tbuckley/cabot-search huggingface dataset:
Abstract P5-19-12: Subgroup analysis on efficacy in the routine treatment - Results of the 2nd interim analysis of BRAWO, the non-interventional trial "Breast Cancer Treatment with Everolimus and Exemestane for HR+ Women"
Authors: Christian Jackisch, Eva-Maria Grischke, Andreas Schneeweiss, Thomas Decker, Christoph Uleer, Frank Förster, Oliver Tomé, Pauline Wimberger, Christian M Kurbacher, Bettina Mueller, Nadia Harbeck, Christoph Mundhenke, Sherko Kuemmel, Mathias Muth, Julia Kreuzeder, Wilhelm Bloch, Hans Tesch, Diana Lüftner, Florian Schütz, Peter A Fasching
Journal: Cancer Research (2015)

Abstract Introduction BRAWO is a German non-interventional study of 3000 patients (pts) with advanced or metastatic, hormone-receptor-positive, HER2-negative breast cancer treated with everolimus (EVE) and exemestane (EXE). We report results of the 2nd preplanned interim analysis (IA) with a data cut-off on 8th July 2014. Methods BRAWO collects data on the routine clinical treatment with EVE and EXE at about 400 sites. Main objectives are to extend the knowledge on a) the efficacy in the clinical routine and the impact of physical activity on efficacy and quality of life, b) prophylaxis and management of stomatitis, and c) the sequence of therapy in the clinical routine. The 2nd IA was defined to take place 12 months after the inclusion of the 500. patient into the documentation. Results Efficacy data will be reported for the first 500 documented pts. Apart from data on the total study population we will present the PFS results for subgroups including pts with or without prior EXE therapy, with or without prior chemotherapy for the advanced setting, with or without visceral metastasis and with regard to the line of treatment in the advanced setting and the extent of physical activity. The respective summary of adverse events for these patients will be presented as well as results on treatment compliance and dosing. Baseline characteristics and medical history as well as insights into treatment sequences before EVE and EXE will further be shown for all enrolled patients with valid baseline documentation (approx. 1200). Conclusion This subgroup analysis will provide insights into the treatment efficacy in the clinical routine and will add to a more comprehensive understanding of the treatment with EVE/EXE. Citation Format: Christian Jackisch, Eva-Maria Grischke, Andreas Schneeweiss, Thomas Decker, Christoph Uleer, Frank Förster, Oliver Tomé, Pauline Wimberger, Christian M Kurbacher, Bettina Mueller, Nadia Harbeck, Christoph Mundhenke, Sherko Kuemmel, Mathias Muth, Julia Kreuzeder, Wilhelm Bloch, Hans Tesch, Diana Lüftner, Florian Schütz, Peter A Fasching. Subgroup analysis on efficacy in the routine treatment - Results of the 2nd interim analysis of BRAWO, the non-interventional trial "Breast Cancer Treatment with Everolimus and Exemestane for HR+ Women" [abstract]. In: Proceedings of the Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2014 Dec 9-13; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2015;75(9 Suppl):Abstract nr P5-19-12.
Abstract P356: The Temporal Relationship Between Body Mass Index and DNA Methylation: Longitudinal Epigenome-Wide Association From the Bogalusa Heart Study
Authors: Dianjianyi Sun, Xiaojing Xu, Xiaoying Fu, Shengxu Li, Camilo Fernandez, Liming Li, Shaoyong Su, Xiaoning Wang, Tao Chen, Yun Lian, Quan-Zhen Li, Wei Chen, Sathanur Srinivasan, Gerald Berenson
Journal: Circulation (2015)

Obesity, as a metabolic disorder, can be either a cause or consequence of epigenetic alterations, but their temporal relationship is unknown. This study assessed the hypothesis that BMI and DNA methylation changes mutually influence each other, dependent on different methylation sites in the human genome. Peripheral leukocyte DNA methylation data on 294,840 CpG sites filtered from 485,577 sites generated by Illumina 450K BeadChip were analyzed in two discovery cohorts (585 whites and 245 blacks) and a longitudinal cohort (95 whites and 43 blacks followed 3.2 years) in the Bogalusa Heart Study (BHS) and 2 replication cohorts (450 twins in Chinese National Twin Study, 456 blacks in Georgia Prevention Institute Epigenetics of Obesity Study). BMI was significantly associated with methylation levels at cg17260706 (negatively), cg13562284 (negatively) and cg15721584 (positively) consistently in the discovery cohorts, and these associations were replicated in both 450 Chinese twins and 456 blacks in the same directions. The temporal relationship analyses in a cross-lagged path analysis model showed a one-directional relation from BMI to methylation changes at cg17260706 in BCL9L gene in both races as seen in the figure. The temporal relationship was different in blacks versus whites for the other two CpGs. In longitudinal analysis of BMI measured 4 or more times over 40 years in the BHS, childhood (p&lt;0.05) and adulthood BMI (p&lt;0.01) and its long-term burden (p&lt;0.01) and increasing trend (p&lt;0.01) were all negatively associated with the methylation level at cg17260706 in 615 whites and 276 blacks. In addition, an SNP in the BCL9L gene (rs586763) was associated with the methylation level at cg17260706 (p&lt;0.05) in blacks only; decreasing slopes of the methylation level at cg17260706 with increasing BMI were significantly different in three genotype groups in blacks (p&lt;0.05), but not in whites. In conclusion, higher BMI results in lower methylation levels at cg17260706 in the BCL9L gene.
High prevalence of ST-78 infection-associated vancomycin-resistant Enterococcus faecium from hospitals in Asunción, Paraguay
Authors: M.A. Khan, J.B. Northwood, R.G.J. Loor, A.T.R. Tholen, E. Riera, M. Falcón, Paraguayan Antimicrobial Network, A. van Belkum, M. van Westreenen, J.P. Hays
Journal: Clinical Microbiology and Infection (2009)
Abstract P390: Relationship between BMI and Risk of Hypertension in an urban Japanese cohort study: the Suita study
Authors: Michikazu Nakai, Makoto Watanabe, Kunihiro Nishimura, Misa Takegami, Yoshihiro Kokubo, Aya Higashiyama, Tomonori Okamura, Yoshihiro Miyamoto
Journal: Circulation (2014)

Objective: The positive relation between body mass index (BMI) and risk of incident hypertension (HT) has been reported mainly in the Western subjects with high BMI. However, there are a few reports in the Asian with relatively lower BMI. This study investigated the relation of BMI with risk of incident HT in the population-based prospective cohort study of Japan, the Suita study. Methods: Participants who had no HT at baseline (1,591 men and 1,973 women) aged 30-84 years were included in this study. BMI categories were defined as following: underweight (BMI&lt;18.5), normal (18.5≤BMI&lt;25.0), and overweight (BMI ≥ 25.0). The Cox proportional hazards model was used to estimate hazard ratios (HRs) of BMI categories for incident HT by sex. HRs were adjusted for age, cigarette smoking and alcohol drinking. The HRs according to quartiles of BMI were also estimated, using the lowest quartile of BMI as a reference. Results: During median follow-up of 7.2 years, 1,325 participants (640 men and 685 women) developed HT. The HR (95% CI) of 1kg/m2 increment of BMI for HT in men and women was 1.08 (1.05-1.11) and 1.10 (1.07-1.12), respectively. When we set a normal BMI as a reference, HR of overweight BMI in men and women was 1.37 (1.13-1.67) and 1.45 (1.18-1.77), whereas HR of underweight BMI in men and women was 0.63 (0.45-0.90) and 0.60 (0.45-0.80), respectively. In addition, compared to the lowest quartile, HR of the highest quartile of BMI in men and women was 1.67 (1.33-2.10, trend p&lt;0.001) and 2.10 (1.67-2.64, trend p&lt;0.001), respectively. Conclusion: In this study, we showed that higher BMI was associated with increased risk of hypertension in both Japanese men and women.
THE ETIOLOGY AND PREVENTION OF ANEMIA IN PREGNANCY
Authors: Maurice B. Strauss
Journal: Annals of Internal Medicine (1935)

Article1 July 1935THE ETIOLOGY AND PREVENTION OF ANEMIA IN PREGNANCYMAURICE B. STRAUSS, M.D.MAURICE B. STRAUSS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-9-1-38 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptPregnancy may be a coincidence in the course of any number of conditions which in themselves cause anemia, such as leukemia, hemolytic jaundice, and chronic blood loss. Furthermore the gravid state may in part be responsible for hemorrhage, pyelitis and puerperal sepsis, each of which may contribute to the development of anemia. Disregarding patients with anemia due to such well recognized causes, there remains a large group of women who during pregnancy develop moderate to severe anemia which has no obvious etiology. Two kinds of such anemia are encountered. One type, hypochromic in character, occurs much more frequently than the...Bibliography1. STRAUSSCASTLE MBWB: Studies of anemia in pregnancy, III, Am. Jr. Med. Sci., 1933, clxxxv, 539-551. Google Scholar2. DAVIESSHELLEY DTU: Some observations on hypochromic anaemia and its relation to pregnancy, Lancet, 1934, ii, 1094-1099. CrossrefGoogle Scholar3. STRAUSS MB: Anemia of infancy from maternal iron deficiency in pregnancy, Jr. Clin. Invest., 1933, xii, 345-353. CrossrefGoogle Scholar4. Corrigan JC, Boston. Google Scholar5. WILLS L: Treatment of "pernicious anaemia of pregnancy" and "tropical anaemia" with special reference to yeast extract as curative agent, Brit. Med. Jr., 1931, i, 1059-1064. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Boston, Massachusetts*Read at the Philadelphia meeting of the American College of Physicians, May 2, 1935.From the Thorndike Memorial Laboratory, Second and Fourth Medical Services (Harvard), Boston City Hospital, and the Departments of Medicine and Tropical Medicine, Harvard Medical School, Boston, Massachusetts. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byClassification and treatment of the anemias of pregnancy 1 July 1935Volume 9, Issue 1Page: 38-41KeywordsAnemiaEtiologyHemolytic jaundiceHemorrhageHospital medicineMedical servicesPregnancyResearch laboratoriesSepsisSevere blood loss ePublished: 1 December 2008 Issue Published: 1 July 1935 PDF downloadLoading ...
Hemic Cell-Associated Mammary Tumor Virus Activity in BALB/cfC3H Mice2
Authors: S. Nandi, Cheryl Helmich, Sandra Haslam
Journal: JNCI Journal of the National Cancer Institute (1974)

Mammary tumor virus (MTV) activity in hemic cells from different sources was studied under various experimental conditions to determine if non-nucleated reticulocytes or nucleated cells are carriers of blood-borne MTV (B-MTV). Comparisons were also made of the titer of MTV activity in hemic cells from different sources and between these cells and mammary tumor cells, which are carriers of B-type particles. Titration of B-MTV activity in blood cells of control, hemorrhagic-anemic, and hypertransfusion-induced polycythemic mice showed a lack of correlation between the numbers of circulating reticulocytes and the titer of MTV. However, the incidence of mammary nodules in polycythemic mice inoculated with mammary-tissue-borne MTV (M-MTV) was less than that of similar mice inoculated with B-MTV. Nucleated hemic cells were separated from the non-nucleated cells by selective lysis of the latter cells with NH4Cl or by immune hemolysis followed by differential centrifugation. Such cell preparations with solely or chiefly nucleated cells nevertheless contained MTV activity. These results indicate that virus activity associated with blood is carried by the nucleated cells (leukocytes and/or hematopoietic stem cells). MTV activity was detectable in nucleated hemic cells from all sources and the titer appeared less in circulating blood cells compared to those from other sources. Thus spleen and blood cells were considered the most suitable sources for B-MTV studies. MTV activity in mammary tumor cells was at least 10 times higher than in the nucleated hemic cells. However, accurate comparison was not feasible without proper identification of the cells containing B-MTV activity.
Menin-MLL inhibitors block oncogenic transformation by MLL-fusion proteins in a fusion partner-independent manner
Authors: S He, B Malik, D Borkin, H Miao, S Shukla, K Kempinska, T Purohit, J Wang, L Chen, B Parkin, S N Malek, G Danet-Desnoyers, A G Muntean, T Cierpicki, J Grembecka
Journal: Leukemia (2015)
Abstract 2515: Synthesis of substituted chromone-2-phenylcarboxamides as anti-breast cancer agents
Authors: Kinfe Ken Redda, Madhavi Gangapuram, Mohammad A. Ghaffari, Suresh Eyunni
Journal: Cancer Research (2014)

Abstract Breast cancer is one of the most commonly diagnosed cancers and causes the second leading cancer deaths in women. The overall survival rate of breast cancer patients has substantially increased during the last decades due to early tumor detection. Unfortunately, the recovery rate of advanced breast cancer by current available drug treatment is still unacceptably low. Although chemotherapy is the main stay of cancer treatment at present, most of the drugs cause general toxicity to any proliferating cells and tend to severely limit the therapeutic values of these drugs. In an attempt to overcome these problems, the synthesis of new anti-breast cancer agents with unique mechanisms of action was developed. Chromones are benzannulated oxygen containing heterocyclic compounds widely distributed in nature that have a -pyrone ring. The chemical core of chromone has been classifies as a privileged structures in drug discovery, due to its uses in a wide variety of pharmacologically active compounds such as anti cancer, anti-HIV, antibacterial and anti-inflammatory agents. Based on these considerations, we attempted the synthesis of novel substituted chromone-2-phenylcarboxamides as anti-breast cancer agents. The starting material chromones-2-carboxylic acid was obtained by the hydrolysis reaction of ethyl esters with the mixture of glacial acetic acid and concentrated HCl (2:1v/v) and the mixture was heated to reflux for 12 h. The acids were obtained in 70-80% yields. A suspension of substituted chromone-2-carboxylic acid in DMF was added to substituted anilines, in the presence of diphenylphosphorylazide and triethylamine. The reaction mixture was stirred at room temperature for 24 h, which furnished the target compounds i.e., substituted chromone-2-phenylcarboxamides. These compounds were evaluated for their cytotoxic effects on MCF-7 ER+ve breast cancer cells, MDA-MB-231 ER-ve breast cancer cell lines and Ishikawa cells using the CellTiter-Glo luminescent cell viability assay. N-(4-hydroxyphenyl)-5,7-dimethoxy-4-oxo-4H-chromene-2-carboxamide showed the most potent cytotoxicity with an IC50 values of 29.5 and 25.7 µM on MCF-7 and Ishikawa cell lines, respectively. This research was supported by National Center for Research Resources and the National Institute of Minority Health and Health Disparities of the National Institutes of Health through Grant Number 8 G12MD007582-28. Citation Format: Kinfe Ken Redda, Madhavi Gangapuram, Mohammad A. Ghaffari, Suresh Eyunni. Synthesis of substituted chromone-2-phenylcarboxamides as anti-breast cancer agents. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2515. doi:10.1158/1538-7445.AM2014-2515
Successful treatment of intravascular papillary endothelial hyperplasia (IPEH) by the beta‐adrenergic antagonist nebivolol
Authors: S. Prey, G. Haberstroh, B. Vergier, A. Taïeb, M. Wassef, K. Ezzedine, C. Léauté‐Labrèze
Journal: British Journal of Dermatology (2011)

Journal Article Successful treatment of intravascular papillary endothelial hyperplasia (IPEH) by the beta‐adrenergic antagonist nebivolol Get access S. Prey, S. Prey Department of Dermatology and National Reference Center for Rare Skin Disorders, Hôpital Pellegrin‐Enfant, INSERM U1035 ‐ Université Victor Segalen Bordeaux 2, Bordeaux, FranceUniversité de Bordeaux, Biothérapies des maladies génétiques et cancers, U1035, F‐33000 Bordeaux, France Search for other works by this author on: Oxford Academic Google Scholar G. Haberstroh, G. Haberstroh 14 avenue Maréchal de Lattre de Tassigny, Mulhouse, France Search for other works by this author on: Oxford Academic Google Scholar B. Vergier, B. Vergier Department of Pathology, Hôpital Haut‐Lévêque Pessac, EA2406 Université Victor Segalen Bordeaux 2, Bordeaux, France Search for other works by this author on: Oxford Academic Google Scholar A. Taïeb, A. Taïeb Department of Dermatology and National Reference Center for Rare Skin Disorders, Hôpital Pellegrin‐Enfant, INSERM U1035 ‐ Université Victor Segalen Bordeaux 2, Bordeaux, FranceUniversité de Bordeaux, Biothérapies des maladies génétiques et cancers, U1035, F‐33000 Bordeaux, France Search for other works by this author on: Oxford Academic Google Scholar M. Wassef, M. Wassef AP‐HP, Department of Pathology, Lariboisière Hospital; University Paris Diderot, Sorbonne Paris Cité, Faculty of Medicine, Paris, France Search for other works by this author on: Oxford Academic Google Scholar K. Ezzedine, K. Ezzedine Department of Dermatology and National Reference Center for Rare Skin Disorders, Hôpital Pellegrin‐Enfant, INSERM U1035 ‐ Université Victor Segalen Bordeaux 2, Bordeaux, FranceT Université de Bordeaux, Biothérapies des maladies génétiques et cancers, U1035, F‐33000 Bordeaux, France E‐mail: sorilla.prey@chu‐bordeaux.fr Search for other works by this author on: Oxford Academic Google Scholar C. Léauté‐Labrèze C. Léauté‐Labrèze Department of Dermatology and National Reference Center for Rare Skin Disorders, Hôpital Pellegrin‐Enfant, INSERM U1035 ‐ Université Victor Segalen Bordeaux 2, Bordeaux, France Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 166, Issue 5, 1 May 2012, Pages 1147–1149, https://doi.org/10.1111/j.1365-2133.2011.10755.x Published: 01 May 2012
Subthalamic Nucleus Deep Brain Stimulation in Parkinson Disease
Authors: Rubens Gisbert Cury, Egberto Reis Barbosa, Daniel Ciampi de Andrade
Journal: JAMA Neurology (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Neurology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Neurology journal
Abstract IA04: Using comprehensive proteomic approaches to map signaling adaptations to BRAF and BRAF/MEK inhibition
Authors: Inna V. Fedorenko, Kim H.T. Paraiso, Bin Fang, John M. Koomen, Keiran S.M. Smalley
Journal: Clinical Cancer Research (2015)

Abstract Although small molecule inhibitors of BRAF have shown great promise in advanced melanoma, resistance is commonplace. Many patients with acquired BRAF and BRAF/MEK inhibitor resistance develop disease at new sites, suggesting that drug-induced selection pressure drives metastasis. Here we used mass spectrometry-based phosphoproteomic screening and network modeling to uncover two novel adaptations to BRAF inhibitor therapy. The first involved ligand-independent EphA2 signaling that led to the adoption of an invasive/metastatic phenotype. The EphA2-mediated invasion was epigenetically mediated, AKT-dependent and was readily reversible upon removal of drug as well as through PI3K or HDAC inhibition. In a human melanoma mouse xenograft model, chronic BRAF inhibition led to the development of metastases, which stained positively for EphA2. A second phosphoproteomic screen showed BRAF inhibition to enhance the survival of both melanoma cells and fibroblasts through the induction of fibronectin (FN)/integrin α5β1 signaling. Adhesion to FN amplified the adaptive EGFR, HER2 and c-MET signals required for PI3K/AKT-mediated survival when BRAF was inhibited. At the same time, BRAF inhibition led, directly and indirectly, to the paracrine release of HGF and neuregulin from fibroblasts, with TGF-β release from the melanoma cells increasing both fibroblast differentiation and survival. These effects were partly mediated through paradoxical MAPK activation in the fibroblasts and could be reversed through BRAF/MEK inhibition. Thus, we have used comprehensive phosphoproteomics to identify two key non-genetic adaptations to BRAF inhibitor therapy that offer new insights into the process of therapeutic escape. Citation Format: Inna V. Fedorenko, Kim H.T. Paraiso, Bin Fang, John M. Koomen, Keiran S.M. Smalley. Using comprehensive proteomic approaches to map signaling adaptations to BRAF and BRAF/MEK inhibition. [abstract]. In: Proceedings of the AACR Precision Medicine Series: Drug Sensitivity and Resistance: Improving Cancer Therapy; Jun 18-21, 2014; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2015;21(4 Suppl): Abstract nr IA04.