tbuckley/cabot-search huggingface dataset:
AB1144-HPR Case Management on Frail Patients in the Rheumatology Department at the Regional University Hospital in Malaga
Authors: L. Cano-Garcia, S. Manrique-Arija, C.M. Romero-Barco, L. Nieves-Martín, N. Mena-Vázquez, M. Rodríguez-Pérez, M.V. Irigoyen-Óyarzabal, F.G. Jiménez-Nuñez, I. Ureña-Garnica, M.D.C. Ordόñez-Cañizares, A. Fernández-Nebro
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Objectives</h3> To determine the features of patients referred to case management and from the case management process at the Regional University Hospital in Malaga. <h3>Methods</h3> <i>Design:</i> Descriptive cross-sectional study. Patients: patients treated in the Rheumatology service at the Regional University Hospital in Malaga and referred to case management from April to November 2013. The case management model is created as a response to the need for greater efficiency in care management due to the new Socio-medical Syndrome situation caused by the ageing of the population, the increase of frail patients and the need for home care. The case management process begins with the rheumatologist identifying a problem to be referred to case management. The rheumatologist contacts the rheumatology nurse specialist who prepares a report and hands it over to the case management nurse of the hospital. The case management nurse of the hospital contacts the primary care center of the patient that manages the petition from the Rheumatology unit. Variables include the basic characteristics of the patients, the Barthel index that measures the dependence in activities of daily living, the main reasons for referral to case management and professionals involved in primary care. <i>Statistical Analysis:</i> Basic descriptive of the results, the Kolmogorov-Smirnov test for the normality of the variables. <h3>Results</h3> From April to November 2013, 16 patients (75% women) with an average age 66.5±13.35 years were referred to case management. Rheumatic diseases in patients were: rheumatoid arthritis (n=10), systemic lupus erythematosus (n=3), scleroderma (n=1), severe osteoporosis (n=1) and psoriatic arthritis (n=1). 87.5% Frail patients with a Barthel index score of severe dependence in 62.5% of cases and of total dependence in 25% of cases. 43.8% lived with relatives, 25% with a professional caregiver and 25% lived alone. The reasons for referral to case management were: domiciliary nursing (50%), professional in-home caregiving (37.5%), help from the primary care center (PCC) staff (25%), information from the primary care physician (PCP) (25%), social problems (18.8%), nursing-home PCP (6.3%). Primary care professionals involved in the care of these patients were: nurses (62.5%), PCPs (37.5%), social workers (50%), community case manager nurses (50%). In 75% of cases the PCC belonged to the districts of Malaga. <h3>Conclusions</h3> Case management is a management tool that integrates primary care and specialty care professionals optimizing resources and improving the quality of health care provided to patients in situations of dependency. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.4555
Abstract 5013: <i>FOXP3</i> is an X-linked prostate tumor suppressor gene that represses <i>MYC</i>
Authors: Wang Lizhong, Runhua Liu, Hiroto Katoh, Yang Liu, Pan Zheng
Journal: Cancer Research (2010)

Abstract Despite clear epidemiological and genetic evidence for X-linked prostate cancer risk, all prostate cancer genes identified are autosomal. Here we report somatic inactivating mutations and deletion of the X-linked FOXP3 gene in human prostate cancer. We first evaluated expression of FOXP3 in both normal and prostate tissue and a reduced FOXP3 expression was wide-spread among prostate cancer samples. We then used fluorescence in situ hybridization (FISH) and determined the deletion of the FOXP3 in the 14% prostate cancer tissues. Our sequencing analyses identified single base-pair changes in 5/20 prostate cancer samples and these somatic mutations of the FOXP3 are functionally inactivating. Lineage-specific ablation of FoxP3 in the mouse prostate epithelial cells leads to prostate hyperplasia and prostate intraepithelial neoplasia. The targeted mutation of the FoxP3 in prostate tissue is sufficient to initiate the process of prostate cancer development. In both normal and malignant prostate tissues, FOXP3 is both necessary and sufficient to transcriptionally repress cMYC, the most commonly over-expressed oncogene in prostate cancer as well as among the aggregates of other cancers. FOXP3 is the first X-linked prostate tumor suppressor in the male. Since the male has only one X chromosome, our data represents a new paradigm of “single-genetic-hit” inactivation-mediated carcinogenesis. 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 5013.
Abstract 4718: Withaferin A, a potent and abundant component of Withania somnifera root extract, reduces myeloid-derived suppressor cell function.
Authors: Pratima Sinha, Suzanne Ostrand-Rosenberg
Journal: Cancer Research (2013)

Abstract Myeloid cells play a crucial role in growth and metastasis of malignant tumors. Tumor infiltrating myeloid cells includes myeloid-derived suppressor cells (MDSC), tumor-associated macrophages (TAMS) and dendritic cells (DC). These cells infiltrate into tumor and suppress tumor immunity by their inherent immune suppressive activity which is enhanced by interactions with each other (cross-talk). Therapeutic strategies targeting manipulation of these cells are being developed. The root extract of the plant Withania somnifera (Ashwagandha) (WRE) has been reported to reduce tumor cell proliferation and angiogenesis. Whether the anti-tumor effects of WRE are due to direct effects on malignant cells, or whether WRE also impacts immune suppressive myeloid cells is unknown. We hypothesize that WRE or its constituents impact tumor infiltrating myeloid cells and thereby boost anti-tumor immunity. HPLC and mass spectrometry analysis revealed that Withaferin A (WA) is the most abundant constituent of Withania somnifera root powder (ChromaDex, Inc. Irvine, CA). In comparison with the other constituents, WA has the most potent effect on reducing suppressive functions of myeloid cells. A prominent effect of MDSC is their production of IL-10 which increases upon cross-talk with macrophages, thus polarizing immunity to a tumor promoting type-2 phenotype. WA reduces inherent and cross-talk induced IL-10 secretion from MDSC in a dose dependent manner. Macrophage secretion of IL-6 and TNFα cytokines that are characteristic of M1-type macrophages and that also increase MDSC accumulation and function, are also reduced by WA. Much of the T cell suppressive activity of MDSC is due to MDSC production of reactive oxygen species (ROS), and WA significantly reduces MDSC production of ROS. Thus adjunctive treatment with WA has the potential to concomitantly reduce myeloid cell mediated immune suppression, to polarize immunity towards a tumor-rejecting type I phenotype, and to facilitate the development of anti-tumor immunity. Supported by NIH RO1CA115880, RO1CA84232, and American Cancer Society IRG-97-153-07 Citation Format: Pratima Sinha, Suzanne Ostrand-Rosenberg. Withaferin A, a potent and abundant component of Withania somnifera root extract, reduces myeloid-derived suppressor cell function. [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 4718. doi:10.1158/1538-7445.AM2013-4718
AB0650 Autoantibody Profile in Systemic Sclerosis Associated Pulmonary Hypertension
Authors: V. Sobanski, S. Nihtyanova, B. Lynch, B. Schreiber, J. Harvey, C. Handler, C. Denton, G. Coghlan
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Pulmonary hypertension (PH) is a severe complication of systemic sclerosis (SSc), affecting around 10% of patients. A recent meta-analysis showed an overall 3-year survival of 52%<sup>1</sup>. The impact of autoantibody on clinical phenotype of PH-SSc patients is not completely established. <h3>Objectives</h3> This study aimed to describe and compare the type of PH and hemodynamic characteristics between different profiles of autoantibody in SSc patients. <h3>Methods</h3> 543 patients diagnosed with PH on right heart catheterisation (mean pulmonary arterial pressure mPAP ≥25mmHg) between 1998 and 2012 were retrieved from our local database. Anti-nuclear antibody (ANA) profiles (n=457) were retrieved from clinical immunology records (missing data in 86 patients). <h3>Results</h3> The distribution of ANA among SSc-PH patients was as follows: anticentromere antibody (ACA) 35%, anti-topoisomerase I (ATA) 12%, anti-RNA polymerase III (ARA) 6%, anti-U1RNP 5%, anti-U3RNP 4%, anti-PM/Scl 2%, anti-Th/To 2%. Seven percent of patients had multiples specificities or anti-dsDNA or anti-Ro/SSa alone. Twelve percent were ANA positive in immunofluorescence and ENA (extractable nuclear antigen) negative. Four percent were ANA negative. Types of PH in patients with different ANA are presented in Fig. 1. In PAH-SSc patients (n=308), significant differences were found between ANA groups for: age at PAH diagnosis (p&lt;0.001), mPAP (p=0.045), FVC (p&lt;0.001) and DLCO (p&lt;0.001). Patients with ACA, ATA, ENA negative and ANA negative had the highest means of age at PAH diagnosis; patients with anti-U3RNP and anti-PM/Scl had the lowest. Patients with ACA had a higher FVC than ATA and ENA negative patients (p&lt;0.05). Patients with ATA and ENA negative had the lowest DLCO. There was a trend for lower mPAP in ATA than in ANA negative patients (p=0.091). No other significant difference in hemodynamic characteristics was found between PAH-SSc patients. <h3>Conclusions</h3> This study provides original data on ANA profile in PH-SSc patients from a large cohort offering quasi-exhaustivity of haemodynamic data. Our data suggests that ANA might provide tools to cluster PH patients in different phenotypes: a phenotype "PAH-like" in ACA, U3RNP, Th-To patients and a phenotype "PH due to lung disease-like" in ATA (ILD), PM/Scl and ARA patients. <h3>References</h3> Lefèvre G et al. Survival and prognostic factors in systemic sclerosis-associated pulmonary hypertension: a systematic review and meta-analysis. Arthritis Rheum. 2013;65(9):2412-23 <h3>Acknowledgements</h3> Vincent Sobanski has received research grants from Association des Sclérodermiques de France, Société Nationale Française de Médecine Interne, Groupe Pasteur-Mutualité, GSK and Institut Servier. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.4495
Endoscopic ultrasound features of mediastinal tuberculosis
Authors: S. Rana, D. Bhasin, K. Singh
Journal: Endoscopy (2011)

We read with interest the article by Fritscher-Ravens et al. [1] on the utility of endoscopic ultrasound (EUS)-guided fine needle aspiration (FNA) in differentiating between tuberculosis and sarcoidosis in patients with granulomatous mediastinal lymphadenopathy. We compliment the authors for conducting such a good study and agree with them that EUS-FNA has a high diagnostic yield for mediastinal tubercular lymphadenopathy; this has also been our experience [2] [3]. Also the ability of EUS-FNA to differentiate between sarcoidosis and tuberculosis, both granulomatous diseases, would be of great help for clinicians treating these two diseases that require different therapies.
Abstract 2211: Quantitative analysis of IGF-1R expression and signaling pathway activation in FFPE xenograft and human tumor tissues
Authors: Sheeno Thyparambil, Todd Hembrough, Liang Cao, David Krizman, Marlene Darfler, Jon Burrows, Lee Helman
Journal: Cancer Research (2011)

Abstract The IGF-1R signal pathway is activated in many cancer types which has led to active clinical development of both antibody and small molecule IGF1R targeted therapeutics. Multiple clinical trials targeting IGF1R are currently underway, however after initial optimism in NSCLC and Ewing's sarcoma, several trials have failed to show efficacy or had severe toxicity. Pretreatment quantitation of tumor IGF1R protein expression remains a challenge due to high homology between IGF1R and the insulin receptor. Thus, there is a need for a specific and quantitative clinical assay for IGF-1R protein expression. The ability to quantify IGF1R expression and determine signaling pathway activation status directly in formalin-fixed paraffin-embedded (FFPE) patient tissue biopsies should help identify and select patients most likely to benefit from anti-IGF1R therapies. We have developed a quantitative IGF1R assay which can be performed directly in FFPE patient tissue. This approach is based on the Liquid Tissue®-SRM technology platform which enables relative and absolute quantification of proteins and their phosphorylation status directly in formalin fixed tissue. The IGF1R- specific SRM assay was developed and preclinically validated on cell lines expressing a range of IGF1R protein. The final assay has a LOD of &amp;lt;20 attomol/ug and an LOQ of ∼35 attomol/ug, values that are well in line with expected levels of expression in primary tumor sourced cell lines and xenograft explants. The expression levels of IGF1R in seven formalin fixed rhabdomyosarcoma (RMS) cell lines were measured by SRM mass spectrometry. We detected a range of IGF1R expression from 68 to 333 amol/ug for these cell lines, values that showed extremely high correlation with antibody based techniques (Cao et al, Cancer Res. 68:8039). We extended this quantitation study by measuring expression of IGF-1R in human rhabdomyosarcoma xenograft explants and a cohort of ∼40 embryonal and alveolar rhabdomyosarcoma tumors. Interestingly, in xenografts treated with a therapeutic IGF1R antibody, tumor regression was seen, and a loss of IGF1R expression was noted by SRM analysis. Our goal is to define expression levels of IGF1R in these tumors, and to validate this assay for use as a companion diagnostic in follow on clinical trials of IGF1R inhibitors. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2211. doi:10.1158/1538-7445.AM2011-2211
The VIM3-AraC regimen followed by autologous stem cell transplantation in refractory or relapsing aggressive non-Hodgkin's lymphoma. A prospective study of 71 consecutive cases
Authors: I Plantier-Colcher, B Dupriez, M Simon, L Detourmignies, JP Jouet, P Fenaux, F Bauters, P Morel
Journal: Leukemia (1999)
Nurses Handbook of Obstetrics
Journal: JAMA (1941)

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Abstract PD07-08: Integrated Genomic Analysis before and after Brief Exposure to Trastuzumab (T): The11q13 and 17q12 Amplicons Are Associated with Response to T+Chemotherapy in Early Stage HER2 Positive Breast Cancer
Authors: LN Harris, Z Liu, A Li, E Sprecher, S Sarkar, K Lezon-Geyda, I Krop, EP Winer, DP. Tuck
Journal: Cancer Research (2010)

Abstract Background: The receptor tyrosine kinase HER2 is overexpressed in 18-20% of breast cancers and is the target of the highly effective therapy, trastuzumab. Coamplicons are frequent in HER2 amplified tumors, yet their role in response to T is not defined. To identify amplicons which might predict response to T in patients we performed gene expression and copy number analysis in tumor tissue from a preoperative trial with brief exposure to T, followed by T+C. Methods: Fresh tumor core biopsies were taken before at a 2 week timepoint after a single dose of T (8mg/m2) from 80 HER2-overpressing, early breast cancer patients enrolled on a clinical trial of T&amp;gt;T+C. Nucleic acids were extracted using Qiagen AllPrep and were analyzed with Illumina Ref8 and Illumina QUAD 610 SNP arrays. Eight commonly amplified regions (11q13, 14q32, 17q12, 20q13, 21q22, 8p22, 8q24) were identified by FISH probe coordinates and copy number calculated using the GPHMM algorithm. Amplification was defined as 4 or more copies of the amplicon. Gene expression was analyzed in Bioconductor using LIMMA analysis. Genomic biomarkers were compared pathologic complete response (pCR) vs objective response (CR+PR) and non-response (SD+PD) by RECIST criteria at the surgical timepoint. Results: There were 50 tumor pairs with adequate RNA for gene expression and 40 baseline tumors for copy number analysis with 28 paired samples. In the 40 baseline biopsies, the 11q13 amplicon was present in 14/40 (35%) of tumors but never seen in tumors with a pCR (t-test; p=0.004975). Of note, in the tumors with amplification of 11q13 there was no evidence of change in copy number after exposure to T, however numbers were small (7 pairs). Gene expression of the 11q13 region showed no significant change in common amplicon genes after one dose of T. The 17q12 amplicon, which harbors the HER2 locus, was amplified in 35/40 (87.5%) of cases - copy number was not associated with response, however, HER2 and GRB7 gene expression levels significantly declined in pCR tumors compared with &amp;lt;pCR (p=0.003). Conclusions: Integrated genomic analysis after brief exposure to T may provide useful predictors for response to T+C in early stage, HER2 positive breast cancer. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr PD07-08.
Abstract 1976: The discovery of mechanisms of resistance to SMO antagonists and the therapeutic implications
Authors: Marion Dorsch, Silvia Buonamici, Juliet Williams, Anlai Wang, Ribo Guo, Anthony Vattay, Kathy Hsiao, Jing Yuan, Lance Ostrom, Paul Fordjour, Dustin Anderson, Michael Morrissey, John Monahan, Joseph Kelleher, Stefan Peukert, Shifeng Pan, Xu Wu, Sauver-Michel Maira, Carlos Garcia-Echeverria, Kimberly Briggs, Neil Watkins, Yung-mae Yao, Christoph Lengauer, Markus Warmuth, William Sellers
Journal: Cancer Research (2010)

Abstract Smoothened (Smo) is a G-protein coupled receptor (GPCR)-like molecule that activates the Hedgehog (Hh) signal transduction pathway. In the resting state, the 12-pass transmembrane protein Patched (Ptch) inhibits Smo activity. When Ptch inhibition is attenuated, Smo signals via a cytosolic complex of proteins leading to activation of the Gli family of transcription factors. Genetic activation of the Hh pathway at or upstream of Smo is linked to tumorigenesis in several cancers. In particular, somatic mutations in Ptch and Smo leading to constitutive pathway activation are found in sporadic medulloblastoma (MB) and basal cell carcinoma (BCC). Evidence suggests that antagonists of Smo may abrogate the tumorigenic phenotype engendered by Ptch inactivation. NVP-LDE225 is a potent and selective orally available Smo antagonist that robustly inhibits Smo-dependent signaling in vitro and in vivo. NVP-LDE225 exerted dose-related anti-tumor activity in vivo in several genetically defined MB models that are driven by mutations in Ptch leading to near complete tumor regression and Hh pathway inhibition. However, following long-term continuous dosing of NVP-LDE225 in medulloblastoma allograft models, evidence of resistance to NVP-LDE225 was observed. Here, we describe our efforts to proactively identify mechanisms of resistance to targeted therapy of Smo. Genome-wide DNA- and RNA-profiling of resistant tumors revealed distinct resistance mechanisms allowing tumors to evade the inhibitory effects of Smo antagonists. Chromosomal amplification of Gli2, a downstream effector of Hh signaling, was identified as one mechanism leading to restoration of pathway signaling despite adequate drug exposure. Additional mining of the gene expression data for pathway signatures that are selectively deregulated in resistant tumors identified increased phosphatidylinositol-3-kinase (PI3K) signaling as another potential resistance mechanism. Probing the functional relevance of increased PI3K signaling, we showed that the combination of NVP-LDE225 with the dual PI3K/mTor inhibitor NVP-BEZ235 markedly delayed the development of resistance. Our findings have important clinical implications for future treatment strategies in medulloblastoma. 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 1976.