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New Insights from Elucidating the Role of LMP1 in Nasopharyngeal Carcinoma
cancers Review New Insights from Elucidating the Role of LMP1 in Nasopharyngeal Carcinoma Kathy H. Y. Shair 1,2,*, Akhil Reddy 1 and Vaughn S. Cooper 2 ID 1 Cancer Virology Program, University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA; [email protected] 2 Department of Microbiology and Molecular Genetics, and Center for Evolutionary Biology and Medicine, University of Pittsburgh, Pittsburgh, PA 15219, USA; [email protected] * Correspondence: [email protected]; Tel.: +1-412-623-7717 Received: 3 March 2018; Accepted: 20 March 2018; Published: 21 March 2018 Abstract: Latent membrane protein 1 (LMP1) is an Epstein-Barr virus (EBV) oncogenic protein that has no intrinsic enzymatic activity or sequence homology to cellular or viral proteins. The oncogenic potential of LMP1 has been ascribed to pleiotropic signaling properties initiated through protein-protein interactions in cytosolic membrane compartments, but the effects of LMP1 extend to nuclear and extracellular processes. Although LMP1 is one of the latent genes required for EBV-immortalization of B cells, the biology of LMP1 in the pathogenesis of the epithelial cancer nasopharyngeal carcinoma (NPC) is more complex. NPC is prevalent in specific regions of the world with high incidence in southeast China. The epidemiology and time interval from seroconversion to NPC onset in adults would suggest the involvement of multiple risk factors that complement the establishment of a latent and persistent EBV infection. The contribution of LMP1 to EBV pathogenesis in polarized epithelia has only recently begun to be elucidated. Furthermore, the LMP1 gene has emerged as one of the most divergent sequences in the EBV genome. -
Paternal Finasteride Treatment Can Influence the Testicular
Article Paternal Finasteride Treatment Can Influence the Testicular Transcriptome Profile of Male Offspring—Preliminary Study Agnieszka Kolasa 1,* , Dorota Rogi ´nska 2 , Sylwia Rzeszotek 1 , Bogusław Machali ´nski 2 and Barbara Wiszniewska 1 1 Department of Histology and Embryology, Pomeranian Medical University (PMU), Powsta´nców Wlkp. 72 Avene, 70-111 Szczecin, Poland; [email protected] (S.R.); [email protected] (B.W.) 2 Department of General Pathology, Pomeranian Medical University, Powsta´nców Wlkp. 72 Avene, 70-111 Szczecin, Poland; [email protected] (D.R.); [email protected] (B.M.) * Correspondence: [email protected]; Tel.: +48-91-466-16-77 Abstract: (1) Background: Hormone-dependent events that occur throughout spermatogenesis during postnatal testis maturation are significant for adult male fertility. Any disturbances in the T/DHT ratio in male progeny born from females fertilized by finasteride-treated male rats (F0:Fin) can result in the impairment of testicular physiology. The goal of this work was to profile the testicular transcriptome in the male filial generation (F1:Fin) from paternal F0:Fin rats. (2) Methods: The subject material for the study were testis from immature and mature male rats born from females fertilized by finasteride-treated rats. Testicular tissues from the offspring were used in microarray analyses. (3) Results: The top 10 genes having the highest and lowest fold change values were mainly those that encoded odoriferous (Olfr: 31, 331, 365, 633, 774, 814, 890, 935, 1109, 1112, 1173, 1251, 1259, 1253, 1383) Citation: Kolasa, A.; Rogi´nska,D.; Vmn1r 50 103 210 211 Vmn2r 3 23 99 RIKEN cDNA 5430402E10 Rzeszotek, S.; Machali´nski,B.; and vomeronasal ( : , , , ; : , , ) receptors and , Wiszniewska, B. -
NOTCH1 Gene Notch 1
NOTCH1 gene notch 1 Normal Function The NOTCH1 gene provides instructions for making a protein called Notch1, a member of the Notch family of receptors. Receptor proteins have specific sites into which certain other proteins, called ligands, fit like keys into locks. Attachment of a ligand to the Notch1 receptor sends signals that are important for normal development of many tissues throughout the body, both before birth and after. Notch1 signaling helps determine the specialization of cells into certain cell types that perform particular functions in the body (cell fate determination). It also plays a role in cell growth and division (proliferation), maturation (differentiation), and self-destruction (apoptosis). The protein produced from the NOTCH1 gene has such diverse functions that the gene is considered both an oncogene and a tumor suppressor. Oncogenes typically promote cell proliferation or survival, and when mutated, they have the potential to cause normal cells to become cancerous. In contrast, tumor suppressors keep cells from growing and dividing too fast or in an uncontrolled way, preventing the development of cancer; mutations that impair tumor suppressors can lead to cancer development. Health Conditions Related to Genetic Changes Adams-Oliver syndrome At least 15 mutations in the NOTCH1 gene have been found to cause Adams-Oliver syndrome, a condition characterized by areas of missing skin (aplasia cutis congenita), usually on the scalp, and malformations of the hands and feet. These mutations are usually inherited and are present in every cell of the body. Some of the NOTCH1 gene mutations involved in Adams-Oliver syndrome lead to production of an abnormally short protein that is likely broken down quickly, causing a shortage of Notch1. -
Selection of Potential Markers for Epithelial Ovarian Cancer with Gene Expression Arrays and Recursive Descent Partition Analysis
Vol. 10, 3291–3300, May 15, 2004 Clinical Cancer Research 3291 Selection of Potential Markers for Epithelial Ovarian Cancer with Gene Expression Arrays and Recursive Descent Partition Analysis Karen H. Lu,2 Andrea P. Patterson,1 Lin Wang,1 that were up-regulated at least 3-fold in epithelial ovarian Rebecca T. Marquez,1 Edward N. Atkinson,3 cancers when compared with normal OSE. In addition, a Keith A. Baggerly,3 Lance R. Ramoth,1 panel of 11 genes known to encode potential tumor markers 5 5 [mucin 1, transmembrane (MUC1), mucin 16 (CA125), me- Daniel G. Rosen, Jinsong Liu, sothelin, WAP four-disulfide core domain 2 (HE4), kal- 6 7 Ingegerd Hellstrom, David Smith, likrein 6, kallikrein 10, matrix metalloproteinase 2, prosta- 7 8 Lynn Hartmann, David Fishman, sin, osteopontin, tetranectin, and inhibin] were similarly Andrew Berchuck,9 Rosemarie Schmandt,2 analyzed. Regina Whitaker,9 David M. Gershenson,2 Results: The 3-fold up-regulated genes were examined Gordon B. Mills,4 and Robert C. Bast, Jr.1 and four genes [Notch homologue 3 (NOTCH3), E2F tran- scription factor 3 (E2F3), GTPase activating protein (RAC- 1Ovarian Cancer Research Laboratory, Department of Experimental Therapeutics, and Departments of 2Gynecologic Oncology, GAP1), and hematological and neurological expressed 1 3Biostatistics, 4Molecular Therapeutics, and 5Pathology, University of (HN1)] distinguished all tumor samples from normal OSE. Texas M. D. Anderson Cancer Center, Houston, Texas; 6Pacific The 3-fold up-regulated genes were analyzed using RDPA, Northwest Research Institute, Seattle, Washington; 7Mayo Clinic, 8 and the combination of elevated claudin 3 (CLDN3) and Rochester, Minnesota; Northwestern University Medical Center, elevated vascular endothelial growth factor (VEGF) distin- Chicago, Illinois; and 9Duke University Medical Center, Durham, North Carolina guished the cancers from normal OSE. -
Ep 2327796 A1
(19) & (11) EP 2 327 796 A1 (12) EUROPEAN PATENT APPLICATION (43) Date of publication: (51) Int Cl.: 01.06.2011 Bulletin 2011/22 C12Q 1/68 (2006.01) (21) Application number: 10184813.3 (22) Date of filing: 09.06.2004 (84) Designated Contracting States: • Spira, Avrum AT BE BG CH CY CZ DE DK EE ES FI FR GB GR Newton, Massachusetts 02465 (US) HU IE IT LI LU MC NL PL PT RO SE SI SK TR (74) Representative: Brown, David Leslie (30) Priority: 10.06.2003 US 477218 P Haseltine Lake LLP Redcliff Quay (62) Document number(s) of the earlier application(s) in 120 Redcliff Street accordance with Art. 76 EPC: Bristol 04776438.6 / 1 633 892 BS1 6HU (GB) (71) Applicant: THE TRUSTEES OF BOSTON Remarks: UNIVERSITY •This application was filed on 30-09-2010 as a Boston, MA 02218 (US) divisional application to the application mentioned under INID code 62. (72) Inventors: •Claims filed after the date of filing of the application/ • Brody, Jerome S. after the date of receipt of the divisional application Newton, Massachusetts 02458 (US) (Rule 68(4) EPC). (54) Detection methods for disorders of the lung (57) The present invention is directed to prognostic vides a minimally invasive sample procurement method and diagnostic methods to assess lung disease risk in combination with the gene expression-based tools for caused by airway pollutants by analyzing expression of the diagnosis and prognosis of diseases of the lung, par- one or more genes belonging to the airway transcriptome ticularly diagnosis and prognosis of lung cancer provided herein. -
Species Functional Analysis Implicate LRP2 in Hypoplastic Left Heart
TOOLS AND RESOURCES Patient-specific genomics and cross- species functional analysis implicate LRP2 in hypoplastic left heart syndrome Jeanne L Theis1†, Georg Vogler2†, Maria A Missinato2†, Xing Li3, Tanja Nielsen2,4, Xin-Xin I Zeng2, Almudena Martinez-Fernandez5, Stanley M Walls2, Anaı¨s Kervadec2, James N Kezos2, Katja Birker2, Jared M Evans3, Megan M O’Byrne3, Zachary C Fogarty3, Andre´ Terzic5,6,7,8, Paul Grossfeld9,10, Karen Ocorr2, Timothy J Nelson6,7,8‡*, Timothy M Olson5,6,8‡*, Alexandre R Colas2‡, Rolf Bodmer2‡* 1Cardiovascular Genetics Research Laboratory, Rochester, United States; 2Development, Aging and Regeneration, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, United States; 3Division of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, United States; 4Doctoral Degrees and Habilitations, Department of Biology, Chemistry, and Pharmacy, Freie Universita¨ t Berlin, Berlin, Germany; 5Department of Cardiovascular Medicine, Mayo Clinic, Rochester, United States; 6Department of Molecular and Pharmacology and Experimental Therapeutics, Mayo Clinic, La Jolla, United States; 7Center for Regenerative Medicine, Mayo Clinic, Rochester, United States; 8Division of Pediatric Cardiology, Department of Pediatric and Adolescent Medicine, Mayo Clinic, *For correspondence: Rochester, United States; 9University of California San Diego, Rady’s Hospital, San [email protected] (TJN); 10 [email protected] (TMO); Diego, United States; Division of General Internal Medicine, Mayo Clinic, [email protected] (RB) Rochester, United States †These authors contributed equally to this work ‡These authors also contributed equally to this work Abstract Congenital heart diseases (CHDs), including hypoplastic left heart syndrome (HLHS), are genetically complex and poorly understood. Here, a multidisciplinary platform was established Competing interests: The to functionally evaluate novel CHD gene candidates, based on whole-genome and iPSC RNA authors declare that no sequencing of a HLHS family-trio. -
Atlas Journal
Atlas of Genetics and Cytogenetics in Oncology and Haematology Home Genes Leukemias Solid Tumours Cancer-Prone Deep Insight Portal Teaching X Y 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 NA Atlas Journal Atlas Journal versus Atlas Database: the accumulation of the issues of the Journal constitutes the body of the Database/Text-Book. TABLE OF CONTENTS Volume 12, Number 2, Mar-Apr Previous Issue / Next Issue 2008 Genes PLAGL1 (Pleomorphic adenoma gene-like 1) (6q24.2). Abbas Abdollahi. Atlas Genet Cytogenet Oncol Haematol 2008; Vol 12 (2): 164-171. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/PLAGL1ID41737ch6q24.html PDCD4 (Programmed Cell Death 4) (10q24). Nancy H Colburn. Atlas Genet Cytogenet Oncol Haematol 2008; Vol 12 (2): 172-177. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/PDCD4ID41675ch10q24.html PAWR (PRKC apoptosis WT1 regulator protein) (12q21.2). Yanming Zhao, Vivek Rangnekar. Atlas Genet Cytogenet Oncol Haematol 2008; Vol 12 (2): 178-183. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/PAWRID41641ch12q21.html NOTCH3 (Notch homolog 3 (Drosophila)) (19p13.12). Tian-Li Wang. Atlas Genet Cytogenet Oncol Haematol 2008; Vol 12 (2): 184-188. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/NOTCH3ID41557ch19p13.html NOTCH1 (Notch homolog 1, translocation-associated (Drosophila)) (9q34.3). Max Cayo, David Yu Greenblatt, Muthusamy Kunnimalaiyaan, Herbert Chen. Atlas Genet Cytogenet Oncol Haematol 2008; Vol 12 (2): 189-205. [Full Text] [PDF] URL : http://atlasgeneticsoncology.org/Genes/NOTCH1ID30ch9q34.html KLK10 (Kallikrein-related peptidase 10) (19q13.41). Liu-Ying Luo, Eleftherios P Diamandis. -
ATP5H&Sol;KCTD2 Locus Is Associated With
Molecular Psychiatry (2014) 19, 682–687 OPEN & 2014 Macmillan Publishers Limited All rights reserved 1359-4184/14 www.nature.com/mp ORIGINAL ARTICLE ATP5H/KCTD2 locus is associated with Alzheimer’s disease risk M Boada1,2,15, C Antu´nez3,15, R Ramı´rez-Lorca4,15, AL DeStefano5,6, A Gonza´lez-Pe´ rez4, J Gaya´n4,JLo´ pez-Arrieta7, MA Ikram8, I Herna´ndez1, J Marı´n3, JJ Gala´n4, JC Bis9, A Mauleo´n1, M Rosende-Roca1, C Moreno-Rey4, V Gudnasson10, FJ Moro´n4, J Velasco4, JM Carrasco4, M Alegret1, A Espinosa1, G Vinyes1, A Lafuente1, L Vargas1, AL Fitzpatrick9, for the Alzheimer’s Disease Neuroimaging Initiative16, LJ Launer11,MESa´ez4,EVa´zquez4, JT Becker12,OLLo´ pez12, M Serrano-Rı´os13,LTa´rraga1, CM van Duijn8, LM Real4, S Seshadri5,6,14 and A Ruiz1,4 To identify loci associated with Alzheimer disease, we conducted a three-stage analysis using existing genome-wide association studies (GWAS) and genotyping in a new sample. In Stage I, all suggestive single-nucleotide polymorphisms (at Po0.001) in a previously reported GWAS of seven independent studies (8082 Alzheimer’s disease (AD) cases; 12 040 controls) were selected, and in Stage II these were examined in an in silico analysis within the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium GWAS (1367 cases and 12904 controls). Six novel signals reaching Po5 Â 10 À 6 were genotyped in an independent Stage III sample (the Fundacio´ ACE data set) of 2200 sporadic AD patients and 2301 controls. We identified a novel association with AD in the adenosine triphosphate (ATP) synthase, H þ transporting, mitochondrial F0 (ATP5H)/Potassium channel tetramerization domain-containing protein 2 (KCTD2) locus, which reached genome-wide significance in the combined discovery and genotyping sample (rs11870474, odds ratio (OR) ¼ 1.58, P ¼ 2.6 Â 10 À 7 in discovery and OR ¼ 1.43, P ¼ 0.004 in Fundacio´ ACE data set; combined OR ¼ 1.53, P ¼ 4.7 Â 10 À 9). -
Genomic Analysis of the HER2/TOP2A Amplicon in Breast
Laboratory Investigation (2008) 88, 491–503 & 2008 USCAP, Inc All rights reserved 0023-6837/08 $30.00 Genomic analysis of the HER2/TOP2A amplicon in breast cancer and breast cancer cell lines Edurne Arriola1,*, Caterina Marchio1,2, David SP Tan1, Suzanne C Drury3, Maryou B Lambros1, Rachael Natrajan1, Socorro Maria Rodriguez-Pinilla4, Alan Mackay1, Narinder Tamber1, Kerry Fenwick1, Chris Jones5, Mitch Dowsett3, Alan Ashworth1 and Jorge S Reis-Filho1 HER2 and TOP2A are targets for the therapeutic agents trastuzumab and anthracyclines and are frequently amplified in breast cancers. The aims of this study were to provide a detailed molecular genetic analysis of the 17q12–q21 amplicon in breast cancers harbouring HER2/TOP2A co-amplification and to investigate additional recurrent co-amplifications in HER2/ TOP2A-co-amplified cancers. In total, 15 breast cancers with HER2 amplification, 10 of which also harboured TOP2A amplification, as defined by chromogenic in situ hybridisation, and 6 breast cancer cell lines known to be amplified for HER2 were subjected to high-resolution microarray-based comparative genomic hybridisation analysis. This revealed that the genomes of 12 cases were characterised by at least one localised region of clustered, relatively narrow peaks of amplification, with each cluster confined to a single chromosome arm (ie ‘firestorm’ pattern) and 3 cases displayed many narrow segments of duplication and deletion affecting the vast majority of chromosomes (ie ‘sawtooth’ pattern). The smallest region of amplification (SRA) on 17q12 in the whole series extended from 34.73 to 35.48 Mb, and encompassed HER2 but not TOP2A.InHER2/TOP2A-co-amplified samples, the SRA extended from 34.73 to 36.54 Mb, spanning a region of B1.8 Mb. -
Hematological and Neurological Expressed 1 (HN1): a Predictive and Pharmacodynamic Biomarker of Metformin Response in Endometrial Cancers
bioRxiv preprint doi: https://doi.org/10.1101/602870; this version posted April 9, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Hematological and Neurological Expressed 1 (HN1): a predictive and pharmacodynamic biomarker of metformin response in endometrial cancers. Nicholas W. Bateman, PhD1,2*, Pang-ning Teng, PhD1*, Erica Hope, MD1*, Brian L. Hood, PhD1, Julie Oliver, MS1, Wei Ao, BS1, Ming Zhou, PhD3, Guisong Wang, MS1, Domenic Tommarello, BS1, Katlin Wilson, BS1, Kelly A. Conrads, PhD1, Chad A. Hamilton, MD1,2, Kathleen M. Darcy, PhD1,2, Yovanni Casablanca, MD1,2, G. Larry Maxwell, MD1-4, Victoria Bae-Jump MD, PhD5, Thomas P. Conrads, PhD1-4 *authors contributed equally to this work. 1Gynecologic Cancer Center of Excellence, Department of Obstetrics and Gynecology, Uniformed Services University and Walter Reed National Military Medical Center, 8901 Wisconsin Avenue, Bethesda 20889, MD, USA. 2The John P. Murtha Cancer Center, Uniformed Services University and Walter Reed National Military Medical Center, 8901 Wisconsin Avenue, Bethesda 20889, MD, USA. 3Inova Schar Cancer Institute, Inova Center for Personalized Health, 3300 Gallows Rd. Falls Church, VA 22042, USA 4Department of Obstetrics and Gynecology, Inova Fairfax Medical Campus, 3300 Gallows Rd. Falls Church, VA 22042, USA. 5University of North Carolina at Chapel Hill, Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Chapel Hill, NC Keywords: metformin, endometrial cancer, proteomics, Hematological and Neurological Expressed 1, HN1, JPT1 Article Category: Research Article Abbreviations: HN1 - Hematological and Neurological Expressed 1 JPT1 - Jupiter microtubule associated homolog 1 EC – endometrial cancer EEC – cndometrioid endometrial cancer Ki-67 – Antigen Ki-67 MS - mass spectrometry MS/MS – tandem mass spectrometry 1 bioRxiv preprint doi: https://doi.org/10.1101/602870; this version posted April 9, 2019. -
The Opium Poppy Genome and Morphinan Production
This is a repository copy of The opium poppy genome and morphinan production.. White Rose Research Online URL for this paper: https://eprints.whiterose.ac.uk/135262/ Version: Accepted Version Article: Guo, Li, Winzer, Thilo Hans orcid.org/0000-0003-0423-9986, Yang, Xiaofei et al. (8 more authors) (2018) The opium poppy genome and morphinan production. Science. pp. 343- 347. ISSN 0036-8075 https://doi.org/10.1126/science.aat4096 Reuse Items deposited in White Rose Research Online are protected by copyright, with all rights reserved unless indicated otherwise. They may be downloaded and/or printed for private study, or other acts as permitted by national copyright laws. The publisher or other rights holders may allow further reproduction and re-use of the full text version. This is indicated by the licence information on the White Rose Research Online record for the item. Takedown If you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing [email protected] including the URL of the record and the reason for the withdrawal request. [email protected] https://eprints.whiterose.ac.uk/ Title: The opium poppy genome and morphinan production Authors: Li Guo1,2,3,†,Thilo Winzer4†, Xiaofei Yang1,5,†, Yi Li4,†, Zemin Ning6,†, Zhesi He4, Roxana Teodor4, Ying Lu7, Tim A. Bowser8, Ian A. Graham4,* and Kai Ye1,2,3,9,* Affiliations: 1MOE Key Lab for Intelligent Networks & Networks Security, School of Electronics and Information Engineering, Xi'an Jiaotong University, Xi’an, 710049 China. 2The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, 710061, China. -
IN CANCER by KATHARINE MELISSA
FUNCTION OF HEMATOPOIETIC- AND NEUROLOGIC-EXPRESSED SEQUENCE 1 (HN1) IN CANCER By KATHARINE MELISSA LAUGHLIN SALAS A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY UNIVERSITY OF FLORIDA 2009 1 © 2009 Katharine Melissa Laughlin Salas 2 I dedicate this work to my dad, mom, brother and four grandparents. 3 ACKNOWLEDGMENTS First of all, I deeply thank my mentor, Dr. Jeffrey K. Harrison, for his time investment and continuous guidance. I especially thank him for encouraging me to become a more critical thinker and a more independent scientist, for helping me polish my presentation and scientific writing skills, and for constantly pushing me to go beyond my own limits. I thank my committee members, Dr. Brian K. Law, Dr. Tomas C. Rowe, Dr. Wolfgang J. Streit and Dr. Edwin M. Meyer, for their helpful counsel, suggestions and support, as well as for providing reagents or instruments that were necessary for this study. I am also very thankful to my undergraduate mentor, Dr. Susan Semple-Rowland, for always looking out for me, even after all these years, and for her valuable advice, encouragement and continuing mentorship. I thank my labmates, Defang Luo and Che Liu, for their company, conversations and technical aid. I also thank everyone who has helped me with parts of this investigation or that have provided reagents or cell lines for this work. I especially thank Dr. Gerry Shaw for providing the excellent antibodies against Hn1, Irene Zolotukhin and Dr. Kenneth Warrington for making and providing the viruses used in this study, Drs.