investigated a possible effect of Phenformin on growth and MYC/MYCN stability in neuroblastoma cells in vitro. SKNBE(2)C and CHP134 neuroblastoma cell lines were treated with various doses (0-2.5mM) of Phenformin for two days. MTS assay was used to assess the effect of Phenformin on growth of the cells. There was a dose-dependent growth suppression of the NB cell lines tested. Phenformin was more effective against growth of SKNBE(2)C than CHP134 cells. The effect of Phenformin on MYC/MYCN expression in four neuroblastoma cell lines [SKNBE(2)C, CHP134, SKNAS, and SY5Y] was also examined by Western blot assay. SKNBE(2)C and CHP134 express MYCN, whereas SKNAS and SY5Y express MYC at high levels. Treatment of these cells with Phenformin at the dose of 1mM for 24 hours resulted in destabilization of MYCN/MYC, suggesting that the growth suppressive effect of Phenformin on neuroblastoma cells was in part due to reduction in MYC/MYCN expression. We are currently examining whether the above observations made in neuroblastoma are also applicable to other neural crest derived tumors. In addition, we are investigating how Phenformin-related mitochondrial dysfunction causes destabilization of MYC/MYCN in neuroblastoma cells. Citation Format: Naohiko Ikegaki, Srah Lomahan, Xao X. Tang. Phenformin is a MYCN/MYC destabilizer that can specifically target neural crest derived tumors. [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 766. doi:10.1158/1538-7445.AM2013-766
Small Study Implicates PCBs in Breast Cancer
Authors: D. Milne
Journal: JNCI Journal of the National Cancer Institute (1992)

Journal Article Small Study Implicates PCBs in Breast Cancer Get access David Milne David Milne Milne is a Toledo-based freelance writer Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 84, Issue 11, 3 June 1992, Pages 834–835, https://doi.org/10.1093/jnci/84.11.834 Published: 03 June 1992
An ongoing measles outbreak in the Federation of Bosnia and Herzegovina, 2014 to 2015
Authors: M Hukic, J Ravlija, S Karakas, M Mulaomerovic, A Dedeic Ljubovic, I Salimović-Besic, M Seremet, S Ahmetagic, A Comor, E Feric
Journal: Eurosurveillance (2015)

Between January 2014 and the beginning of February 2015, the Federal Institute of Public Health in the Federation of Bosnia and Herzegovina has reported 3,804 measles cases. Notable transmission has been observed in three Central Bosnia Canton municipalities: Bugojno, Fojnica and Travnik. Most cases were unvaccinated 2,680 (70%) or of unknown vaccination status 755 (20%). Health authorities have been checking vaccination records and performing necessary prevention measures. The epidemic is still ongoing.
Endoscopic ultrasound education in Russian Federation
Authors: SY Orlov, ED Fedorov, ZV Galkova
Journal: Endoscopy (2006)

First attempts to perform endoscopic ultrasonography (EUS) in the frame of clinical approbation of EUS-prototypes were made in Russia in 1984 and in 1987, but regular introduction of this method in the clinical practice began only in 1997. Systematic training of specialists began a year later and in 2004 Olympus Endoscopy Training Center, based at our clinic was officially approved. During this period 45 endoscopists of 30 clinics from 4 countries have completed their training, including 26 clinics in Russia. In addition 5 doctors had EUS training course in Japan and 3– in Europe.
EVALUATION OF RENAL TRANSPLANT FAILURE WITH RADIONUCLIDE SCINTIGRAPHY (RNS) AND MAGNETIC RESONANCE IMAGING (MRI): A COMPARATIVE STUDY.
Authors: Mark S. Goldsmith, Doina E. Tanasescu, John V. Crues, Lalitha Ramanna, Michael B. Brachman, Alan D. Waxman
Journal: Clinical Nuclear Medicine (1986)

Goldsmith, Mark S.; Tanasescu, Doina E.; Crues, John V. III; Ramanna, Lalitha; Brachman, Michael B.; Waxman, Alan D. Author Information
1050 HUMAN LIVER CARCINOMAS RECRUIT MESENCHYMAL STEM/STROMAL CELLS THAT CAN PROMOTE TUMOR GROWTH VIA PARACRINE SIGNALING
Authors: P. Hernanda, A. Pedroza-Gonzales, L.J.W. van der Laan, H.L.A. Janssen, M.P. Peppelenbosch, Q. Pan
Journal: Journal of Hepatology (2013)
THU0568 Effectiveness of Educational Programs for Knee and Hip Osteoarthritis Pain and Quality of Life in Primary Care Patients
Authors: M. Protopopov, S. Lapshina, L. Myasoutova
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Knee and hip joints are the two most prevalent sites of osteoarthritis (OA). Pain and functional limitations are the two major factors influencing the quality of life in patients with OA. Few studies assessed the effect of educational programs on clinical features of OA in primary care. <h3>Objectives</h3> To determine the influence of participation in educational programs performed by healthcare professionals on pain levels and quality of life in patients with knee and hip OA. <h3>Methods</h3> 32 patients with symptomatic hip and knee OA (radiographic stages II-IV) participated in educational program for primary care patients with OA. Patients participated in once-a-month 2-hour classes performed by healthcare professionals. VAS pain, WOMAC (Likert Scale) and overall satisfaction with provided medical aid score (0-100 mm VAS scale) were measured at the baseline and after 3 months. Work productivity was assessed using the Work Productivity and Activity Impairment (WPAI) questionnaire. The comparison group included 30 patients with hip and knee OA comparable by age, sex and baseline VAS and WOMAC scores. <h3>Results</h3> After 3 months a significant improvements were found for VAS pain score (study group - 49.3±7.3- baseline, 34.2±4.8 - 3 months, control group - 50.1±6.9- baseline, 48.2±6.9 - 3 months p&lt;0,05), WOMAC overall score (study group - 33.7±4.5- baseline, 27.6±3.9 - 3 months, control group - 34.2±4.8 - baseline, 32.9±4.0 - 3 months, p&lt;0.05), as well as WOMAC pain and physical function scores in patients who participated in educational program. 81,9% of patients achieved pain relief of ≥ 3 points in the WOMAC pain subscale. Both presenteism and absenteeism percent were significantly higher in the control group patients (32% of productive time while at work and 14% through absenteeism) compared to intervention group patients (24% of productive time while at work and 6% through absenteeism) after 3 months. The overall satisfaction with provided medical aid score measured by VAS scale was higher in the study group patients compared to controls (79.3±10.2 vs 55.8±14.0, p&lt;0.05). <h3>Conclusions</h3> Participation of patients with symptomatic knee and hip OA in educational programs performed by healthcare professionals can decrease pain, increase quality of life and work performance. <h3>Disclosure of Interest</h3> None Declared