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Cell Circuitry || Science Teaches English || The Chicken Genome Is Hot || Magnets in Medicine SEPTEMBER 2002 www.hhmi.org/bulletin Leading Doublea Life It’s a stretch, but doctors who work bench to bedside say they wouldn’t do it any other way. FEATURES 14 On Human Terms 24 The Evolutionary War A small—some say too small—group of Efforts to undermine evolution education have physician-scientists believes the best science evolved into a 21st-century marketing cam- requires patient contact. paign that relies on legal acumen, manipulation By Marlene Cimons of scientific literature and grassroots tactics. 20 Engineering the Cell By Trisha Gura Adam Arkin sees the cell as a mechanical system. He hopes to transform molecular 28 Call of the Wild biology into a kind of cellular engineering Could quirky, new animal models help scien- and in the process, learn how to move cells tists learn how to regenerate human limbs or from sickness to health. avert the debilitating effects of a stroke? By M. Mitchell Waldrop By Kathryn Brown 24 In front of a crowd of 1,500, Ohio’s Board of Education heard testimony on whether students should learn about intelligent design in science class. DEPARTMENTS 2 NOTA BENE 33 PERSPECTIVE ulletin Intelligent Design Is a Cop-Out 4 LETTERS September 2002 || Volume 15 Number 3 NEWS AND NOTES HHMI TRUSTEES PRESIDENT’S LETTER 5 JAMES A. BAKER, III, ESQ. 34 Senior Partner, Baker & Botts A Creative Influence In from the Fields ALEXANDER G. BEARN, M.D. Executive Officer, American Philosophical Society 35 Lost on the Tip of the Tongue Adjunct Professor, The Rockefeller University UP FRONT Professor Emeritus of Medicine, Cornell University Medical College 36 Biology by Numbers FRANK WILLIAM GAY 6 Follow the Songbird Former President and Chief Executive Officer, SUMMA Corporation JAMES H. -
The Role of Hepatitis C Virus in Hepatocellular Carcinoma U
Viruses in cancer cell plasticity: the role of hepatitis C virus in hepatocellular carcinoma U. Hibner, D. Gregoire To cite this version: U. Hibner, D. Gregoire. Viruses in cancer cell plasticity: the role of hepatitis C virus in hepato- cellular carcinoma. Contemporary Oncology, Termedia Publishing House, 2015, 19 (1A), pp.A62–7. 10.5114/wo.2014.47132. hal-02187396 HAL Id: hal-02187396 https://hal.archives-ouvertes.fr/hal-02187396 Submitted on 2 Jun 2021 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Distributed under a Creative Commons Attribution - NonCommercial - ShareAlike| 4.0 International License Review Viruses are considered as causative agents of a significant proportion of human cancers. While the very Viruses in cancer cell plasticity: stringent criteria used for their clas- sification probably lead to an under- estimation, only six human viruses the role of hepatitis C virus are currently classified as oncogenic. In this review we give a brief histor- in hepatocellular carcinoma ical account of the discovery of on- cogenic viruses and then analyse the mechanisms underlying the infectious causes of cancer. We discuss viral strategies that evolved to ensure vi- Urszula Hibner1,2,3, Damien Grégoire1,2,3 rus propagation and spread can alter cellular homeostasis in a way that increases the probability of oncogen- 1Institut de Génétique Moléculaire de Montpellier, CNRS, UMR 5535, Montpellier, France ic transformation and acquisition of 2Université Montpellier 2, Montpellier, France stem cell phenotype. -
Medical Advisory Board September 1, 2006–August 31, 2007
hoWard hughes medical iNstitute 2007 annual report What’s Next h o W ard hughes medical i 4000 oNes Bridge road chevy chase, marylaNd 20815-6789 www.hhmi.org N stitute 2007 a nn ual report What’s Next Letter from the president 2 The primary purpose and objective of the conversation: wiLLiam r. Lummis 6 Howard Hughes Medical Institute shall be the promotion of human knowledge within the CREDITS thiNkiNg field of the basic sciences (principally the field of like medical research and education) and the a scieNtist 8 effective application thereof for the benefit of mankind. Page 1 Page 25 Page 43 Page 50 seeiNg Illustration by Riccardo Vecchio Südhof: Paul Fetters; Fuchs: Janelia Farm lab: © Photography Neurotoxin (Brunger & Chapman): Page 3 Matthew Septimus; SCNT images: by Brad Feinknopf; First level of Rongsheng Jin and Axel Brunger; iN Bruce Weller Blake Porch and Chris Vargas/HHMI lab building: © Photography by Shadlen: Paul Fetters; Mouse Page 6 Page 26 Brad Feinknopf (Tsai): Li-Huei Tsai; Zoghbi: Agapito NeW Illustration by Riccardo Vecchio Arabidopsis: Laboratory of Joanne Page 44 Sanchez/Baylor College 14 Page 8 Chory; Chory: Courtesy of Salk Janelia Farm guest housing: © Jeff Page 51 Ways Illustration by Riccardo Vecchio Institute Goldberg/Esto; Dudman: Matthew Szostak: Mark Wilson; Evans: Fred Page 10 Page 27 Septimus; Lee: Oliver Wien; Greaves/PR Newswire, © HHMI; Mello: Erika Larsen; Hannon: Zack Rosenthal: Paul Fetters; Students: Leonardo: Paul Fetters; Riddiford: Steitz: Harold Shapiro; Lefkowitz: capacity Seckler/AP, © HHMI; Lowe: Zack Paul Fetters; Map: Reprinted by Paul Fetters; Truman: Paul Fetters Stewart Waller/PR Newswire, Seckler/AP, © HHMI permission from Macmillan Page 46 © HHMI for Page 12 Publishers, Ltd.: Nature vol. -
The Role of Model Organisms in the History of Mitosis Research
Downloaded from http://cshperspectives.cshlp.org/ on September 30, 2021 - Published by Cold Spring Harbor Laboratory Press The Role of Model Organisms in the History of Mitosis Research Mitsuhiro Yanagida Okinawa Institute of Science and Technology Graduate University, Okinawa 904-0495, Japan Correspondence: [email protected] Mitosis is a cell-cycle stage during which condensed chromosomes migrate to the middle of the cell and segregate into two daughter nuclei before cytokinesis (cell division) with the aid of a dynamic mitotic spindle. The history of mitosis research is quite long, commencing well before the discovery of DNA as the repository of genetic information. However, great and rapid progress has been made since the introduction of recombinant DNA technology and discovery of universal cell-cycle control. A large number of conserved eukaryotic genes required for the progression from early to late mitotic stages have been discovered, confirm- ing that DNA replication and mitosis are the two main events in the cell-division cycle. In this article, a historical overview of mitosis is given, emphasizing the importance of diverse model organisms that have been used to solve fundamental questions about mitosis. Onko Chisin—An attempt to discover new truths by checkpoint [SAC]), then metaphase (in which studying the past through scrutiny of the old. the chromosomes are aligned in the middle of cell), anaphase A (in which identical sister chro- matids comprising individual chromosomes LARGE SALAMANDER CHROMOSOMES separate and move toward opposite poles of ENABLED THE FIRST DESCRIPTION the cell), anaphase B (in which the spindle elon- OF MITOSIS gates as the chromosomes approach the poles), itosis means “thread” in Greek. -
Gurdon Institute 20122011 PROSPECTUS / ANNUAL REPORT 20112010
The Wellcome Trust/Cancer Research UK Gurdon Institute 20122011 PROSPECTUS / ANNUAL REPORT 20112010 Gurdon I N S T I T U T E PROSPECTUS 2012 ANNUAL REPORT 2011 http://www.gurdon.cam.ac.uk CONTENTS THE INSTITUTE IN 2011 INTRODUCTION........................................................................................................................................3 HISTORICAL BACKGROUND..........................................................................................................4 CENTRAL SUPPORT SERVICES....................................................................................................5 FUNDING.........................................................................................................................................................5 RETREAT............................................................................................................................................................5 RESEARCH GROUPS.........................................................................................................6 MEMBERS OF THE INSTITUTE................................................................................44 CATEGORIES OF APPOINTMENT..............................................................................44 POSTGRADUATE OPPORTUNITIES..........................................................................44 SENIOR GROUP LEADERS.............................................................................................44 GROUP LEADERS.......................................................................................................................48 -
Sensitive Detection of Oncoviruses Integrated Into a Comprehensive Tumor Immuno-Genomics Platform #3788
Sensitive detection of oncoviruses integrated into a comprehensive tumor immuno-genomics platform #3788 Gábor Bartha, Robin Li, Shujun Luo, John West, Richard Chen Personalis, Inc. | 1330 O’Brien Dr., Menlo Park, CA 94025 Contact: [email protected] Introduction Results Mixed Oncoviral Cell Lines We obtained 22 cell lines from ATCC containing HPV16, HPV18, HPV45, HPV68, HBV, EBV, KSHV, HTLV1 and HTLV2 in which the oncoviruses HPV, HBV, HCV and EBV viruses are causally EBV Cell Lines were known to be in the tumors from which the cell lines were created. In the ATCC samples we detected 23 out of 23 oncoviruses expected in linked to over 11% of cancers worldwide while both the DNA and RNA. We detected all the different types of oncoviruses that we targeted except for HCV because it wasn’t in any sample. In all KSHV, HTLV and MCV are linked to an additional To test the ability of the platform to detect oncoviruses, we identified a set of 11 EBV cell lines from but one case the signals were strong. 1%. As use of immunotherapy expands to a Coriell in which EBV was used as a transformant. We detected EBV in all the Coriell cell lines in both broader variety of cancers, it is important to DNA and RNA indicating strong sensitivity of the platform. Wide dynamic ranGe suggests quantification Detected in DNA Detected in RNA Virus Tissue Notes understand how these oncoviruses may be may be possible as well. In the DNA and RNA there were no detections of any other oncovirus EBV EBV EBV HodGkin’s lymphoma Per ATCC : “The cells are EBNA positive" indicating high specificity. -
Nucleotide Sequences in Mouse DNA and RNA Specific for Moloney Sarcoma Virus
Proc. Nati. Acad. Sci. USA Vol. 73, No. 10, pp. 3705-3709, October 1976 Microbiology Nucleotide sequences in mouse DNA and RNA specific for Moloney sarcoma virus (murine sarcoma virus/RNA tumor virus/nucleic acid hybridization/gene evolution/sarcoma-specific nucleotide sequence) ARTHUR E. FRANKEL AND PETER J. FISCHINGER Laboratory of Viral Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20014 Communicated by Howard M. Temin, July 12,1976 ABSTRACT Complementary DNA (cDNA) synthesized (3). Laboratory strains of oncoviruses do contain information by Moloney murine sarcoma virus (M-MSV) was separated into that is different from the spontaneously released oncovirus of two parts, the first, termed MSV-specific cDNA, composed of the species Of nucleotide sequences found only in M-MSV viral RNA, and the (6, 7). these, the sarcomagenic oncoviruses gen- second, termed MSV-MuLV common cDNA, composed of nu- erally contain both a set of nucleotide sequences shared with cleotide sequences that were found in both M-MSV and murine leukosis-leukemia viruses, and another set of sequences that are leukemia virus (MuLV) viral RNAs. RNA complementary to the dissimilar from those of other oncoviruses of the species (6-10). MSV-specific cDNA was not found in several other MSV iso- Complementary DNA (cDNA) can be transcribed from sar- lates, nor in ecotropic MuLV, mouse mammary tumor virus, or coma virus RNA by the viral endogenous DNA polymerase. several murine xenotropic oncoviruses. Cellular DNA of several The cDNA represents both the "shared" and the species was examined for the presence of nucleotide sequences "specific" complementary to MSV-specific cDNA. Cells transformed by moieties of the sarcoma virus genome. -
Ordered Proteolysis in Anaphase Inactivates Plk1 To
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by PubMed Central JCBArticle Ordered proteolysis in anaphase inactivates Plk1 to contribute to proper mitotic exit in human cells Catherine Lindon and Jonathon Pines Wellcome Trust/Cancer Research UK Gurdon Institute and Department of Zoology, University of Cambridge, Cambridge CB2 1QR, England, UK e have found that key mitotic regulators show identified a putative destruction box in Plk1 that is required distinct patterns of degradation during exit from for degradation of Plk1 in anaphase, and have examined W mitosis in human cells. Using a live-cell assay for the effect of nondegradable Plk1 on mitotic exit. Our results proteolysis, we show that two of these regulators, polo-like show that Plk1 proteolysis contributes to the inactivation of kinase 1 (Plk1) and Aurora A, are degraded at different Plk1 in anaphase, and that this is required for the proper times after the anaphase-promoting complex/cyclosome control of mitotic exit and cytokinesis. Our experiments (APC/C) switches from binding Cdc20 to Cdh1. Therefore, reveal a role for APC/C-mediated proteolysis in exit from events in addition to the switch from Cdc20 to Cdh1 control mitosis in human cells. the proteolysis of APC/CCdh1 substrates in vivo. We have Introduction In animal cells, the regulated proteolysis of cyclin A, cyclin APC/C switches from its Cdc20- to Cdh1-activated form, or B1, and securin during mitosis are all essential for the proper whether they are degraded at distinct times, perhaps to coor- timing of events leading up to separation of sister chromatids dinate exit from mitosis. -
2007 Keio Medical Science Prize Winner Announcement
FOR IMMEDIATE RELEASE http://www.keio.ac.jp/ September 26, 2007 2007 Keio Medical Science Prize Winner Announcement Keio University presents the “Keio Medical Science Prize” to researchers in recognition of their outstanding achievements in the fields of medical or life sciences. It is the only prize of its kind to be awarded by a Japanese university. The 12th Keio Medical Science Prize will be awarded to Dr. Brian J. Druker and Dr. Hiroaki Mitsuya. Brian J. Druker, M.D. Investigator, Howard Hughes Medical Institute Director, Oregon Health & Science University Cancer Institute JELD-WEN Chair of Leukemia Research For the development of a molecular-targeted drug for chronic myelogenous leukemia Hiroaki Mitsuya, M.D., Ph.D. Professor, Department of Hematology, Department of Rheumatology and Clinical Immunology, Division of Infections Diseases, Graduate School of Medical and Pharmaceutical Sciences, Kumamoto University Chief and Principal Investigator, Experimental Retrovirology Section Center for Cancer Research National Cancer Institute For the development of anti-AIDS drugs Award Ceremony and Commemorative Symposium The award ceremony and a commemorative lecture given by the prize winners will be held on December 4, 2007 and a commemorative symposium will take place on December 5. Both events will be held at the Keio University School of Medicine (Shinanomachi Campus). Please see the contact information below to inquire about interviews or photographs. Attachments : (1) About the Keio University Medical Science Fund (2)2007 Prize Winner: Brian J. Druker(Theme, CV, other information) (3)2007 Prize Winner: Hiroaki Mitsuya(Theme, CV, other information) (4)2007 Keio Medical Science Prize Award Ceremony/Commemorative Lecture/ Commemorative Symposium Inquiries: Keio University Medical Science Fund(Ms. -
Cancer Patients Have a Higher Risk Regarding COVID-19–And Vice Versa?
pharmaceuticals Opinion Cancer Patients Have a Higher Risk Regarding COVID-19–and Vice Versa? Franz Geisslinger, Angelika M. Vollmar and Karin Bartel * Pharmaceutical Biology, Department Pharmacy, Ludwig-Maximilians-University of Munich, 81377 Munich, Germany; [email protected] (F.G.); [email protected] (A.M.V.) * Correspondence: [email protected] Received: 29 May 2020; Accepted: 3 July 2020; Published: 6 July 2020 Abstract: The world is currently suffering from a pandemic which has claimed the lives of over 230,000 people to date. The responsible virus is called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and causes the coronavirus disease 2019 (COVID-19), which is mainly characterized by fever, cough and shortness of breath. In severe cases, the disease can lead to respiratory distress syndrome and septic shock, which are mostly fatal for the patient. The severity of disease progression was hypothesized to be related to an overshooting immune response and was correlated with age and comorbidities, including cancer. A lot of research has lately been focused on the pathogenesis and acute consequences of COVID-19. However, the possibility of long-term consequences caused by viral infections which has been shown for other viruses are not to be neglected. In this regard, this opinion discusses the interplay of SARS-CoV-2 infection and cancer with special focus on the inflammatory immune response and tissue damage caused by infection. We summarize the available literature on COVID-19 suggesting an increased risk for severe disease progression in cancer patients, and we discuss the possibility that SARS-CoV-2 could contribute to cancer development. -
Human Papillomaviruses and Epstein–Barr Virus Interactions in Colorectal Cancer: a Brief Review
pathogens Review Human Papillomaviruses and Epstein–Barr Virus Interactions in Colorectal Cancer: A Brief Review 1,2, 1,2, 1, 1,2, Queenie Fernandes y, Ishita Gupta y, Semir Vranic * and Ala-Eddin Al Moustafa * 1 College of Medicine, QU Health, Qatar University, Doha 2713, Qatar; [email protected] (Q.F.); [email protected] (I.G.) 2 Biomedical Research Centre, Qatar University, Doha 2713, Qatar * Correspondence: [email protected] (S.V.); [email protected] (A.-E.A.M.); Tel.:+974-4403-7873 (S.V.); +974-4403-7817 (A.-E.A.M.) Both authors contributed equally to this review. y Received: 9 March 2020; Accepted: 7 April 2020; Published: 20 April 2020 Abstract: Human papillomaviruses (HPVs) and the Epstein–Barr virus (EBV) are the most common oncoviruses, contributing to approximately 10%–15% of all malignancies. Oncoproteins of high-risk HPVs (E5 and E6/E7), as well as EBV (LMP1, LMP2A and EBNA1), play a principal role in the onset and progression of several human carcinomas, including head and neck, cervical and colorectal. Oncoproteins of high-risk HPVs and EBV can cooperate to initiate and/or enhance epithelial-mesenchymal transition (EMT) events, which represents one of the hallmarks of cancer progression and metastasis. Although the role of these oncoviruses in several cancers is well established, their role in the pathogenesis of colorectal cancer is still nascent. This review presents an overview of the most recent advances related to the presence and role of high-risk HPVs and EBV in colorectal cancer, with an emphasis on their cooperation in colorectal carcinogenesis. -
Pnas11052ackreviewers 5098..5136
Acknowledgment of Reviewers, 2013 The PNAS editors would like to thank all the individuals who dedicated their considerable time and expertise to the journal by serving as reviewers in 2013. Their generous contribution is deeply appreciated. A Harald Ade Takaaki Akaike Heather Allen Ariel Amir Scott Aaronson Karen Adelman Katerina Akassoglou Icarus Allen Ido Amit Stuart Aaronson Zach Adelman Arne Akbar John Allen Angelika Amon Adam Abate Pia Adelroth Erol Akcay Karen Allen Hubert Amrein Abul Abbas David Adelson Mark Akeson Lisa Allen Serge Amselem Tarek Abbas Alan Aderem Anna Akhmanova Nicola Allen Derk Amsen Jonathan Abbatt Neil Adger Shizuo Akira Paul Allen Esther Amstad Shahal Abbo Noam Adir Ramesh Akkina Philip Allen I. Jonathan Amster Patrick Abbot Jess Adkins Klaus Aktories Toby Allen Ronald Amundson Albert Abbott Elizabeth Adkins-Regan Muhammad Alam James Allison Katrin Amunts Geoff Abbott Roee Admon Eric Alani Mead Allison Myron Amusia Larry Abbott Walter Adriani Pietro Alano Isabel Allona Gynheung An Nicholas Abbott Ruedi Aebersold Cedric Alaux Robin Allshire Zhiqiang An Rasha Abdel Rahman Ueli Aebi Maher Alayyoubi Abigail Allwood Ranjit Anand Zalfa Abdel-Malek Martin Aeschlimann Richard Alba Julian Allwood Beau Ances Minori Abe Ruslan Afasizhev Salim Al-Babili Eric Alm David Andelman Kathryn Abel Markus Affolter Salvatore Albani Benjamin Alman John Anderies Asa Abeliovich Dritan Agalliu Silas Alben Steven Almo Gregor Anderluh John Aber David Agard Mark Alber Douglas Almond Bogi Andersen Geoff Abers Aneel Aggarwal Reka Albert Genevieve Almouzni George Andersen Rohan Abeyaratne Anurag Agrawal R. Craig Albertson Noga Alon Gregers Andersen Susan Abmayr Arun Agrawal Roy Alcalay Uri Alon Ken Andersen Ehab Abouheif Paul Agris Antonio Alcami Claudio Alonso Olaf Andersen Soman Abraham H.