tbuckley/cabot-search huggingface dataset:
SAT0349 Duration of Steroid Treatment in Polymyalgia Rheumatica
Authors: E. Tang, P. Shah, F. McKenna
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> The duration of steroid treatment in polymyalgia rheumatic (PMR) is variable. Some patients do not have raised inflammatory markers and anecdotal evidence suggests they may need a shorter duration of treatment. In order to evaluate parameters that may predict the duration of steroid treatment we have undertaken a retrospective analysis of patients on our database with a diagnosis of PMR. <h3>Methods</h3> We evaluated patients who presented with new onset PMR to the Trafford Rheumatology Unit between 2005 and 2010. Following a 14 day therapeutic trial of prednisolone 20mg od and a diagnosis of PMR confirmed by a consultant rheumatologist, all patients received a standard reducing regime of prednisolone, reducing every 2 weeks to initial maintenance of alternate day 10mg/5mg after 2 months (if possible). Doses were increased for recurrence of symptoms. After 6 months the dose was reduced to 5mg od if they had not required a dose increase and tailed off once asymptomatic on 5mg od for 6 months. All patients were followed for 10 years or until drug free remission. The electronic records were reviewed for demographic data, blood count, inflammatory markers, liver enzymes, immunology, and duration of treatment prior to drug free remission. <h3>Results</h3> 96 patients were evaluated. 15 were excluded from analysis if they had incomplete documentation or because of a positive rheumatoid factor, other immunology or revised diagnosis. The mean age was 68yrs; range 53–90yrs. Female to male ratio was 2.8:1. The median duration of symptoms prior to presentation was 4.5 months (1–36 months). At diagnosis 14% of patients were anaemic, mean CRP was 35mg/l, mean ESR was 45mm/hr and 26% had normal inflammatory markers. Only 1% of patients had raised liver enzymes. 44% were able to reduce to 5mg prednisolone after 6 months and a further 6% after 9 months. The mean duration of steroid treatment for all patients was 30 months (13–108 months). For patients with a normal ESR and CRP at diagnosis, the mean duration of steroids was 22 months compared with 32 months with raised ESR and 35 months with raised CRP. 10% relapsed after steroid withdrawal. 2 patients remained on long term steroids. <h3>Conclusions</h3> Approximately 25% of patients with PMR do not have raised inflammatory markers at diagnosis and have shorter total duration of steroids (mean 22 months). Almost half can reduce prednisolone to 5mg after 6 months. The average duration of steroids prior to drug free remission is almost 3 yrs in patients with raised inflammatory markers at diagnosis. 10% relapse after gradual steroid withdrawal. <h3>Disclosure of Interest</h3> None declared
SAT0456 Long-Term Effects of Treatment on The Progression of Structural Changes in Knee Osteoarthritis: 6-Year Follow-Up
Authors: J. Marte-Pelletier, J.P. Raynauld, F. Abram, P. Delorme, J.P. Pelletier
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> The Osteoarthritis Initiative (OAI) is the largest knee osteoarthritis observational cohort. It provides the possibility to study the evolution of OA structural changes over time and the associated risk factors. It also allows the potential disease-modifying OA drug effects to be explored in patients over time. <h3>Objectives</h3> This study aimed to examine, for the first time, the long-term (6-year) protective effect of combined glucosamine (Glu) and chondroitin sulfate (CS) treatment on OA knee cartilage volume using the OAI cohort. <h3>Methods</h3> Participants from the OAI Progression and Incidence sub-cohorts who had MRI data on the target knee at baseline and at 6 years and with a JSW greater than 1 mm, and information on the Glu/CS consumption were included (n=1593). The participants were stratified into two main groups based on whether or not they had medial meniscal extrusion at baseline, and the former group (n=429) were further stratified into subgroups based on their exposure time: not exposed, 1 year, 2 to 3 years, and 4 to 6 years. MRI assessments were done using fully automated quantitative technologies<sup>1,2</sup>. Statistical analysis included the Jonckheere-Terpstra trend test as well as multivariate analysis test. <h3>Results</h3> Findings indicate that in participants with knee OA, treatment with the combined Glu/CS significantly reduced the loss of cartilage in the global knee associated with the lateral compartment. Moreover, the extent of the treatment9s positive effect was also found to be related to the exposure time to treatment, the protective effect at 6 years being significant in participants who were exposed to 2 or more years of treatment. <h3>Conclusions</h3> The findings of this study are in line with previous data showing chondroprotective effects of glucosamine and chondroitin sulfate treatment with preferential effects, and provide future support for the long-term structure-modifying effects of such treatment in knee osteoarthritis subjects. <h3>References</h3> Dodin P, Pelletier JP, Martel-Pelletier J, Abram F. IEEE Trans Biomed Eng. 2010;57:2699–711. Dodin P, Abram F, Pelletier JP, Martel-Pelletier J. J Biomed Graph Comput. 2013;3:51–65. <h3>Disclosure of Interest</h3> J. Marte-Pelletier Shareholder of: Arthrolab Inc., Grant/research support from: Bioiberica, Consultant for: Bioiberica, J. P. Raynauld: None declared, F. Abram: None declared, P. Delorme: None declared, J. P. Pelletier Shareholder of: Arthrolab Inc., Grant/research support from: Bioiberica, Consultant for: Bioiberica, Speakers bureau: Bioiberica
A Novel, Oncogenic CSF2RB Mutation Found in a Primary Leukemia Sample Results in Constitutive Signaling, Increased Receptor Stability, and Formation of Intermolecular Complexes
Authors: Kevin M Watanabe-Smith, Cristina E. Tognon, Jeffrey W. Tyner, Brian J. Druker, Anupriya Agarwal
Journal: Blood (2015)
Expansion of T or B Lymphocytes after Unrelated Cord Blood (UCB) Allogeneic Stem Cell Transplantation in Adults Correlates with CMV Reactivation and Is Associated with a Better Outcome
Authors: Yannick Le Bris, Thierry Guillaume, Marina Iliaquer, Jerome Martin, Pierre Peterlin, Audrey Menard, Marion Eveillard, Soraya Wuilleme, Nelly Robillard, Jacques Delaunay, Mohamad Mohty, Alice Garnier, Philippe Moreau, Marie C Bene, Patrice Chevallier
Journal: Blood (2015)
A Randomized Open-Label Study To Evaluate The Efficacy Of Azacitidine For Post-Remission Therapy Of Acute Myeloid Leukemia In Elderly Patients (QOLESS AZA-AMLE)
Authors: Esther Natalie Oliva, Stella Santarone, Pietro Leoni, Caterina Alati, Antonio Volpe, Nicola Cascavilla, Anna Candoni, Pellegrino Musto, Fortunato Morabito, Francesco Di Raimondo, Patrizia Cufari, Irene Santacaterina, Iolanda Vincelli, Debora Capelli, Alessandra Freyrie, Prassede Salutari, Paolo Di Bartolomeo, Bruno Martino, Francesca Ronco, Agostino Cortelezzi
Journal: Blood (2013)
Human Metapneumovirus Infection in Adult Patients after Allogeneic Hemopoietic Stem Cell Transplantation.
Authors: Anna A. Colombo, Alessandra Algarotti, Maurizia Debiaggi, Maurizio Parea, Letizia Zenone Bragotti, Paolo Bernasconi, Daniela Caldera, Filippo Canducci, Mario Lazzarino, Emilio P. Alessandrino
Journal: Blood (2005)
Prospective, Multinational/Regional, Non-Interventional Study to Assess Treatment Practices in Anemia Patients Prone to Iron Overload: Results from the 3-Year Transfusional Hemosiderosis Registry (TORS)
Authors: Noppadol Siritanaratkul, Jong Wook Lee, Jun Ma, Mustafa Pehlivan, Elena Volodicheva, Qian Jiang, Fatiha Grifi, Bor-Sheng Ko, Raymond Wong, Vernon Louw, Abderrahim Khelif, Ali El-Ali, Jackie Han, Alfonso Losco, Osman Ilhan
Journal: Blood (2015)
FRI0384 Healthcare Utilization and Direct Medical Costs of Giant Cell Arteritis
Authors: M.J. Koster, S. Achenbach, C.S. Crowson, H. Maradit-Kremers, E.L. Matteson, K.J. Warrington
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Giant cell arteritis (GCA) is the most common systemic vasculitis in patients aged ≥50 years. Few studies have evaluated the economic impact of this condition and have been limited to inpatient-only data sources. Although the majority of healthcare for patients with GCA is provided as an outpatient, utilization and costs from this healthcare sector is largely unknown. <h3>Objectives</h3> To determine the health care utilization and direct medical cost of GCA in a population-based cohort. <h3>Methods</h3> This study utilized a retrospective, population-based cohort of patients diagnosed with GCA, as defined by 1990 ACR criteria, in 1982–2009 and a reference cohort of patients without GCA matched on age, sex, and calendar year from the same population. Standardized cost data (inflation-adjusted to 2014 dollars) for 1987–2014 and outpatient utilization data for 1995–2014 were obtained from the Mayo Clinic Cost Data Warehouse and analyzed from one year before and up to five years after the GCA diagnosis/index date. Utilization and costs were compared between GCA and non-GCA cohorts using signed rank two-tailed paired analyses. <h3>Results</h3> The GCA cohort consisted of 147 patients (118 female, 29 male) with a mean (±SD) age of 77.2 (±8.2). The non-GCA cohort comprised 147 patients with a mean (±SD) age of 76.9 (±8.5) years. During the year preceding diagnosis, excess healthcare cost related to GCA was only significantly increased in the month immediately preceding GCA diagnosis [mean (±SD) excess cost $1127 (±5154)]. Following diagnosis, significant annual excess outpatient cost was observed for patients with GCA in each of the first four years [mean excess cost (±SD): 0–1 yrs $1307 (±15581), p&lt;0.001; 1–2yrs $908 (±5917), p=0.009; 2–3 yrs $1324 (±4648), p=0.007; 3–4 yrs $609 (±4596), p=0.04] but was similar between GCA and non-GCA subjects in the 5th year. There were no significant differences in inpatient costs between GCA and non-GCA subjects. Patients with GCA had higher utilization of laboratory visit days annually for each of the first 3 years following diagnosis, as well as increased outpatient physician visits and combined radiology for years 0–1, 1–2, and 3–4 years (figure). Ophthalmologic procedures/surgery were increased for years 0–1, 1–2, and 4–5. Emergency medicine visits, musculoskeletal and cardiovascular procedures/surgery were similar between GCA and non-GCA groups throughout the study period. <h3>Conclusions</h3> Direct medical costs were increased in the month preceding and outpatient costs were increased in the first 4 years following GCA diagnosis and then return to levels similar to non-GCA subjects. A higher utilization of outpatient physician, laboratory and radiology visits, as well as ophthalmologic procedures among these patients accounts for the observed increased cost of care. <h3>Disclosure of Interest</h3> None declared
Molecular Pathways: Understanding and Targeting Mutant Spliceosomal Proteins
Authors: Akihide Yoshimi, Omar Abdel-Wahab
Journal: Clinical Cancer Research (2016)

Abstract Splicing of precursor messenger RNA is a critical step in regulating gene expression, and major advances are being made in understanding the composition and structure of the enzymatic complex that performs splicing, which is termed the “spliceosome.” In parallel, there has been increased appreciation for diverse mechanisms by which alterations in splicing contribute to cancer pathogenesis. Key among these include change-of-function mutations in genes encoding spliceosomal proteins. Such mutations are among the most common genetic alterations in myeloid and lymphoid leukemias, making efforts to therapeutically target cells bearing these mutations critical. To this end, recent studies have clarified that pharmacologic modulation of splicing may be preferentially lethal for cells bearing spliceosomal mutations and may also have a role in the therapy of MYC-driven cancers. This has culminated in the initiation of a clinical trial of a novel oral spliceosome modulatory compound targeting the SF3B complex, and several novel alternative approaches to target splicing are in development as reviewed here. There is now, therefore, a great need to understand the mechanistic basis of altered spliceosomal function in cancers and to study the effects of spliceosomal modulatory compounds in preclinical settings and in well-designed clinical trials. Clin Cancer Res; 23(2); 336–41. ©2016 AACR.
An International Multi-Center Study To Define the Application of Microarray-Based Gene Expression Profiling in the Diagnosis and Sub-Classification of Leukemia (MILE Study): Analysis of Completed Stage I with 2030 Patients Achieved a 95.4% Accuracy.
Authors: Torsten Haferlach, Alexander Kohlmann, Giuseppe Basso, Marie-Christine Bene, James R. Downing, Sheilla Shurtleff, Jesus M. Hernandez, Wolf-Karsten Hofmann, Thomas J. Kipps, Truus Te Kronnie, Wei-Min Liu, Elisabeth MacIntyre, Ken Mills, Claude Preudhomme, Sabina Chiaretti, Laura Z. Rassenti, John de Vos, Allen Yeoh, Evelyn Koay, Peter Papenhausen, Mickey Williams, Lothar Wieczorek, Robert Foa
Journal: Blood (2007)
Effect of Post-Thaw Washing Prior to Transplantation of Umbilical Cord Blood Units (UCB) That Were Depleted of Plasma but Not of Red Blood Cells.
Authors: Robert Chow, David Gjertson, Joseph Rosenthal, Auayporn Nademanee, Chatchada Karanes, Tang-Her Jaing, Michael Graham, Patrick Tan, Lawrence Petz
Journal: Blood (2005)
Abstract 3842: Expression analysis of SMYD5 in breast cancer and normal tissues
Authors: João Nunes de Matos Neto, Maíra de Azevedo Feitosa Araujo, Doralina do Amaral Rabello, Andrea Barretto Motoyama, Diego Madureira de Oliveira, Fabio Pittella Silva
Journal: Cancer Research (2015)

Abstract Lysine methyltransferases are a group of enzymes that carry a SET domain, which catalyzes the addition of methyl groups to specific lysine residues. Several lysine methyltransferases have been described to be involved in human carcinogenesis. The SMYD family of methyltransferases constitutes a group of five genes that encodes proteins bearing a SET and a MYND domain, whose activity have not yet been completely characterized. Although deregulation of SMYD family members has been reported to contribute to cancer progression through several different mechanisms, to date a clear relationship of SMYD5 with breast cancer, the second most frequent cancer worldwide and the most common among women, was not determined. In the present study we investigated the expression profile of SMYD5 in breast tumors and adjacent non-tumor samples, in breast cancer cell lines and in several normal tissues. qPCR revealed SMYD5 mRNA expression level was downregulated in 7 breast cancer cell lines when compared to normal breast tissues. Relative expression of SMYD5 in breast tumors and normal breast samples revealed a significant (p&amp;lt;0.001) reduction of SMYD5 expression in tumors comparing to the non-cancerous breast samples. These findings led us to investigate the role of SMYD5 in cell proliferation. We observed that reduction of SMYD5 expression by shRNA in HEK293 cells induced acceleration in culture growth. Moreover, the generation of MDA-MB-231 tumor sublines expressing varying levels of SMYD5 revealed different proliferative profiles. SMYD5 expression inversely correlated with growth rate in highly proliferative cultures. However, slow proliferating cells (i.e. long doubling time) do not seem to be affected by SMYD5 levels. This observation indicates that specific subgroup of highly proliferative cells may depend on SMYD5 downregulation to exhibit this phenotype. In addition, we found that SMYD5 has a sub-cellular distribution similar to other SMYD family proteins suggesting it may exert enzymatic activity in both cytosolic and nuclear substrates. Taken together, our data indicates a possible role for SMYD5 in modulating breast carcinogenesis through epigenetic alterations, probably acting as tumor suppressor. Note: This abstract was not presented at the meeting. Citation Format: João Nunes de Matos Neto, Maíra de Azevedo Feitosa Araujo, Doralina do Amaral Rabello, Andrea Barretto Motoyama, Diego Madureira de Oliveira, Fabio Pittella Silva. Expression analysis of SMYD5 in breast cancer and normal tissues. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3842. doi:10.1158/1538-7445.AM2015-3842
Allogeneic Stem Cell Transplantation (SCT) for Multiple Myeloma (MM) - What Has Changed? : A CIBMTR Analysis From 1989 – 2005.
Authors: Shaji Kumar, Smriti Shrestha, Mei-Jie Zhang, Angela Dispenzieri, Gustavo A. Milone, Sagar Lonial, Parameswaran N. Hari
Journal: Blood (2009)
miR-126 Regulates Distinct Self-Renewal Outcomes in Normal and Malignant Hematopoietic Stem Cells
Authors: Eric R. Lechman, Bernhard Gentner, Stanley W.K. Ng, Erwin M. Schoof, Peter van Galen, James A. Kennedy, Silvia Nucera, Fabio Ciceri, Kerstin B. Kaufmann, Naoya Takayama, Stephanie M. Dobson, Aaron Trotman-Grant, Gabriela Krivdova, Janneke Elzinga, Amanda Mitchell, Björn Nilsson, Karin G. Hermans, Kolja Eppert, Rene Marke, Ruth Isserlin, Veronique Voisin, Gary D. Bader, Peter W. Zandstra, Todd R. Golub, Benjamin L. Ebert, Jun Lu, Mark Minden, Jean C.Y. Wang, Luigi Naldini, John E. Dick
Journal: Cancer Cell (2016)

(Cancer Cell 29, 214–228; February 8, 2016) During figure preparation for this article, the authors inadvertently duplicated representative flow plots within Figure 3A (gated plot on left and lower right plot) and within Figures 4A and 4B (CTRL, AML17 and 126OE, AML17). The authors regret this error and apologize for any confusion that it may have caused. These errors have now been corrected in the figures here and in the article online.Figure 3Enforced Expression and Knockdown of miR-126 Alters the Proliferation and Differentiation Status of Primitive 8227 AML Cells (original)View Large Image Figure ViewerDownload Hi-res image Download (PPT)Figure 4Enforced Expression of miR-126 Expands Primary AML LSC (corrected)View Large Image Figure ViewerDownload Hi-res image Download (PPT)Figure 4Enforced Expression of miR-126 Expands Primary AML LSC (original)View Large Image Figure ViewerDownload Hi-res image Download (PPT) miR-126 Regulates Distinct Self-Renewal Outcomes in Normal and Malignant Hematopoietic Stem CellsLechman et al.Cancer CellJanuary 28, 2016In BriefLechman et al. show that miR-126 targets the PI3K/AKT/MTOR signaling pathway to preserve quiescence, increase self-renewal, and promote chemotherapy resistance of acute myeloid leukemia stem cells (LSC). Reducing the miR-126 level impairs LSC maintenance in contrast to expanding normal hematopoietic stem cells. Full-Text PDF Open Access
AB0598 Does The Presence of Anti-Citrullinated Protein Antibodies Change The Presentation of Systemic Sclerosis?
Authors: G. Laustriat, Y. Degboe, A. Ruyssen-Witrand, A. Constantin, T. Barnetche, D. Adoue, A. Cantagrel
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background</h3> Systemic sclerosis (SSc) is one of the most complex and heterogeneous systemic disease. The diagnosis can be helped by the positivity of different characteristic auto-antibodies steered toward topoisomerase I, centromeric protein, RNA polymerase and fibrillarin. Different presentations of the disease can be associated with some specificities of auto-antibodies. Recently, some studies have reported the presence of anti-citrullinated protein antibodies (ACPA) in patients with SSc. <h3>Objectives</h3> We have conducted a systematic literature review in order to define the prevalence of ACPA in SSc, and to observe their influence on clinical and paraclinical presentation of the disease. <h3>Methods</h3> Literature search was performed in PubMed Medline database on 15 february 2015. Publication were identified through a search that used the terms: ("systemic sclerosis"(MeSH) and "ACPA or anti-CCP or rheumatoid factor or cohort or value diagnostic"). In a first step, we have selected all cohorts over 50 patients with SSc and ACPA identification. In a second step we have included all studies in which the clinical profile of scleroderma was detailed according to their ACPA status. Meta-analyses were performed when there were two or more studies with similar clinical description. <h3>Results</h3> For the first question, we identified 13 observational studies merging 1231 patients with SSc. ACPAs were positive for 113 patients, giving a prevalence of ACPA in SSc of 9.2%. In a second step, we identified 9 studies reporting clinical and paraclinical aspects according to their ACPA status. Information was enough to perform a meta-analysis for arthralgia, arthritis, joint erosions, skin sclerosis, pulmonary arterial hypertension, pulmonary fibrosis and gastrooesophageal reflux. We found a significant association between ACPA positivity and the presence of arthritis (OR: 25.48 [11.82–54.47]), joint erosions on X-rays (OR: 13.06 [4.68–36.43]), pulmonary arterial hypertension (OR: 7.72 [2.38 – 25.5]), and pulmonary fibrosis (OR: 2.75 [1,21–6.24]) (Fig 1). <h3>Conclusions</h3> ACPA prevalence in scleroderma is 9.2%. Our systematic literature review shows a significant increased risk for erosive arthritis, pulmonary hypertension and pulmonary fibrosis in ACPA positive SSc. ACPA should be systematically included in the check-up of systemic sclerosis. <h3>Disclosure of Interest</h3> None declared
SP0035 Development of Eular Standardised Procedures for Rheumatology Ultrasound Imaging (RHUS)
Authors: I. Möller
Journal: Annals of the Rheumatic Diseases (2016)

The objectives of this EULAR Project are: To update the technical requirements for performing musculoskeletal ultrasound (MSUS) of the essential lesions present in rheumatic diseases accessible by MSUS including patient position, initial probe placement, scanning method and US landmarks. To develop procedures for additional MSUS assessment of additional musculoskeletal lesions/ abnormalities related to rheumatic diseases accessible to ultrasound evaluation. To develop procedures for ultrasound scanning of non-musculoskeletal anatomic regions of importance in rheumatologic practice that are readily accessible to ultrasound evaluation (i.e. large vessels, salivary glands, ligaments, and peripheral nerves). The creation of a concise illustrated manual of these procedures including internet access to video-clips accessible to all with interest in incorporating RHUS in their practice. <h3>Disclosure of Interest</h3> None declared
Chronic Inhibition of Mitochondrial Translation Alters Metabolism and Stemness in AML
Authors: Jhas Bozhena, Shrivani Sriskanthadevan, Marko Skrtic, Mahadeo A. Sukhai, Veronique Voisin, Yulia Jitkova, Marcela Gronda, Rose Hurren, Xiaoming Wang, Rob C. Laister, Gary D. Bader, Mark D. Minden, Aaron D. Schimmer
Journal: Blood (2012)
Unmet Needs for Symptom Control in Essential Thrombocythemia with Front Line Therapy
Authors: Holly Geyer, Robyn M. Scherber, Heidi Kosiorek, Amylou C. Dueck, Jean-Jacques Kiladjian, Stefanie Slot, Zhijian Xiao, Sonja Zweegman, Federico Sackmann, Ana Kerguelen Fuentes, Dolores Hernandez-Maraver, Konstanze Döhner, Claire N. Harrison, Deepti Radia, Pablo J. Muxi, Carlos Besses, Francisco Cervantes, Peter L. Johansson, Bjorn Andreasson, Alessandro Rambaldi, Tiziano Barbui, Karin Bonatz, Andreas Reiter, Francoise Boyer, Gabriel Etienne, Jean-Christophe Ianotto, Dana Ranta, Lydia Roy, Jean-Yves Cahn, Norman I Maldonado, Giovanni Barosi, Maria Ferrari, Robert Peter Gale, Gunnar Birgegard, Zefeng Xu, Yu Zhang, Xiujuan Sun, Junqing Xu, Peihong Zhang, Peter A. te Boekhorst, Suzan Commandeur, Harry C. Schouten, Heike L Pahl, Martin Griesshammer, Frank Stegelmann, Thomas Lehmann, Alessandro M. Vannucchi, Francesco Passamonti, Jan Samuelsson, Ruben A. Mesa
Journal: Blood (2015)