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ASM Journals Eliminate Impact Factor Information from Journal Websites
ASM Journals Eliminate Impact Factor Information from Journal Websites The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Casadevall, A., S. Bertuzzi, M. J. Buchmeier, R. J. Davis, H. Drake, F. C. Fang, J. Gilbert, et al. 2016. “ASM Journals Eliminate Impact Factor Information from Journal Websites.” mSphere 1 (4): e00184-16. doi:10.1128/mSphere.00184-16. http:// dx.doi.org/10.1128/mSphere.00184-16. Published Version doi:10.1128/mSphere.00184-16 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:27822275 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 EDITORIAL crossmark ASM Journals Eliminate Impact Factor Information from Journal Websites Arturo Casadevall,a Editor in Chief, mBio®, Stefano Bertuzzi,b Chief Executive Officer, ASM, Michael J. Buchmeier,c Editor in Chief, Microbiology and Molecular Biology Reviews®, Roger J. Davis,d Editor in Chief, Molecular and Cellular Biology®, Harold Drake,e Editor in Chief, Applied and Environmental Microbiology®, Ferric C. Fang,f Editor in Chief, Infection and Immunity®, Jack Gilbert,g Editor in Chief, mSystems™, Barbara M. Goldman,b Director, Journals, ASM, Michael J. Imperiale,h Editor in Chief, mSphere™, Philip Matsumura,i Editor, Genome Announcements™, Alexander J. McAdam,j Editor in Chief, Journal of Clinical Microbiology®, Marcela F. Pasetti,k Editor in Chief, Clinical and Vaccine Immunology®, Rozanne M. -
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. -
Clinical Molecular Genetics in the Uk C.1975–C.2000
CLINICAL MOLECULAR GENETICS IN THE UK c.1975–c.2000 The transcript of a Witness Seminar held by the History of Modern Biomedicine Research Group, Queen Mary, University of London, on 5 February 2013 Edited by E M Jones and E M Tansey Volume 48 2014 ©The Trustee of the Wellcome Trust, London, 2014 First published by Queen Mary, University of London, 2014 The History of Modern Biomedicine Research Group is funded by the Wellcome Trust, which is a registered charity, no. 210183. ISBN 978 0 90223 888 6 All volumes are freely available online at www.history.qmul.ac.uk/research/modbiomed/ wellcome_witnesses/ Please cite as: Jones E M, Tansey E M. (eds) (2014) Clinical Molecular Genetics in the UK c.1975–c.2000. Wellcome Witnesses to Contemporary Medicine, vol. 48. London: Queen Mary, University of London. CONTENTS What is a Witness Seminar? v Acknowledgements E M Tansey and E M Jones vii Illustrations and credits ix Abbreviations xi Ancillary guides xiii Introduction Professor Bob Williamson xv Transcript Edited by E M Jones and E M Tansey 1 Appendix 1 Photograph, with key, of delegates attending The Molecular Biology of Thalassaemia conference in Kolimbari, Crete, 1978 88 Appendix 2 Extracts from the University of Leiden postgraduate course Restriction Fragment Length Polymorphisms and Human Genetics, 1982 91 Appendix 3 Archival material of the Clinical Molecular Genetics Society 95 Biographical notes 101 References 113 Index 131 Witness Seminars: Meetings and Publications 143 WHAT IS A WITNESS SEMINAR? The Witness Seminar is a specialized form of oral history, where several individuals associated with a particular set of circumstances or events are invited to meet together to discuss, debate, and agree or disagree about their memories. -
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. -
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. -
Holmes Washington 0250E 22
©Copyright 2020 Daniel Holmes Identification of Targetable Vulnerabilities During Latent KSHV Infection Daniel Holmes A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy University of Washington 2020 Reading Committee: Michael Lagunoff, Chair Adam Philip Geballe Jason G Smith Program Authorized to Offer Degree: Department of Microbiology University of Washington Abstract Identification of Targetable Vulnerabilities During Latent KSHV Infection Daniel Holmes Chair of the Supervisory Committee: Professor Michael Lagunoff Department of Microbiology Viruses are defined as obligate intracellular parasites that require host processes to repli- cate. Latent virus life cycles are no exception to this definition, as viruses are still reliant on host machinery for continued proliferation and maintenance of viral genomes, even in the absence of lytic replication. In this thesis, I used essentiality screening to identify host factors on which Kaposi's Sarcoma Associated Herpesvirus (KSHV) relies for the proliferation and survival of latently infected cells. KSHV is the etiological agent of Kaposi's Sarcoma (KS), an endothelial cell-based tumor where more than 90% of the endothelial cells in the tumor are latently infected with KSHV. While traditional therapies for herpesviruses target lytic replication, the prevalence of latency in KS necessitates exploration of options for intervening in this stage of the viral life cycle. I performed CRISPR/Cas9 screening using lentiviral vec- tors encoding a library of single guide RNAs (sgRNAs) targeting every protein coding gene in the human genome. I compared mock infected and KSHV infected endothelial cells eight days post infection to identify genes essential to latent KSHV infection. -
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. -
Historischer Abriss
Historischer Abriss 1970 Geschichte der Zellbiologie im Überblick Entdeckung der reversen Transkription durch H. (Kapitel 1.1) Temin und D. Baitimare 17. Jahrhundert 1972 Bezeichnung der porenartigen Strukturen des Fluid-mosaic-Modell der Zellmembran (S. Singer Korks als "Zellen" durch R. Hooke und G. Nicholson) Identifizierung von Amöben und Bakterien im 1973 durch A. van Leeuwenhoek Mikroskop Erstes rekombinantes DNA-Molekül 1838 1975 Entdeckung, dass Pflanzen aus Zellen aufgebaut Erzeugung von monoklonalen Antikörpern durch sind (M. Schleiden) C. Milstein und G. Köhler 1839 1976 Beschreibung der Zelle als strukturelle Einheit des Entdeckung des v-src-Onkogens durch H. Varmus Lebens durch T. Schwann und M. Bishop Um 1850 Aufklärung des Rearrangements von Immunglobu Mendel-Vererbungsgesetze lingenen durch S. Tonegawa 1855 1977 Erkenntnis, dass Zellen nur durch Teilung aus an Entdeckung der rezeptorvermittelten Endozytose deren Zellen entstehen (R . Virchow) durch M. Brown und ]. Goldstein 1911 1980 Tumorinduktion durch Viren (P. Rous) Isolierung von G-Proteinen durch A. Gilman 1945 1982 Erstes elektronenmikroskopisches Bild einer intak Prionenhypothese von S. Prusiner ten Zelle durch K. R. Porter, A. Claude und E. F. DNA-Sequenzierungsmethoden nach Sanger und Fullam Gilbert 1951 1983 Erste In-vitro-Kultur von humanen Zellen durch Erfindung der Polymerasekettenreaktionsmethode G. Gey (HeLa) durch K. Mullis 1953 1989 Modell der DNA-Doppelhelix durch]. Watson und Erzeugung von Knockout-Mäusen durch M. Cap F. Crick pechi 1961 1996 Entschlüsselung des genetischen Kodes durch M. Verwendung DNA-Mikroarrays zur Analyse der Nirenberg Genexpression Operon Modell von F. ]acob und ]. Monod Chemiosmotische Theorie der oxidativen Phospho 2000 rylierung von P. Mitchell Vollständige Sequenz des humanen Genoms Ganten I Ruckpaul (Hrsg.) Grundlagen der Molekularen Medizin, 2. -
B I O T E C H I N T H E S U N S H I N E S T A
BIOTECH IN THE SUNSHINE STATE December 2009 American Society for Biochemistry and Molecular Biology ASBMB2011 SPECIAL SYMPOSIA CALL FOR PROPOSALS Partner with the American Society for Biochemistry and Molecular Biology to bring your community together! ASBMB Special Symposia provides you, as a specialized researcher, a unique opportunity to present cutting-edge science mixed with active networking opportunities in an intimate setting. How We’re Different: Format: Majority of talks selected from abstracts, invited speakers, 2-4 days in length Attendee: 60- 200 attendees, including investigators, industry professionals, graduate and postdoctoral students Venues: Unique locations near natural resources that enable time for outdoor recreation and networking opportunities Funding: ASBMB provides initial funding as well as staff support! Learn More About Special Symposia and Proposal Submission Guidelines at www.asbmb.org/meetings Proposals Due March 1, 2010 ATodayFullPageAd_2011_Proposal Submission2.indd 1 11/23/2009 10:50:10 AM contents DECEMBER 2009 On the cover: ASBMB hopes that your holidays are filled with society news lots of serotonin. 2 Letters to the Editor IMAGE: REBECCA HANNA 20 4 President’s Message 7 Washington Update 8 News from the Hill 11 Member Spotlight 12 Retrospective: Mahlon Hoagland (1921-2009) A retrospective 15 Retrospective: on Mahlon Charles Tanford (1921-2009) Hoagland. 12 2010 annual meeting 18 Nobel Laureate Claims the 2010 Herbert Tabor Lectureship 19 Kinase Researcher Named Recipient of FASEB Award special interest 20 Centerpieces: Burnham Institute Touches Down in Orlando departments 26 Education and Training Regulating 30 Minority Affairs transcriptional activity. 32 BioBits 32 34 Career Insights 36 Lipid News resources Scientific Meeting Calendar podcast summary online only Check out the latest ASBMB podcast, in which Journal of Biological Chemistry Associate Editor James N. -
Can a Virus Cause Cancer: a Look Into the History and Significance of Oncoviruses
UC Berkeley Berkeley Scientific Journal Title Can A Virus Cause Cancer: A Look Into The History And Significance Of Oncoviruses Permalink https://escholarship.org/uc/item/6c57612p Journal Berkeley Scientific Journal, 14(1) ISSN 1097-0967 Author Rwazavian, Niema Publication Date 2011 DOI 10.5070/BS3141007638 Peer reviewed|Undergraduate eScholarship.org Powered by the California Digital Library University of California CA N A VIRU S CA U S E CA NCER ? A LOOK IN T O T HE HI st ORY A ND SIGNIFIC A NCE OF ONCO V IRU S E S Niema Rwazavian The IMPORTANC E OF ONCOVIRUS E S (van Epps 2005). Although many in the scientific Cancer, a disease caused by unregulated cell community were unconvinced of the role of viruses in growth, is often attributed to chemical carcinogens cancer, research on the subject nevertheless continued. (e.g. tobacco), hormonal imbalances (e.g. high levels of In 1933, Richard Shope discovered the first mammalian estrogen), or genetics (e.g. breast cancer susceptibility oncovirus, cottontail rabbit papillomavirus (CRPV), gene 1). While cancer can originate from any number which could infect cottontail rabbits, and in 1936, John of sources, many people fail to recognize another Bittner discovered the mouse mammary tumor virus important etiology: oncoviruses, or cancer-causing (MMTV), which could be transmitted from mothers to pups via breast milk (Javier and Butle 2008). By the 1960s, with the additional “…despite limited awareness, oncoviruses are discovery of the murine leukemia BSJ virus (MLV) in mice and the SV40 nevertheless important because they represent virus in rhesus monkeys, researchers over 17% of the global cancer burden.” began to acknowledge the possibility that viruses could be linked to human cancers as well. -
Editors' Statement on Considerations of Biodefence and Biosecurity
EDITORIAL Editors’ statement on considerations of biodefence and biosecurity The threat of bioterrorism requires active consideration by scientists. On 9 January 2003, the US National Academy of Sciences held a discussion on the balance between scientific openness and security. The next day, a group of editors met to discuss the issues with specific reference to the scientific publication process. The following statement has emerged from that meeting. The principles dis- cussed will be considered and followed through by Nature Medicine The process of scientific publication, is a view, shared by nearly all, that there is FOURTH: We recognize that on occasions through which new findings are reviewed information that, although we cannot an editor may conclude that the potential for quality and then presented to the rest now capture it with lists or definitions, harm of publication outweighs the poten- of the scientific community and the pub- presents enough risk of use by terrorists tial societal benefits. Under such circum- lic, is a vital element in our national life. that it should not be published. How and stances, the paper should be modified, or New discoveries reported in research pa- by what processes it might be identified not be published. Scientific information is pers have helped improve the human con- will continue to challenge us, because – as also communicated by other means: semi- dition in myriad ways: protecting public all present acknowledged — it is also true nars, meetings, electronic posting, etc. health, multiplying agricultural yields, that open publication brings benefits not Journals and scientific societies can play fostering technological development and only to public health but also in efforts to an important role in encouraging investi- economic growth, and enhancing global combat terrorism.