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RADIATION SAFETY OFFICE Table of Contents
Center for Radiological Research − 630 W. 168th St., New York, NY 10032 − http://crr-cu.org ANNUAL REPORT 2007 Eric J. Hall Director Howard B. Lieberman Editor Jinshuang Lu Assistant Editor CENTER FOR RADIOLOGICAL RESEARCH • ANNUAL REPORT 2007 Table of Contents CONTENTS.................................................................................................................................................................................1 COLLABORATING DEPARTMENTS AND INSTITUTIONS....................................................................................................4 ACKNOWLEDGEMENT OF SUPPORT.....................................................................................................................................4 RELATED WEB SITES..............................................................................................................................................................4 INTRODUCTION ........................................................................................................................................................................5 STAFF NEWS .............................................................................................................................................................................6 COLUMBIA COLLOQUIUM AND LABORATORY SEMINARS..............................................................................................7 STAFF LISTING .........................................................................................................................................................................8 -
Role of Nuclear Receptors in Central Nervous System Development and Associated Diseases
Role of Nuclear Receptors in Central Nervous System Development and Associated Diseases The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Olivares, Ana Maria, Oscar Andrés Moreno-Ramos, and Neena B. Haider. 2015. “Role of Nuclear Receptors in Central Nervous System Development and Associated Diseases.” Journal of Experimental Neuroscience 9 (Suppl 2): 93-121. doi:10.4137/JEN.S25480. http:// dx.doi.org/10.4137/JEN.S25480. Published Version doi:10.4137/JEN.S25480 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:27320246 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Journal name: Journal of Experimental Neuroscience Journal type: Review Year: 2015 Volume: 9(S2) Role of Nuclear Receptors in Central Nervous System Running head verso: Olivares et al Development and Associated Diseases Running head recto: Nuclear receptors development and associated diseases Supplementary Issue: Molecular and Cellular Mechanisms of Neurodegeneration Ana Maria Olivares1, Oscar Andrés Moreno-Ramos2 and Neena B. Haider1 1Department of Ophthalmology, Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA. 2Departamento de Ciencias Biológicas, Facultad de Ciencias, Universidad de los Andes, Bogotá, Colombia. ABSTRACT: The nuclear hormone receptor (NHR) superfamily is composed of a wide range of receptors involved in a myriad of important biological processes, including development, growth, metabolism, and maintenance. -
Interplay Between P53 and Epigenetic Pathways in Cancer
University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations 2016 Interplay Between P53 and Epigenetic Pathways in Cancer Jiajun Zhu University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Biology Commons, Cell Biology Commons, and the Molecular Biology Commons Recommended Citation Zhu, Jiajun, "Interplay Between P53 and Epigenetic Pathways in Cancer" (2016). Publicly Accessible Penn Dissertations. 2130. https://repository.upenn.edu/edissertations/2130 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/2130 For more information, please contact [email protected]. Interplay Between P53 and Epigenetic Pathways in Cancer Abstract The human TP53 gene encodes the most potent tumor suppressor protein p53. More than half of all human cancers contain mutations in the TP53 gene, while the majority of the remaining cases involve other mechanisms to inactivate wild-type p53 function. In the first part of my dissertation research, I have explored the mechanism of suppressed wild-type p53 activity in teratocarcinoma. In the teratocarcinoma cell line NTera2, we show that wild-type p53 is mono-methylated at Lysine 370 and Lysine 382. These post-translational modifications contribute ot the compromised tumor suppressive activity of p53 despite a high level of wild-type protein in NTera2 cells. This study provides evidence for an epigenetic mechanism that cancer cells can exploit to inactivate p53 wild-type function. The paradigm provides insight into understanding the modes of p53 regulation, and can likely be applied to other cancer types with wild-type p53 proteins. On the other hand, cancers with TP53 mutations are mostly found to contain missense substitutions of the TP53 gene, resulting in expression of full length, but mutant forms of p53 that confer tumor-promoting “gain-of-function” (GOF) to cancer. -
Peter F. Andrews Sportswriting and Broadcasting Resume [email protected] | Twitter: @Pfandrews | Pfandrews.Wordpress.Com
Peter F. Andrews Sportswriting and Broadcasting Resume [email protected] | Twitter: @pfandrews | pfandrews.wordpress.com RELEVANT EXPERIENCE Philly Soccer Page Staff Writer & Columnist, 2014-present: Published over 100 posts, including match reports, game analysis, commentary, and news recaps, about the Philadelphia Union and U.S. National Teams. Covered MLS matches, World Cup qualifiers, Copa America Centenario matches, and an MLS All-Star Game at eight different venues across the United States and Canada. Coordinated the launch of PSP’s Patreon campaign, which helps finance the site. Appeared as a guest on one episode of KYW Radio’s “The Philly Soccer Show.” Basketball Court Podcast Host & Producer, 2016-present: Produced a semi-regular podcast exploring the “what-ifs” in the history of the National Basketball Association, presented in a humorous faux-courtroom style. Hosted alongside Sam Tydings and Miles Johnson. Guests on the podcast include writers for SBNation and SLAM Magazine. On The Vine Podcast Host & Producer, 2014-present: Produced a weekly live podcast on Mixlr during the Ivy League basketball season with writers from Ivy Hoops Online and other sites covering the league. Co-hosted with IHO editor-in- chief Michael Tony. Featured over 30 guests in three seasons. Columbia Daily Spectator Sports Columnist, Fall 2012-Spring 2014: Wrote a bi-weekly column for Columbia’s student newspaper analyzing and providing personal reflections on Columbia’s athletic teams and what it means to be a sports fan. Spectrum Blogger, Fall 2013: Wrote a series of blog posts (“All-22”) which analyzed specific plays from Columbia football games to help the average Columbia student better understand football. -
Epigenomic and Transcriptional Regulation of Hepatic Metabolism by REV-ERB and Hdac3
University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations 2013 Epigenomic and Transcriptional Regulation of Hepatic Metabolism by REV-ERB and Hdac3 Dan Feng University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Genetics Commons, and the Molecular Biology Commons Recommended Citation Feng, Dan, "Epigenomic and Transcriptional Regulation of Hepatic Metabolism by REV-ERB and Hdac3" (2013). Publicly Accessible Penn Dissertations. 633. https://repository.upenn.edu/edissertations/633 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/633 For more information, please contact [email protected]. Epigenomic and Transcriptional Regulation of Hepatic Metabolism by REV-ERB and Hdac3 Abstract Metabolic activities are regulated by the circadian clock, and disruption of the clock exacerbates metabolic diseases including obesity and diabetes. Transcriptomic studies in metabolic organs suggested that the circadian clock drives the circadian expression of important metabolic genes. Here we show that histone deacetylase 3 (HDAC3) is recruited to the mouse liver genome in a circadian manner. Histone acetylation is inversely related to HDAC3 binding, and this rhythm is lost when HDAC3 is absent. Diurnal recruitment of HDAC3 corresponds to the expression pattern of REV-ERBα, an important component of the circadian clock. REV-ERBα colocalizes with HDAC3 near genes regulating lipid metabolism, and deletion of HDAC3 or Rev-erbα in mouse liver causes hepatic steatosis. Thus, genomic recruitment of HDAC3 by REV-ERBα directs a circadian rhythm of histone acetylation and gene expression required for normal hepatic lipid homeostasis. In addition, we reported that the REV-ERBα paralog, REV- ERBβ also displays circadian binding similar to that of REV-ERBα. -
Circadian Modulation of Genome-Wide Rxr Binding in Mouse Liver Tissue
Unicentre CH-1015 Lausanne http://serval.unil.ch Year : 2019 CIRCADIAN MODULATION OF GENOME-WIDE RXR BINDING IN MOUSE LIVER TISSUE Trang Khanh Bao Trang Khanh Bao, 2019, CIRCADIAN MODULATION OF GENOME-WIDE RXR BINDING IN MOUSE LIVER TISSUE Originally published at : Thesis, University of Lausanne Posted at the University of Lausanne Open Archive http://serval.unil.ch Document URN : urn:nbn:ch:serval-BIB_C4CE7516215F0 Droits d’auteur L'Université de Lausanne attire expressément l'attention des utilisateurs sur le fait que tous les documents publiés dans l'Archive SERVAL sont protégés par le droit d'auteur, conformément à la loi fédérale sur le droit d'auteur et les droits voisins (LDA). A ce titre, il est indispensable d'obtenir le consentement préalable de l'auteur et/ou de l’éditeur avant toute utilisation d'une oeuvre ou d'une partie d'une oeuvre ne relevant pas d'une utilisation à des fins personnelles au sens de la LDA (art. 19, al. 1 lettre a). A défaut, tout contrevenant s'expose aux sanctions prévues par cette loi. Nous déclinons toute responsabilité en la matière. Copyright The University of Lausanne expressly draws the attention of users to the fact that all documents published in the SERVAL Archive are protected by copyright in accordance with federal law on copyright and similar rights (LDA). Accordingly it is indispensable to obtain prior consent from the author and/or publisher before any use of a work or part of a work for purposes other than personal use within the meaning of LDA (art. 19, para. -
Nuclear Security Today
The History and Future of Planetary Threats: Nuclear Security Today Welcome LEE BOLLINGER Speaker ERNEST J. MONIZ Panelists ROBERT JERVIS KEREN YARHI-MILO DAVID BRENNER Moderators WILMOT G. JAMES ALEX N. HALLIDAY THE WORLD FACES THE HIGHEST RISK of use of a nuclear weapon since the Cuban Mis- sile Crisis, largely due to heightened concern about the potential for blunder or miscalculation. In a virtual event held on 17 November 2020, former Secretary of Energy and Co-Chair and Chief Executive Officer of the Nuclear Threat Initiative Ernest J. Moniz discussed today’s nu- clear challenges—and the urgent need to return to diplomacy, diligence, and both technologi- cal and policy innovation to reduce these threats. The webinar was co-sponsored by the Insti- tute for Social and Economic Research and Policy (ISERP), Columbia University’s Earth Insti- tute, Columbia University’s Programs in Global Health at the Vagelos College of Physicians and Surgeons, and The Academy of Political Science. The webinar was the first inaugural event of The History and Future of Planetary Threats series. In this series, ISERP convenes meetings to examine the history of, as well as contempo- rary catastrophic risks and hazards, whether natural, accident or deliberate, in the following domains: geological, biological, epidemic infectious disease, environmental, chemical, extreme weather, radiological and nuclear, or combinations of these. By catastrophic we understand to mean classes of events that could lead to sudden, extraordinary, widespread disaster beyond the collective capacity of national and international organizations and the private sector to control, causing severe disruptions in normal social functioning, heavy tolls in terms of mor- bidity and mortality, and major economic losses; in sum, events that may well cause a change in the direction of history. -
Retinoid-Induced Apoptosis in Normal and Neoplastic Tissues
Cell Death and Differentiation (1998) 5, 11 ± 19 1998 Stockton Press All rights reserved 13509047/98 $12.00 Review Retinoid-induced apoptosis in normal and neoplastic tissues Laszlo Nagy1,3,4, Vilmos A. Thomazy1, Richard A. Heyman2 retinoic acid receptor (RAR), which belongs to the superfamily and Peter J.A. Davies1,3 of ligand-activated transcription factors (nuclear receptors) revolutionized our understanding as to how retinoids exert 1 Department of Pharmacology, University of Texas-Houston, Medical School, their pleiotropic effects (for reviews see Chambon (1996); Houston, Texas 77225 USA Mangelsdorf et al (1994)). Members of the nuclear receptor 2 Ligand Pharmaceuticals, San Diego, California, 92121 USA superfamily mediate the biological effects of many hormones, 3 Corresponding author: PJAD, tel: 713-500-7480; fax: 713-500-7455; vitamins and drugs (i.e. steroid hormones, thyroid hormones, e-mail: [email protected] 4 vitamin D, prostaglandin-J (PG-J ) and drugs that activate Present address for correspondence: The Salk Institute for Biological Studies, 2 2 Gene Expression Laboratory, La Jolla, California 92037; peroxisomal proliferation). There are two families of retinoid tel: (619) 453-4100 fax:(619) 455-1349; e-mail: [email protected] receptors, Retinoid X Receptors (RXRs) that bind 9-cis retinoic acid (9-cis RA) and Retinoic Acid Receptors (RARs) Received 18.8.97; revised 19.9.97; accepted 22.9.97 that bind both 9-cis RA and all-trans retinoic acid (ATRA) (for Edited by M. Piacentini reviews see Chambon 1996; Mangelsdorf et al, 1994)). Each of these receptor families includes at least three distinct genes, (RARa,b and g; RXRa,b and g) that through differential Abstract promoter usage and alternative splicing, give rise to a large number of distinct retinoid receptor proteins (for reviews see Vitamin A and its derivatives (collectively referred to as Chambon 1996; Mangelsdorf et al, 1994). -
Retinoid X Receptor Is Necessary to Establish the S-Opsin Gradient In
Retinoid X Receptor ␥ Is Necessary to Establish the S-opsin Gradient in Cone Photoreceptors of the Developing Mouse Retina Melanie R. Roberts,1,2 Anita Hendrickson,2 Christopher R. McGuire,2 and Thomas A. Reh2 PURPOSE. The retinoid X receptors (RXRs) are members of the tion, they also have demonstrated some isoform-specific family of ligand-dependent nuclear hormone receptors. One of functions. For example, RXR␣ heterodimerizes with retinoic these genes, RXR␥, is expressed in highly restricted regions of acid receptors (RARs) to regulate retinal growth and cardiac the developing central nervous system (CNS), including the development.4 retina. Although previous studies have localized RXR␥ to de- Although all three isoforms are expressed in the developing veloping cone photoreceptors in several species, its function nervous system, RXR␥ has the most restricted and develop- in these cells is unknown. A prior study showed that thyroid mentally regulated expression. It is expressed in the develop- hormone receptor 2 (TR2) is necessary to establish proper ing striatum, part of the tegmentum, the pituitary, the ventral cone patterning in mice by activating medium-wavelength (M) horns of the spinal cord,3,5 and the retina.6 RXR␥-null mice cone opsin and suppressing short-wavelength (S) cone opsin. show isoform-specific defects in both striatal and hippocampal Thyroid hormone receptors often regulate gene transcription function, although RXR can partially compensate for the loss as heterodimeric complexes with RXRs. of RXR␥ in the striatum.2,7,8 RXR␥ has also been identified in 6,9,10 METHODS. To determine whether RXR␥ cooperates with TR2 the developing retina of Xenopus, chicks, and mice. -
Multi-Omics Signatures and Translational Potential to Improve Thyroid Cancer Patient Outcome
cancers Review Multi-omics Signatures and Translational Potential to Improve Thyroid Cancer Patient Outcome Myriem Boufraqech and Naris Nilubol * Surgical Oncology Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20817, USA; [email protected] * Correspondence: [email protected] Received: 13 November 2019; Accepted: 3 December 2019; Published: 10 December 2019 Abstract: Recent advances in high-throughput molecular and multi-omics technologies have improved our understanding of the molecular changes associated with thyroid cancer initiation and progression. The translation into clinical use based on molecular profiling of thyroid tumors has allowed a significant improvement in patient risk stratification and in the identification of targeted therapies, and thereby better personalized disease management and outcome. This review compiles the following: (1) the major molecular alterations of the genome, epigenome, transcriptome, proteome, and metabolome found in all subtypes of thyroid cancer, thus demonstrating the complexity of these tumors and (2) the great translational potential of multi-omics studies to improve patient outcome. Keywords: genomic; proteomic; methylation; microRNA; thyroid cancer 1. Introduction The incidence of thyroid cancer has been increasing by almost 300% in the past four decades with an estimated 54,000 patients diagnosed each year in the United States [1]. Thyroid cancer is the fifth most common cancer in women. Earlier data has suggested that the rising incidence of thyroid cancer has been due to the increased detection of small, commonly incidental, and subclinical papillary thyroid cancer (PTC) with indolent behavior [1–4], however, the more recent analysis of the Surveillance, Epidemiology, and End Results (SEER) cancer registry data has shown an increase in advanced-stage PTC and PTC larger than 5 cm which were believed to be clinically detectable or were symptomatic [5]. -
Nuclear Receptor Regulation of a Luminal Breast
NUCLEAR RECEPTOR REGULATION OF A LUMINAL BREAST CANCER STEM CELL POPULATION by LYNSEY MAE FETTIG B.A., University of North Dakota, 2009 B.S., University of Minnesota, 2011 A thesis submitted to the Faculty of the Graduate School of the University of Colorado in partial fulfillment of the requirements for the degree of Doctor of Philosophy Cancer Biology Program 2019 This thesis for the Doctor of Philosophy degree by Lynsey Mae Fettig has been approved for the Cancer Biology Program by Rebecca Schweppe, Chair David Bentley Peter Kabos Maranke Koster Diana Cittelly Jennifer Richer Carol A. Sartorius, Advisor Date: May 17, 2019 ii Fettig, Lynsey Mae (Ph.D., Cancer Biology) Nuclear Receptor Regulation of a Luminal Breast Cancer Stem Cell Population Thesis directed by Professor Carol A. Sartorius ABSTRACT Crosstalk between nuclear receptors is emerging as important in regulating breast cancer (BC) treatment response and progression. Estrogen receptor (ER), progesterone receptor (PR), and retinoic acid receptor (RARα) are all co-expressed in luminal subtype BCs that are generally associated with good prognosis. This is mainly due to the success of endocrine therapies targeting ER. However, eventual resistance to endocrine therapy is a long-standing clinical problem that affects ~30% of patients. About half of all luminal tumors contain subpopulations of ER negative cells that express cytokeratin 5 (CK5). CK5+ cells exhibit cancer stem cell (CSC) properties such as resistance to chemo- and endocrine therapies, and enhanced tumor initiating potential. In previous work we identified that progesterone (P4) expands the population of CK5+ BC cells and that retinoids block such expansion. -
Similarities and Differences in the Transcriptional Control of Expression
Similarities and differences in the transcriptional PNAS PLUS control of expression of the mouse TSLP gene in skin epidermis and intestinal epithelium Krishna Priya Gantia,b,c, Atish Mukherjia,b,c,1, Milan Surjita,b,c,d,1, Mei Lia,b, and Pierre Chambona,b,c,2 aInstitut de Génétique et de Biologie Moléculaire et Cellulaire (CNRS UMR7104, INSERM U964), Illkirch 67404, France; bUniversity of Strasbourg Institute for Advanced Study, F-67083 Strasbourg, France; cCollège de France, 75005 Paris, France; and dTranslational Health Science and Technology Institute, National Capital Region Biotech Science Cluster, Faridabad-121001, India Contributed by Pierre Chambon, December 20, 2016 (sent for review November 18, 2016; reviewed by Christophe Benoist, Didier Picard, and Filippo M. Rijli) We previously reported that selective ablation of the nuclear corepressor-bound unliganded RXR-α (or RXR-β)/VDR and receptors retinoid X receptor (RXR)-α and RXR-β in mouse epidermal RXR-α (or RXR-β)/RAR-γ heterodimers bound to VDR and keratinocytes (RXR-αβep−/−) or a topical application of active vitamin RAR response elements (VDRE and RARE, respectively). Thus, D3 (VD3) and/or all-trans retinoic acid (RA) on wild-type mouse skin RXR-α and RXR-β ablations, which release both heterodimers induces a human atopic dermatitis-like phenotype that is triggered from their DBS, might abolish repression and allow other pro- by an increased expression of the thymic stromal lymphopoietin moter-bound transcription factors (TFs) to stimulate TSLP tran- (TSLP) proinflammatory