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Whole-Genome Microarray Detects Deletions and Loss of Heterozygosity of Chromosome 3 Occurring Exclusively in Metastasizing Uveal Melanoma
Anatomy and Pathology Whole-Genome Microarray Detects Deletions and Loss of Heterozygosity of Chromosome 3 Occurring Exclusively in Metastasizing Uveal Melanoma Sarah L. Lake,1 Sarah E. Coupland,1 Azzam F. G. Taktak,2 and Bertil E. Damato3 PURPOSE. To detect deletions and loss of heterozygosity of disease is fatal in 92% of patients within 2 years of diagnosis. chromosome 3 in a rare subset of fatal, disomy 3 uveal mela- Clinical and histopathologic risk factors for UM metastasis noma (UM), undetectable by fluorescence in situ hybridization include large basal tumor diameter (LBD), ciliary body involve- (FISH). ment, epithelioid cytomorphology, extracellular matrix peri- ϩ ETHODS odic acid-Schiff-positive (PAS ) loops, and high mitotic M . Multiplex ligation-dependent probe amplification 3,4 5 (MLPA) with the P027 UM assay was performed on formalin- count. Prescher et al. showed that a nonrandom genetic fixed, paraffin-embedded (FFPE) whole tumor sections from 19 change, monosomy 3, correlates strongly with metastatic death, and the correlation has since been confirmed by several disomy 3 metastasizing UMs. Whole-genome microarray analy- 3,6–10 ses using a single-nucleotide polymorphism microarray (aSNP) groups. Consequently, fluorescence in situ hybridization were performed on frozen tissue samples from four fatal dis- (FISH) detection of chromosome 3 using a centromeric probe omy 3 metastasizing UMs and three disomy 3 tumors with Ͼ5 became routine practice for UM prognostication; however, 5% years’ metastasis-free survival. to 20% of disomy 3 UM patients unexpectedly develop metas- tases.11 Attempts have therefore been made to identify the RESULTS. Two metastasizing UMs that had been classified as minimal region(s) of deletion on chromosome 3.12–15 Despite disomy 3 by FISH analysis of a small tumor sample were found these studies, little progress has been made in defining the key on MLPA analysis to show monosomy 3. -
Meta-Analysis of Nasopharyngeal Carcinoma
BMC Genomics BioMed Central Research article Open Access Meta-analysis of nasopharyngeal carcinoma microarray data explores mechanism of EBV-regulated neoplastic transformation Xia Chen†1,2, Shuang Liang†1, WenLing Zheng1,3, ZhiJun Liao1, Tao Shang1 and WenLi Ma*1 Address: 1Institute of Genetic Engineering, Southern Medical University, Guangzhou, PR China, 2Xiangya Pingkuang associated hospital, Pingxiang, Jiangxi, PR China and 3Southern Genomics Research Center, Guangzhou, Guangdong, PR China Email: Xia Chen - [email protected]; Shuang Liang - [email protected]; WenLing Zheng - [email protected]; ZhiJun Liao - [email protected]; Tao Shang - [email protected]; WenLi Ma* - [email protected] * Corresponding author †Equal contributors Published: 7 July 2008 Received: 16 February 2008 Accepted: 7 July 2008 BMC Genomics 2008, 9:322 doi:10.1186/1471-2164-9-322 This article is available from: http://www.biomedcentral.com/1471-2164/9/322 © 2008 Chen et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: Epstein-Barr virus (EBV) presumably plays an important role in the pathogenesis of nasopharyngeal carcinoma (NPC), but the molecular mechanism of EBV-dependent neoplastic transformation is not well understood. The combination of bioinformatics with evidences from biological experiments paved a new way to gain more insights into the molecular mechanism of cancer. Results: We profiled gene expression using a meta-analysis approach. Two sets of meta-genes were obtained. Meta-A genes were identified by finding those commonly activated/deactivated upon EBV infection/reactivation. -
Identification of Genes Concordantly Expressed with Atoh1 During Inner Ear Development
Original Article doi: 10.5115/acb.2011.44.1.69 pISSN 2093-3665 eISSN 2093-3673 Identification of genes concordantly expressed with Atoh1 during inner ear development Heejei Yoon, Dong Jin Lee, Myoung Hee Kim, Jinwoong Bok Department of Anatomy, Brain Korea 21 Project for Medical Science, College of Medicine, Yonsei University, Seoul, Korea Abstract: The inner ear is composed of a cochlear duct and five vestibular organs in which mechanosensory hair cells play critical roles in receiving and relaying sound and balance signals to the brain. To identify novel genes associated with hair cell differentiation or function, we analyzed an archived gene expression dataset from embryonic mouse inner ear tissues. Since atonal homolog 1a (Atoh1) is a well known factor required for hair cell differentiation, we searched for genes expressed in a similar pattern with Atoh1 during inner ear development. The list from our analysis includes many genes previously reported to be involved in hair cell differentiation such as Myo6, Tecta, Myo7a, Cdh23, Atp6v1b1, and Gfi1. In addition, we identified many other genes that have not been associated with hair cell differentiation, including Tekt2, Spag6, Smpx, Lmod1, Myh7b, Kif9, Ttyh1, Scn11a and Cnga2. We examined expression patterns of some of the newly identified genes using real-time polymerase chain reaction and in situ hybridization. For example, Smpx and Tekt2, which are regulators for cytoskeletal dynamics, were shown specifically expressed in the hair cells, suggesting a possible role in hair cell differentiation or function. Here, by re- analyzing archived genetic profiling data, we identified a list of novel genes possibly involved in hair cell differentiation. -
Genomic Profiling of Adult Acute Lymphoblastic Leukemia by Single
SUPPLEMENTARY APPENDIX Genomic profiling of adult acute lymphoblastic leukemia by single nucleotide polymorphism oligonucleotide microarray and comparison to pediatric acute lymphoblastic leukemia Ryoko Okamoto,1 Seishi Ogawa,2 Daniel Nowak,1 Norihiko Kawamata,1 Tadayuki Akagi,1,3 Motohiro Kato,2 Masashi Sanada,2 Tamara Weiss,4 Claudia Haferlach,4 Martin Dugas,5 Christian Ruckert,5 Torsten Haferlach,4 and H. Phillip Koeffler1,6 1Division of Hematology and Oncology, Cedars-Sinai Medical Center, UCLA School of Medicine, Los Angeles, CA, USA; 2Cancer Genomics Project, Graduate School of Medicine, University of Tokyo, Tokyo, Japan; 3Department of Stem Cell Biology, Graduate School of Medical Science, Kanazawa University 4MLL Munich Leukemia Laboratory, Munich, Germany; 5Department of Medical Informatics and Biomathematics, University of Münster, Münster, Germany; 6Cancer Science Institute of Singapore, National University of Singapore, Singapore Citation: Okamoto R, Ogawa S, Nowak D, Kawamata N, Akagi T, Kato M, Sanada M, Weiss T, Haferlach C, Dugas M, Ruckert C, Haferlach T, and Koeffler HP. Genomic profiling of adult acute lymphoblastic leukemia by single nucleotide polymorphism oligonu- cleotide microarray and comparison to pediatric acute lymphoblastic leukemia. Haematologica 2010;95(9):1481-1488. doi:10.3324/haematol.2009.011114 Online Supplementary Data ed by PCR of genomic DNA and subsequent direct sequencing of SNP in a region of CNN-LOH in an ALL sample versus the corresponding Design and Methods matched normal sample (Online Supplementary -
The DEK Oncoprotein and Its Emerging Roles in Gene Regulation
Leukemia (2015) 29, 1632–1636 © 2015 Macmillan Publishers Limited All rights reserved 0887-6924/15 www.nature.com/leu CONCISE REVIEW The DEK oncoprotein and its emerging roles in gene regulation C Sandén and U Gullberg The DEK oncogene is highly expressed in cells from most human tissues and overexpressed in a large and growing number of cancers. It also fuses with the NUP214 gene to form the DEK-NUP214 fusion gene in a subset of acute myeloid leukemia. Originally characterized as a member of this translocation, DEK has since been implicated in epigenetic and transcriptional regulation, but its role in these processes is still elusive and intriguingly complex. Similarly multifaceted is its contribution to cellular transformation, affecting multiple cellular processes such as self-renewal, proliferation, differentiation, senescence and apoptosis. Recently, the roles of the DEK and DEK-NUP214 proteins have been elucidated by global analysis of DNA binding and gene expression, as well as multiple functional studies. This review outlines recent advances in the understanding of the basic functions of the DEK protein and its role in leukemogenesis. Leukemia (2015) 29, 1632–1636; doi:10.1038/leu.2015.72 INTRODUCTION DNA-binding structure in the C-terminal end of the protein 18 The DEK gene was originally discovered as a fusion partner in the (Figure 1). The specificity of the binding between DEK and DNA (6;9)(p23;q34) chromosomal translocation in acute myeloid has been investigated in several studies, demonstrating that it leukemia (AML), described in detail below.1 Since then, DEK has depends on either the sequence or the structure of the chromatin been shown to be expressed in most human cells and tissues and and that it correlates with the transcriptional activity of the gene. -
University of London Thesis Z C
REFERENCE ONLY UNIVERSITY OF LONDON THESIS Degree Year Name of Author Z C G f h j > COPYRIGHT This is a thesis accepted for a Higher Degree of the University of London. It is an unpublished typescript and the copyright is held by the author. All persons consulting the thesis must read and abide by the Copyright Declaration below. COPYRIGHT DECLARATION I recognise that the copyright of the above-described thesis rests with the author and that no quotation from it or information derived from it may be published without the prior written consent of the author. LOANS Theses may not be lent to individuals, but the Senate House Library may lend a copy to approved libraries within the United Kingdom, for consultation solely on the premises of those libraries. Application should be made to: Inter-Library Loans, Senate House Library, Senate House, Malet Street, London WC1E 7HU. REPRODUCTION University of London theses may not be reproduced without explicit written permission from the Senate House Library. Enquiries should be addressed to the Theses Section of the Library. Regulations concerning reproduction vary according to the date of acceptance of the thesis and are listed below as guidelines. A. Before 1962. Permission granted only upon the prior written consent of the author. (The Senate House Library will provide addresses where possible). B. 1962- 1974. In many cases the author has agreed to permit copying upon completion of a Copyright Declaration. C. 1975 - 1988. Most theses may be copied upon completion of a Copyright Declaration. D. 1989 onwards. Most theses may be copied. -
Real-Time PCR Analysis of Af4 and Dek Genes Expression in Acute Promyelocytic Leukemia T (15; 17) Patients
EXPERIMENTAL and MOLECULAR MEDICINE, Vol. 36, No. 3, 279-282, June 2004 Real-Time PCR analysis of af4 and dek genes expression in acute promyelocytic leukemia t (15; 17) patients Hakan Savli1, Sema Sirma2, Keywords: af4; APL; dek; Gene expression; Real Time Balint Nagy3, Melih Aktan4, PCR Guncag Dincol4, Zafer Salcioglu5, 4 2,6 Nazan Sarper and Ugur Ozbek Introduction 1 Department of Medical Biology Translocation associated gene fusions are well known Medical Faculty, University of Kocaeli, Kocaeli, Turkey, incidents in acute myeloid leukemia while the other 2Departments of Genetics genetic changes are less known. Acute promyelocytic Institute for Experimental Medicine (DETAE) leukaemia (APL) which is characterized by a recip- Istanbul University, Istanbul, Turkey rocal t (15; 17) translocation of fusing the pml gene 31st Department of Obstetrics and Gynecology to the retinoic acid receptor alpha (rar-alpha) gene, Semmelweis University, Budapest, Hungary but probably there are more oncogenes responsible 4Istanbul Medical Faculty, Istanbul University, Istanbul, Turkey in APL pathogenesis. Among several newly identified 5SSK Bakirkoy Hospital, Istanbul, Turkey oncogenes, dek and af4 are attractive targets for 6Corresponding author: Tel, 90-533-4275272; researchers interested with leukemia. Single role of Fax, 90-212-6311351; E-mail, [email protected] translocation partners dek and af4 genes in leuke- mogenesis have been shown in previous studies Accepted 12 May 2004 (Domer et al., 1993; Larramendy et al., 2002). We also found that dek and af4 genes were down Abbreviations: APL, acute promyelocytic leukaemia regulated during vitamin D dependent differentiation of acute promyelocytic leukaemia cell line HL-60 cells, in our previous studies, using cDNA array technology (Savli et al., 2002). -
(BPA) Exposure Biomarkers in Ovarian Cancer
Journal of Clinical Medicine Article Identification of Potential Bisphenol A (BPA) Exposure Biomarkers in Ovarian Cancer Aeman Zahra 1, Qiduo Dong 1, Marcia Hall 1,2 , Jeyarooban Jeyaneethi 1, Elisabete Silva 1, Emmanouil Karteris 1,* and Cristina Sisu 1,* 1 Biosciences, College of Health, Medicine and Life Sciences, Brunel University London, Uxbridge UB8 3PH, UK; [email protected] (A.Z.); [email protected] (Q.D.); [email protected] (M.H.); [email protected] (J.J.); [email protected] (E.S.) 2 Mount Vernon Cancer Centre, Northwood HA6 2RN, UK * Correspondence: [email protected] (E.K.); [email protected] (C.S.) Abstract: Endocrine-disrupting chemicals (EDCs) can exert multiple deleterious effects and have been implicated in carcinogenesis. The xenoestrogen Bisphenol A (BPA) that is found in various consumer products has been involved in the dysregulation of numerous signalling pathways. In this paper, we present the analysis of a set of 94 genes that have been shown to be dysregulated in presence of BPA in ovarian cancer cell lines since we hypothesised that these genes might be of biomarker potential. This study sought to identify biomarkers of disease and biomarkers of disease- associated exposure. In silico analyses took place using gene expression data extracted from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) databases. Differential expression was further validated at protein level using immunohistochemistry on an ovarian cancer tissue microarray. We found that 14 out of 94 genes are solely dysregulated in the presence of BPA, while the remaining 80 genes are already dysregulated (p-value < 0.05) in their expression pattern Citation: Zahra, A.; Dong, Q.; Hall, as a consequence of the disease. -
Anti-CST2 / Cystatin SA Antibody (ARG59583)
Product datasheet [email protected] ARG59583 Package: 100 μl anti-CST2 / Cystatin SA antibody Store at: -20°C Summary Product Description Rabbit Polyclonal antibody recognizes CST2 / Cystatin SA Tested Reactivity Ms Tested Application WB Host Rabbit Clonality Polyclonal Isotype IgG Target Name CST2 / Cystatin SA Antigen Species Human Immunogen Recombinant fusion protein corresponding to aa. 20-141 of Human CST2 (NP_001313.1). Conjugation Un-conjugated Alternate Names Cystatin-2; Cystatin-SA; Cystatin-S5 Application Instructions Application table Application Dilution WB 1:500 - 1:2000 Application Note * The dilutions indicate recommended starting dilutions and the optimal dilutions or concentrations should be determined by the scientist. Positive Control Mouse heart Calculated Mw 16 kDa Observed Size 16 kDa Properties Form Liquid Purification Affinity purified. Buffer PBS (pH 7.3), 0.02% Sodium azide and 50% Glycerol. Preservative 0.02% Sodium azide Stabilizer 50% Glycerol Storage instruction For continuous use, store undiluted antibody at 2-8°C for up to a week. For long-term storage, aliquot and store at -20°C. Storage in frost free freezers is not recommended. Avoid repeated freeze/thaw cycles. Suggest spin the vial prior to opening. The antibody solution should be gently mixed before use. Note For laboratory research only, not for drug, diagnostic or other use. www.arigobio.com 1/2 Bioinformation Gene Symbol CST2 Gene Full Name cystatin SA Background The cystatin superfamily encompasses proteins that contain multiple cystatin-like sequences. Some of the members are active cysteine protease inhibitors, while others have lost or perhaps never acquired this inhibitory activity. There are three inhibitory families in the superfamily, including the type 1 cystatins (stefins), type 2 cystatins and the kininogens. -
The Oncoprotein DEK Affects the Outcome of PARP1/2 Inhibition
bioRxiv preprint doi: https://doi.org/10.1101/555003; this version posted February 19, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 1 The oncoprotein DEK affects the outcome of 2 PARP1/2 inhibition during replication stress 3 Magdalena Ganz1¶, Christopher Vogel1¶, Christina Czada1, Vera Jörke1, Rebecca 4 Kleiner1, Agnieszka Pierzynska-Mach2,3, Francesca Cella Zanacchi2,4, Alberto 5 Diaspro2,5, Ferdinand Kappes6, Alexander Bürkle7, and Elisa Ferrando-May1* 6 1Department of Biology, Bioimaging Center, University of Konstanz, Konstanz, 7 Germany 8 2Nanoscopy and NIC@IIT, Istituto Italiano di Tecnologia, Genoa, Italy 9 3Department of Experimental Oncology, European Institute of Oncology, Milan, Italy 10 4Biophysics Institute (IBF), National Research Council (CNR), Genoa, Italy 11 5DIFILAB, Department of Physics, University of Genoa, Genoa, Italy 12 6Xi’an Jiaotong-Liverpool University, Dushu Lake Higher Education Town, Suzhou, 13 China 14 7Department of Biology, Molecular Toxicology Group, University of Konstanz, 15 Konstanz, Germany 16 17 Short title: DEK and PARP in replication stress 18 19 * Corresponding author 20 email: [email protected] 21 22 ¶These authors contributed equally to this work bioRxiv preprint doi: https://doi.org/10.1101/555003; this version posted February 19, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. -
Functional Annotation of a Full-Length Mouse Cdna Collection
articles Functional annotation of a full-length mouse cDNA collection The RIKEN Genome Exploration Research Group Phase II Team and the FANTOM Consortium* ...............................................................................................................................* A full list of authors appears at the end of the paper ............................................................................................................................................. The RIKEN Mouse Gene Encyclopaedia Project, a systematic approach to determining the full coding potential of the mouse genome, involves collection and sequencing of full-length complementary DNAs and physical mapping of the corresponding genes to the mouse genome. We organized an international functional annotation meeting (FANTOM) to annotate the ®rst 21,076 cDNAs to be analysed in this project. Here we describe the ®rst RIKEN clone collection, which is one of the largest described for any organism. Analysis of these cDNAs extends known gene families and identi®es new ones. In mammals and higher plants, interpreting the genome sequence is Annotation of cDNAs not straightforward: coding regions are interspersed with noncod- An international meeting was held to facilitate functional annota- ing DNA, and an individual gene may give rise to many gene tion of the cDNA sequences. Participants contributed to the devel- products. Thus, genomic sequence cannot be reliably decoded to opment of a web-based annotation interface that should expedite identify the spectrum of messenger RNAs (the transcriptome) and future annotation of additional clones in the Mouse Gene Encyclo- their corresponding protein products (the proteome). This problem paedia project. We agreed on annotation vocabularies and the is illustrated by the different estimates of the number of human application of Gene Ontology (GO) terms (http://genome.gsc. genes (30,000, 35,000 and 120,000)1±3. -
Functional Specialization of Human Salivary Glands and Origins of Proteins Intrinsic to Human Saliva
UCSF UC San Francisco Previously Published Works Title Functional Specialization of Human Salivary Glands and Origins of Proteins Intrinsic to Human Saliva. Permalink https://escholarship.org/uc/item/95h5g8mq Journal Cell reports, 33(7) ISSN 2211-1247 Authors Saitou, Marie Gaylord, Eliza A Xu, Erica et al. Publication Date 2020-11-01 DOI 10.1016/j.celrep.2020.108402 Peer reviewed eScholarship.org Powered by the California Digital Library University of California HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Cell Rep Manuscript Author . Author manuscript; Manuscript Author available in PMC 2020 November 30. Published in final edited form as: Cell Rep. 2020 November 17; 33(7): 108402. doi:10.1016/j.celrep.2020.108402. Functional Specialization of Human Salivary Glands and Origins of Proteins Intrinsic to Human Saliva Marie Saitou1,2,3, Eliza A. Gaylord4, Erica Xu1,7, Alison J. May4, Lubov Neznanova5, Sara Nathan4, Anissa Grawe4, Jolie Chang6, William Ryan6, Stefan Ruhl5,*, Sarah M. Knox4,*, Omer Gokcumen1,8,* 1Department of Biological Sciences, University at Buffalo, The State University of New York, Buffalo, NY, U.S.A 2Section of Genetic Medicine, Department of Medicine, University of Chicago, Chicago, IL, U.S.A 3Faculty of Biosciences, Norwegian University of Life Sciences, Ås, Viken, Norway 4Program in Craniofacial Biology, Department of Cell and Tissue Biology, School of Dentistry, University of California, San Francisco, CA, U.S.A 5Department of Oral Biology, School of Dental Medicine, University at Buffalo, The State University of New York, Buffalo, NY, U.S.A 6Department of Otolaryngology, School of Medicine, University of California, San Francisco, CA, U.S.A 7Present address: Weill-Cornell Medical College, Physiology and Biophysics Department 8Lead Contact SUMMARY Salivary proteins are essential for maintaining health in the oral cavity and proximal digestive tract, and they serve as potential diagnostic markers for monitoring human health and disease.