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Bayesian Hierarchical Modeling of High-Throughput Genomic Data with Applications to Cancer Bioinformatics and Stem Cell Differentiation
BAYESIAN HIERARCHICAL MODELING OF HIGH-THROUGHPUT GENOMIC DATA WITH APPLICATIONS TO CANCER BIOINFORMATICS AND STEM CELL DIFFERENTIATION by Keegan D. Korthauer A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Statistics) at the UNIVERSITY OF WISCONSIN–MADISON 2015 Date of final oral examination: 05/04/15 The dissertation is approved by the following members of the Final Oral Committee: Christina Kendziorski, Professor, Biostatistics and Medical Informatics Michael A. Newton, Professor, Statistics Sunduz Kele¸s,Professor, Biostatistics and Medical Informatics Sijian Wang, Associate Professor, Biostatistics and Medical Informatics Michael N. Gould, Professor, Oncology © Copyright by Keegan D. Korthauer 2015 All Rights Reserved i in memory of my grandparents Ma and Pa FL Grandma and John ii ACKNOWLEDGMENTS First and foremost, I am deeply grateful to my thesis advisor Christina Kendziorski for her invaluable advice, enthusiastic support, and unending patience throughout my time at UW-Madison. She has provided sound wisdom on everything from methodological principles to the intricacies of academic research. I especially appreciate that she has always encouraged me to eke out my own path and I attribute a great deal of credit to her for the successes I have achieved thus far. I also owe special thanks to my committee member Professor Michael Newton, who guided me through one of my first collaborative research experiences and has continued to provide key advice on my thesis research. I am also indebted to the other members of my thesis committee, Professor Sunduz Kele¸s,Professor Sijian Wang, and Professor Michael Gould, whose valuable comments, questions, and suggestions have greatly improved this dissertation. -
Investigation of Key Genes and Pathways in Inhibition of Oxycodone on Vincristine-Induced Microglia Activation by Using Bioinformatics Analysis
Hindawi Disease Markers Volume 2019, Article ID 3521746, 10 pages https://doi.org/10.1155/2019/3521746 Research Article Investigation of Key Genes and Pathways in Inhibition of Oxycodone on Vincristine-Induced Microglia Activation by Using Bioinformatics Analysis Wei Liu,1 Jishi Ye,2 and Hong Yan 1 1Department of Anesthesiology, the Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430014, China 2Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060 Hubei, China Correspondence should be addressed to Hong Yan; [email protected] Received 2 November 2018; Accepted 31 December 2018; Published 10 February 2019 Academic Editor: Hubertus Himmerich Copyright © 2019 Wei Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction. The neurobiological mechanisms underlying the chemotherapy-induced neuropathic pain are only partially understood. Among them, microglia activation was identified as the key component of neuropathic pain. The aim of this study was to identify differentially expressed genes (DEGs) and pathways associated with vincristine-induced neuropathic pain by using bioinformatics analysis and observe the effects of oxycodone on these DEG expressions in a vincristine-induced microglia activation model. Methods. Based on microarray profile GSE53897, we identified DEGs between vincristine-induced neuropathic pain rats and the control group. Using the ToppGene database, the prioritization DEGs were screened and performed by gene ontology (GO) and signaling pathway enrichment. A protein-protein interaction (PPI) network was used to explore the relationship among DEGs. -
Use of Genomic Tools to Discover the Cause of Champagne Dilution Coat Color in Horses and to Map the Genetic Cause of Extreme Lordosis in American Saddlebred Horses
University of Kentucky UKnowledge Theses and Dissertations--Veterinary Science Veterinary Science 2014 USE OF GENOMIC TOOLS TO DISCOVER THE CAUSE OF CHAMPAGNE DILUTION COAT COLOR IN HORSES AND TO MAP THE GENETIC CAUSE OF EXTREME LORDOSIS IN AMERICAN SADDLEBRED HORSES Deborah G. Cook University of Kentucky, [email protected] Right click to open a feedback form in a new tab to let us know how this document benefits ou.y Recommended Citation Cook, Deborah G., "USE OF GENOMIC TOOLS TO DISCOVER THE CAUSE OF CHAMPAGNE DILUTION COAT COLOR IN HORSES AND TO MAP THE GENETIC CAUSE OF EXTREME LORDOSIS IN AMERICAN SADDLEBRED HORSES" (2014). Theses and Dissertations--Veterinary Science. 15. https://uknowledge.uky.edu/gluck_etds/15 This Doctoral Dissertation is brought to you for free and open access by the Veterinary Science at UKnowledge. It has been accepted for inclusion in Theses and Dissertations--Veterinary Science by an authorized administrator of UKnowledge. For more information, please contact [email protected]. STUDENT AGREEMENT: I represent that my thesis or dissertation and abstract are my original work. Proper attribution has been given to all outside sources. I understand that I am solely responsible for obtaining any needed copyright permissions. I have obtained needed written permission statement(s) from the owner(s) of each third-party copyrighted matter to be included in my work, allowing electronic distribution (if such use is not permitted by the fair use doctrine) which will be submitted to UKnowledge as Additional File. I hereby grant to The University of Kentucky and its agents the irrevocable, non-exclusive, and royalty-free license to archive and make accessible my work in whole or in part in all forms of media, now or hereafter known. -
Functional Genomics Atlas of Synovial Fibroblasts Defining Rheumatoid Arthritis
medRxiv preprint doi: https://doi.org/10.1101/2020.12.16.20248230; this version posted December 18, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Functional genomics atlas of synovial fibroblasts defining rheumatoid arthritis heritability Xiangyu Ge1*, Mojca Frank-Bertoncelj2*, Kerstin Klein2, Amanda Mcgovern1, Tadeja Kuret2,3, Miranda Houtman2, Blaž Burja2,3, Raphael Micheroli2, Miriam Marks4, Andrew Filer5,6, Christopher D. Buckley5,6,7, Gisela Orozco1, Oliver Distler2, Andrew P Morris1, Paul Martin1, Stephen Eyre1* & Caroline Ospelt2*,# 1Versus Arthritis Centre for Genetics and Genomics, School of Biological Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK 2Department of Rheumatology, Center of Experimental Rheumatology, University Hospital Zurich, University of Zurich, Zurich, Switzerland 3Department of Rheumatology, University Medical Centre, Ljubljana, Slovenia 4Schulthess Klinik, Zurich, Switzerland 5Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK 6NIHR Birmingham Biomedical Research Centre, University Hospitals Birmingham NHS Foundation Trust, University of Birmingham, Birmingham, UK 7Kennedy Institute of Rheumatology, University of Oxford Roosevelt Drive Headington Oxford UK *These authors contributed equally #corresponding author: [email protected] NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. 1 medRxiv preprint doi: https://doi.org/10.1101/2020.12.16.20248230; this version posted December 18, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. -
Supplemental Information
Supplemental information Dissection of the genomic structure of the miR-183/96/182 gene. Previously, we showed that the miR-183/96/182 cluster is an intergenic miRNA cluster, located in a ~60-kb interval between the genes encoding nuclear respiratory factor-1 (Nrf1) and ubiquitin-conjugating enzyme E2H (Ube2h) on mouse chr6qA3.3 (1). To start to uncover the genomic structure of the miR- 183/96/182 gene, we first studied genomic features around miR-183/96/182 in the UCSC genome browser (http://genome.UCSC.edu/), and identified two CpG islands 3.4-6.5 kb 5’ of pre-miR-183, the most 5’ miRNA of the cluster (Fig. 1A; Fig. S1 and Seq. S1). A cDNA clone, AK044220, located at 3.2-4.6 kb 5’ to pre-miR-183, encompasses the second CpG island (Fig. 1A; Fig. S1). We hypothesized that this cDNA clone was derived from 5’ exon(s) of the primary transcript of the miR-183/96/182 gene, as CpG islands are often associated with promoters (2). Supporting this hypothesis, multiple expressed sequences detected by gene-trap clones, including clone D016D06 (3, 4), were co-localized with the cDNA clone AK044220 (Fig. 1A; Fig. S1). Clone D016D06, deposited by the German GeneTrap Consortium (GGTC) (http://tikus.gsf.de) (3, 4), was derived from insertion of a retroviral construct, rFlpROSAβgeo in 129S2 ES cells (Fig. 1A and C). The rFlpROSAβgeo construct carries a promoterless reporter gene, the β−geo cassette - an in-frame fusion of the β-galactosidase and neomycin resistance (Neor) gene (5), with a splicing acceptor (SA) immediately upstream, and a polyA signal downstream of the β−geo cassette (Fig. -
Whole Exome Sequencing in Families at High Risk for Hodgkin Lymphoma: Identification of a Predisposing Mutation in the KDR Gene
Hodgkin Lymphoma SUPPLEMENTARY APPENDIX Whole exome sequencing in families at high risk for Hodgkin lymphoma: identification of a predisposing mutation in the KDR gene Melissa Rotunno, 1 Mary L. McMaster, 1 Joseph Boland, 2 Sara Bass, 2 Xijun Zhang, 2 Laurie Burdett, 2 Belynda Hicks, 2 Sarangan Ravichandran, 3 Brian T. Luke, 3 Meredith Yeager, 2 Laura Fontaine, 4 Paula L. Hyland, 1 Alisa M. Goldstein, 1 NCI DCEG Cancer Sequencing Working Group, NCI DCEG Cancer Genomics Research Laboratory, Stephen J. Chanock, 5 Neil E. Caporaso, 1 Margaret A. Tucker, 6 and Lynn R. Goldin 1 1Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 2Cancer Genomics Research Laboratory, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 3Ad - vanced Biomedical Computing Center, Leidos Biomedical Research Inc.; Frederick National Laboratory for Cancer Research, Frederick, MD; 4Westat, Inc., Rockville MD; 5Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; and 6Human Genetics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA ©2016 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol.2015.135475 Received: August 19, 2015. Accepted: January 7, 2016. Pre-published: June 13, 2016. Correspondence: [email protected] Supplemental Author Information: NCI DCEG Cancer Sequencing Working Group: Mark H. Greene, Allan Hildesheim, Nan Hu, Maria Theresa Landi, Jennifer Loud, Phuong Mai, Lisa Mirabello, Lindsay Morton, Dilys Parry, Anand Pathak, Douglas R. Stewart, Philip R. Taylor, Geoffrey S. Tobias, Xiaohong R. Yang, Guoqin Yu NCI DCEG Cancer Genomics Research Laboratory: Salma Chowdhury, Michael Cullen, Casey Dagnall, Herbert Higson, Amy A. -
GWAS for Meat and Carcass Traits
G3: Genes|Genomes|Genetics Early Online, published on July 11, 2019 as doi:10.1534/g3.119.400452 GWAS for meat and carcass traits using imputed sequence level genotypes in pooled F2- designs in pigs Clemens Falker-Gieske,*,1,2 Iulia Blaj,†,2 Siegfried Preuß,‡ Jörn Bennewitz,‡ Georg Thaller,† Jens Tetens*,§ *Department of Animal Sciences, Georg-August-University, 37077 Göttingen, Germany. †Institute of Animal Breeding and Husbandry, Kiel University, 24118 Kiel, Germany. ‡Institute of Animal Husbandry and Breeding, University of Hohenheim, 70599 Stuttgart, Germany. §Center for Integrated Breeding Research, Georg-August-University, 37077 Göttingen, Germany. 1 © The Author(s) 2013. Published by the Genetics Society of America. Running title: Sequence level GWAS in pooled F2 pigs Keywords Genome wide association study Whole genome sequencing Imputation Meat, carcass, and production traits Variant calling 1Corresponding author: Clemens Falker-Gieske, Georg-August-University Goettingen, Department of Animal Sciences, Division Functional Breeding, Burckhardtweg 2, 37077 Goettingen, (+49) 551-39-23669 2contributed equally. 2 ABSTRACT In order to gain insight into the genetic architecture of economically important traits in pigs and to derive suitable genetic markers to improve these traits in breeding programs, many studies have been conducted to map quantitative trait loci. Shortcomings of these studies were low mapping resolution, large confidence intervals for quantitative trait loci-positions and large linkage disequilibrium blocks. Here, we overcome these shortcomings by pooling four large F2 designs to produce smaller linkage disequilibrium blocks and by resequencing the founder generation at high coverage and the F1 generation at low coverage for subsequent imputation of the F2 generation to whole genome sequencing marker density. -
Original Article a Database and Functional Annotation of NF-Κb Target Genes
Int J Clin Exp Med 2016;9(5):7986-7995 www.ijcem.com /ISSN:1940-5901/IJCEM0019172 Original Article A database and functional annotation of NF-κB target genes Yang Yang, Jian Wu, Jinke Wang The State Key Laboratory of Bioelectronics, Southeast University, Nanjing 210096, People’s Republic of China Received November 4, 2015; Accepted February 10, 2016; Epub May 15, 2016; Published May 30, 2016 Abstract: Backgrounds: The previous studies show that the transcription factor NF-κB always be induced by many inducers, and can regulate the expressions of many genes. The aim of the present study is to explore the database and functional annotation of NF-κB target genes. Methods: In this study, we manually collected the most complete listing of all NF-κB target genes identified to date, including the NF-κB microRNA target genes and built the database of NF-κB target genes with the detailed information of each target gene and annotated it by DAVID tools. Results: The NF-κB target genes database was established (http://tfdb.seu.edu.cn/nfkb/). The collected data confirmed that NF-κB maintains multitudinous biological functions and possesses the considerable complexity and diversity in regulation the expression of corresponding target genes set. The data showed that the NF-κB was a central regula- tor of the stress response, immune response and cellular metabolic processes. NF-κB involved in bone disease, immunological disease and cardiovascular disease, various cancers and nervous disease. NF-κB can modulate the expression activity of other transcriptional factors. Inhibition of IKK and IκBα phosphorylation, the decrease of nuclear translocation of p65 and the reduction of intracellular glutathione level determined the up-regulation or down-regulation of expression of NF-κB target genes. -
A Draft Map of the Human Proteome
ARTICLE doi:10.1038/nature13302 A draft map of the human proteome Min-Sik Kim1,2, Sneha M. Pinto3, Derese Getnet1,4, Raja Sekhar Nirujogi3, Srikanth S. Manda3, Raghothama Chaerkady1,2, Anil K. Madugundu3, Dhanashree S. Kelkar3, Ruth Isserlin5, Shobhit Jain5, Joji K. Thomas3, Babylakshmi Muthusamy3, Pamela Leal-Rojas1,6, Praveen Kumar3, Nandini A. Sahasrabuddhe3, Lavanya Balakrishnan3, Jayshree Advani3, Bijesh George3, Santosh Renuse3, Lakshmi Dhevi N. Selvan3, Arun H. Patil3, Vishalakshi Nanjappa3, Aneesha Radhakrishnan3, Samarjeet Prasad1, Tejaswini Subbannayya3, Rajesh Raju3, Manish Kumar3, Sreelakshmi K. Sreenivasamurthy3, Arivusudar Marimuthu3, Gajanan J. Sathe3, Sandip Chavan3, Keshava K. Datta3, Yashwanth Subbannayya3, Apeksha Sahu3, Soujanya D. Yelamanchi3, Savita Jayaram3, Pavithra Rajagopalan3, Jyoti Sharma3, Krishna R. Murthy3, Nazia Syed3, Renu Goel3, Aafaque A. Khan3, Sartaj Ahmad3, Gourav Dey3, Keshav Mudgal7, Aditi Chatterjee3, Tai-Chung Huang1, Jun Zhong1, Xinyan Wu1,2, Patrick G. Shaw1, Donald Freed1, Muhammad S. Zahari2, Kanchan K. Mukherjee8, Subramanian Shankar9, Anita Mahadevan10,11, Henry Lam12, Christopher J. Mitchell1, Susarla Krishna Shankar10,11, Parthasarathy Satishchandra13, John T. Schroeder14, Ravi Sirdeshmukh3, Anirban Maitra15,16, Steven D. Leach1,17, Charles G. Drake16,18, Marc K. Halushka15, T. S. Keshava Prasad3, Ralph H. Hruban15,16, Candace L. Kerr19{, Gary D. Bader5, Christine A. Iacobuzio-Donahue15,16,17, Harsha Gowda3 & Akhilesh Pandey1,2,3,4,15,16,20 The availability of human genome sequence has transformed biomedical research over the past decade. However, an equiv- alent map for the human proteome with direct measurements of proteins and peptides does not exist yet. Here we present a draft map of the human proteome using high-resolution Fourier-transform mass spectrometry. -
Transcriptomics Analysis and Its Applications in Cancer
Transcriptomics analysis and its applications in cancer Alejandra Cervera Taboada Research Program in Systems Oncology Research Programs Unit Biochemistry and Developmental Biology Medicum Faculty of Medicine University of Helsinki Finland Academic dissertation To be publicly discussed, with the permission of the Faculty of Medicine of the University of Helsinki, on the 14th of December 2020, at 15 o’clock. The defence is open for audience through remote access. Helsinki 2020 Supervisor Sampsa Hautaniemi, DTech, Professor Research Program in Systems Oncology Research Programs Unit Biochemistry and Developmental Biology Medicum Faculty of Medicine University of Helsinki Helsinki, Finland Reviewers appointed by the Faculty Rolf Skotheim, PhD Department of Molecular Oncology, Institute for Cancer Research, Oslo University Hospital-Radiumhospitalet Oslo, Norway Joaquin Dopazo, PhD, Director Clinical Bioinformatics Area Fundación Progreso y Salud Universidad de Valencia Sevilla, Spain Opponent appointed by the Faculty Carla Daniela Robles Espinoza, PhD International Laboratory for Human Genome Research, National Autonomous University of Mexico Juriquilla, Mexico Faculty of Medicine Doctoral Programme in Biomedicine ISBN 978-951-51-6865-8 (paperback) ISBN 978-951-51-6866-5 (PDF) http://ethesis.helsinki.fi Unigrafia Oy Helsinki 2020 The Faculty of Medicine uses the Urkund system (plagiarism recognition) to exam- ine all doctoral dissertations. "We reveal ourselves in the metaphors we choose for depicting the cosmos in miniature." - Stephen Jay Gould To Antonio, Abstract Cancer is a collection of diseases that combined are one of the leading causes of deaths worldwide. Although great strides have been made in finding cures for certain cancers, the heterogeneity caused by both the tissue in which cancer originates and the mutations acquired in the cell’s DNA results in unsuccessful treatments for some patients. -
Atypical Chromosome Abnormalities in Acute Myeloid Leukemia Type M4
Genetics and Molecular Biology, 30, 1, 6-9 (2007) Copyright by the Brazilian Society of Genetics. Printed in Brazil www.sbg.org.br Short Communication Atypical chromosome abnormalities in acute myeloid leukemia type M4 Agnes C. Fett-Conte1, Roseli Viscardi Estrela2, Cristina B. Vendrame-Goloni3, Andréa B. Carvalho-Salles1, Octávio Ricci-Júnior4 and Marileila Varella-Garcia5 1Departamento de Biologia Molecular, Faculdade de Medicina de São José do Rio Preto, São José do Rio Preto, SP, Brazil. 2Austa Hospital, São José do Rio Preto, SP, Brazil. 3Departamento de Biologia, Instituto de Biociências, Letras e Ciências Exatas, Universidade Estadual Paulista, São José do Rio Preto, SP, Brazil. 4Hemocentro, São José do Rio Preto, SP, Brazil. 5Comprehensive Cancer Center, University of Colorado, Denver, CO, USA. Abstract This study reports an adult AML-M4 patient with atypical chromosomal aberrations present in all dividing bone mar- row cell at diagnosis: t(1;8)(p32.1;q24.2), der(9)t(9;10)(q22;?), and ins(19;9)(p13.3;q22q34) that may have origi- nated transcripts with leukemogenic potential. Key words: acute myeloid leukemia, chromosomal abnormalities, chromosomal translocations. Received: February 10, 2006; Accepted: June 22, 2006. Acute non-lymphocytic or myelogenous leukemia (Mitelman Database of Chromosome Aberration in Cancer (ANLL or AML) represents a hematopoietic malignancy 2006). Karyotype is generally an important prognostic fac- characterized by abnormal cell proliferation and stalled dif- tor in AML, a favorable prognosis being associated with ferentiation leading to the accumulation of immature cells minor karyotypic changes, low frequency of abnormal in the marrow itself, in peripheral blood and eventually in bone marrow cells and changes specifically involving the other tissues. -
Expression Profiling of Sexually Dimorphic Genes in the Japanese
www.nature.com/scientificreports OPEN Expression profling of sexually dimorphic genes in the Japanese quail, Coturnix japonica Miki Okuno1,5, Shuntaro Miyamoto2,5, Takehiko Itoh1, Masahide Seki3, Yutaka Suzuki3, Shusei Mizushima2,4 & Asato Kuroiwa2,4* Research on avian sex determination has focused on the chicken. In this study, we established the utility of another widely used animal model, the Japanese quail (Coturnix japonica), for clarifying the molecular mechanisms underlying gonadal sex diferentiation. In particular, we performed comprehensive gene expression profling of embryonic gonads at three stages (HH27, HH31 and HH38) by mRNA-seq. We classifed the expression patterns of 4,815 genes into nine clusters according to the extent of change between stages. Cluster 2 (characterized by an initial increase and steady levels thereafter), including 495 and 310 genes expressed in males and females, respectively, contained fve key genes involved in gonadal sex diferentiation. A GO analysis showed that genes in this cluster are related to developmental processes including reproductive structure development and developmental processes involved in reproduction were signifcant, suggesting that expression profling is an efective approach to identify novel candidate genes. Based on RNA-seq data and in situ hybridization, the expression patterns and localization of most key genes for gonadal sex diferentiation corresponded well to those of the chicken. Our results support the efectiveness of the Japanese quail as a model for studies gonadal sex diferentiation in birds. In birds, males are homogametic (ZZ) and females are heterogametic (ZW). Te sex determination mechanism involving gene(s) on the sex chromosome is highly conserved among birds. In chickens, sex determination is thought to occur afer embryonic day (E) 4.5, corresponding to Hamburger and Hamilton stage1 24 (HH24).