DOCSLIB.ORG

PCDHB2 (Human) Recombinant Protein (P01)

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
PCDHB2 (Human) Recombinant Protein (P01) Produktinformation Diagnostik & molekulare Diagnostik Laborgeräte & Service Zellkultur & Verbrauchsmaterial Forschungsprodukte & Biochemikalien Weitere Information auf den folgenden Seiten! See the following pages for more information! Lieferung & Zahlungsart Lieferung: frei Haus Bestellung auf Rechnung SZABO-SCANDIC Lieferung: € 10,- HandelsgmbH & Co KG Erstbestellung Vorauskassa Quellenstraße 110, A-1100 Wien T. +43(0)1 489 3961-0 Zuschläge F. +43(0)1 489 3961-7 [email protected] • Mindermengenzuschlag www.szabo-scandic.com • Trockeneiszuschlag • Gefahrgutzuschlag linkedin.com/company/szaboscandic • Expressversand facebook.com/szaboscandic PCDHB2 (Human) Recombinant Purification: Glutathione Sepharose 4 Fast Flow Protein (P01) Storage Buffer: 50 mM Tris-HCI, 10 mM reduced Glutathione, pH=8.0 in the elution buffer. Catalog Number: H00056133-P01 Storage Instruction: Store at -80°C. Aliquot to avoid Regulation Status: For research use only (RUO) repeated freezing and thawing. Product Description: Human PCDHB2 full-length ORF Entrez GeneID: 56133 ( AAH98575.1, 1 a.a. - 798 a.a.) recombinant protein with GST-tag at N-terminal. Gene Symbol: PCDHB2 Sequence: Gene Alias: MGC111392, PCDH-BETA2 MEAGEGKERVPKQRQVLIFFVLLGIAQASCQPRHYSV AEETESGSFVANLLKDLGLEIGELAVRGARVVSKGKK Gene Summary: This gene is a member of the MHLQFDRQTGDLLLNEKLDREELCGPTEPCVLPFQVL protocadherin beta gene cluster, one of three related LENPLQFFQAELRIRDVNDHSPVFLDKEILLKIPESITPG gene clusters tandemly linked on chromosome five. The TTFLIERAQDLDVGTNSLQNYTISPNFHFHLNLQDSLD gene clusters demonstrate an unusual genomic GIILPQLVLNRALDREEQPEIRLTLTALDGGSPPRSGTA organization similar to that of B-cell and T-cell receptor LVRIEVVDINDNVPEFAKLLYEVQIPEDSPVGSQVAIVS gene clusters. The beta cluster contains 16 genes and 3 ARDLDIGTNGEISYAFSQASEDIRKTFRLSAKSGELLLR pseudogenes, each encoding 6 extracellular cadherin QKLDFESIQTYTVNIQATDGGGLSGTCVVFVQVMDLN domains and a cytoplasmic tail that deviates from others DNPPELTMSTLINQIPENLQDTLIAVFSVSDPDSGDNG in the cadherin superfamily. The extracellular domains RMVCSIQDDLPFFLKPSVENFYTLVISTALDRETRSEY interact in a homophilic manner to specify differential NITITVTDFGTPRLKTEHNITVLVSDVNDNAPAFTQTSY cell-cell connections. Unlike the alpha and gamma TLFVRENNSPALHIGSVSATDRDSGTNAQVTYSLLPPQ clusters, the transcripts from these genes are made up DPHLPLASLVSINADNGHLFALQSLDYEALQAFEFRVG of only one large exon, not sharing common 3' exons as AADRGSPALSSEALVRVLVLDANDNSPFVLYPLQNGS expected. These neural cadherin-like cell adhesion APCTELVPRAAEPGYLVTKVVAVDGDSGQNAWLSYQ proteins are integral plasma membrane proteins. Their LLKATEPGLFGVWAHNGEVRTARLLRERDAAKQRLVV specific functions are unknown but they most likely play LVKDNGEPPRSATATLHVLLVDGFSQPYLLLPEAAPAQ a critical role in the establishment and function of AQADLLTVYLVVALASVSSLFLFSVLLFVAVRLCRRSR specific cell-cell neural connections. [provided by AASVGRCSVPEGPFPGQMVDVSGTGTLSQSYQYEVC RefSeq] LTGESGTNEFKFLKPIIPNFVAQGAERVSEANPSFRKS FEFT Host: Wheat Germ (in vitro) Theoretical MW (kDa): 113.7 Applications: AP, Array, ELISA, WB-Re (See our web site product page for detailed applications information) Protocols: See our web site at http://www.abnova.com/support/protocols.asp or product page for detailed protocols Preparation Method: in vitro wheat germ expression system Page 1/1 Powered by TCPDF (www.tcpdf.org).
Load more

Recommended publications
  • Supplementary Table 1: Adhesion Genes Data Set
    Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like,
    [Show full text]
  • Research Progress on DNA Methylation in Hepatocellular Carcinoma
    998 Review Article Research progress on DNA methylation in hepatocellular carcinoma Yongchang Zheng*, Xin Wang*, Feihu Xie, Zhaoqi Gu, Li He, Shunda Du, Haitao Zhao, Yiyao Xu, Xin Lu, Yilei Mao, Xinting Sang, Haifeng Xu, Tianyi Chi Department of Liver Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China Contributions: (I) Conception and design: Y Zheng, H Xu, T Chi; (II) Administrative support: X Sang, Z Gu, L He, S Du, H Zhao, Y Xu, X Lu, Y Mao; (III) Provision of study materials or patients: Y Zheng, X Wang; (IV) Collection and assembly of data: Y Zheng, X Wang; (V) Data analysis and interpretation: X Wang, F Xie; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. *These authors contributed equally to this work. Correspondence to: Haifeng Xu, MD. Department of Liver Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China. Email: [email protected]; Tianyi Chi, MD. Department of Liver Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China. Email: [email protected]. Abstract: Hepatocellular carcinoma (HCC) is a common malignant tumor with high incidence and morbidity worldwide. The pathogenesis and progression of HCC are closely related to abnormal epigenetic regulation of hepatocytes. DNA methylation is an important regulatory mechanism in epigenetics which has been deeply and widely investigated. Along with the development of high-throughput sequencing techniques, including high-throughput gene chip analysis and next generation sequencing, great progress was achieved toward the understanding of the epigenetic regulation of HCC.
    [Show full text]
  • Role of the Chromosome Architectural Factor SMCHD1 in X-Chromosome Inactivation, Gene Regulation, and Disease in Humans
    HIGHLIGHTED ARTICLE | INVESTIGATION Role of the Chromosome Architectural Factor SMCHD1 in X-Chromosome Inactivation, Gene Regulation, and Disease in Humans Chen-Yu Wang,*,† Harrison Brand,‡,§,**,†† Natalie D. Shaw,‡‡,§§ Michael E. Talkowski,‡,§,**,†† and Jeannie T. Lee*,†,1 *Department of Molecular Biology, ††Center for Human Genetic Research, and ‡‡Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114, †Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, ‡Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, §Program in Medical and Population Genetics and **Center for Mendelian Genomics, Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, §§National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709 ORCID IDs: 0000-0002-3912-5113 (C.-Y.W.); 0000-0001-7786-8850 (J.T.L.) ABSTRACT Structural maintenance of chromosomes flexible hinge domain-containing 1 (SMCHD1) is an architectural factor critical for X-chromosome inactivation (XCI) and the repression of select autosomal gene clusters. In mice, homozygous nonsense mutations in Smchd1 cause female-specific embryonic lethality due to an XCI defect. However, although human mutations in SMCHD1 are associated with congenital arhinia and facioscapulohumeral muscular dystrophy type 2 (FSHD2), the diseases do not show a sex- specific bias, despite the essential nature of XCI in humans. To investigate whether there is a dosage imbalance for the sex chromo- somes, we here analyze transcriptomic data from arhinia and FSHD2 patient blood and muscle cells. We find that X-linked dosage compensation is maintained in these patients. In mice, SMCHD1 controls not only protocadherin (Pcdh) gene clusters, but also Hox genes critical for craniofacial development.
    [Show full text]
  • Peripheral Nerve Single-Cell Analysis Identifies Mesenchymal Ligands That Promote Axonal Growth
    Research Article: New Research Development Peripheral Nerve Single-Cell Analysis Identifies Mesenchymal Ligands that Promote Axonal Growth Jeremy S. Toma,1 Konstantina Karamboulas,1,ª Matthew J. Carr,1,2,ª Adelaida Kolaj,1,3 Scott A. Yuzwa,1 Neemat Mahmud,1,3 Mekayla A. Storer,1 David R. Kaplan,1,2,4 and Freda D. Miller1,2,3,4 https://doi.org/10.1523/ENEURO.0066-20.2020 1Program in Neurosciences and Mental Health, Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada, 2Institute of Medical Sciences University of Toronto, Toronto, Ontario M5G 1A8, Canada, 3Department of Physiology, University of Toronto, Toronto, Ontario M5G 1A8, Canada, and 4Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5G 1A8, Canada Abstract Peripheral nerves provide a supportive growth environment for developing and regenerating axons and are es- sential for maintenance and repair of many non-neural tissues. This capacity has largely been ascribed to paracrine factors secreted by nerve-resident Schwann cells. Here, we used single-cell transcriptional profiling to identify ligands made by different injured rodent nerve cell types and have combined this with cell-surface mass spectrometry to computationally model potential paracrine interactions with peripheral neurons. These analyses show that peripheral nerves make many ligands predicted to act on peripheral and CNS neurons, in- cluding known and previously uncharacterized ligands. While Schwann cells are an important ligand source within injured nerves, more than half of the predicted ligands are made by nerve-resident mesenchymal cells, including the endoneurial cells most closely associated with peripheral axons. At least three of these mesen- chymal ligands, ANGPT1, CCL11, and VEGFC, promote growth when locally applied on sympathetic axons.
    [Show full text]
  • Predict AID Targeting in Non-Ig Genes Multiple Transcription Factor
    Downloaded from http://www.jimmunol.org/ by guest on September 26, 2021 is online at: average * The Journal of Immunology published online 20 March 2013 from submission to initial decision 4 weeks from acceptance to publication Multiple Transcription Factor Binding Sites Predict AID Targeting in Non-Ig Genes Jamie L. Duke, Man Liu, Gur Yaari, Ashraf M. Khalil, Mary M. Tomayko, Mark J. Shlomchik, David G. Schatz and Steven H. Kleinstein J Immunol http://www.jimmunol.org/content/early/2013/03/20/jimmun ol.1202547 Submit online. Every submission reviewed by practicing scientists ? is published twice each month by http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://www.jimmunol.org/content/suppl/2013/03/20/jimmunol.120254 7.DC1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2013 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 26, 2021. Published March 20, 2013, doi:10.4049/jimmunol.1202547 The Journal of Immunology Multiple Transcription Factor Binding Sites Predict AID Targeting in Non-Ig Genes Jamie L. Duke,* Man Liu,†,1 Gur Yaari,‡ Ashraf M. Khalil,x Mary M. Tomayko,{ Mark J. Shlomchik,†,x David G.
    [Show full text]
  • New Possible Targetable Genes for Future Treatment of Mixed Lineage Leukemia Senol Dogan* International Burch University, Sarajevo, Bosnia and Herzegovina
    etrics iom & B B f io o l s t a a n t Dogan, J Biom Biostat 2017, 8:3 r i s u t i o c J s Journal of Biometrics & Biostatistics DOI: 10.4172/2155-6180.1000349 ISSN: 2155-6180 Research Ar ticleArticle Open Access New Possible Targetable Genes for Future Treatment of Mixed Lineage Leukemia Senol Dogan* International Burch University, Sarajevo, Bosnia and Herzegovina Abstract Aim of study: Leukemia has different subtypes, which present unique clinical and molecular characteristics. MLL (Mixed Lineage Leukemia) is one of the new different subtypes than AML and ALL. Materials and Methods: Genomic characterization is the main key understanding the differences of MLL by analysis of differential gene expression, methylation patterns and mutational spectra that were compared and analyzed between MLL and AML types (n=197). Results: According to the genomic characterization of MLL, differentially expressed 114 genes were selected and 37 of them targeted genes having more than 2 fold expression change, including HOXA9, CFH, DDX4, MSH4, MSMB, TWIST1, ZSWIM2, POU6F2. To measure the aberrant methylation is the second genomic characterization of this research because the rearrangements of MLL gene leading to aberrant methylation. The methylation data were compared between cancer and control, so high methylated genes have been detected between MLL and AML types. The methylation loci were categorized into two groups: ≥ 10 fold difference and ≥ 5 and ≤ 10 fold difference. Some of the genes high methylated more than one location such as; RAET1E, HSD17B2, RNASE11, DGK1, POU6F2, NAGS, PIK3C2G, GADL1, and KRT13. In addition to that, analysis of somatic mutation gives us that CFH has the highest point mutation 9,92%.
    [Show full text]
  • Remote Memory and Cortical Synaptic Plasticity Require Neuronal CCCTC-Binding Factor (CTCF)
    5042 • The Journal of Neuroscience, May 30, 2018 • 38(22):5042–5052 Cellular/Molecular Remote Memory and Cortical Synaptic Plasticity Require Neuronal CCCTC-Binding Factor (CTCF) X Somi Kim,1* Nam-Kyung Yu,1* Kyu-Won Shim,2 XJi-il Kim,1 X Hyopil Kim,1 Dae Hee Han,1 XJa Eun Choi,1 X Seung-Woo Lee,1 X Dong Il Choi,1 Myung Won Kim,1 Dong-Sung Lee,3 Kyungmin Lee,4 Niels Galjart,5 X Yong-Seok Lee,6 XJae-Hyung Lee,7 and XBong-Kiun Kaang1 1Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul 08826, South Korea, 2Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul 08826, South Korea, 3Salk Institute for Biological Studies, La Jolla, California 92130, 4Department of Anatomy, Graduate School of Medicine, Kyungpook National University, Daegu 700-422, Korea, 5Department of Cell Biology and Genetics, 3000 CA Rotterdam, The Netherlands, 6Department of Physiology, Seoul National University College of Medicine, Seoul 03080, South Korea, and 7Department of Life and Nanopharmaceutical Sciences, Department of Maxillofacial Biomedical Engineering, School of Dentistry, Kyung Hee University, Seoul 02447, South Korea The molecular mechanism of long-term memory has been extensively studied in the context of the hippocampus-dependent recent memory examined within several days. However, months-old remote memory maintained in the cortex for long-term has not been investigated much at the molecular level yet. Various epigenetic mechanisms are known to be important for long-term memory, but how the 3D chromatin architecture and its regulator molecules contribute to neuronal plasticity and systems consolidation is still largely unknown.
    [Show full text]
  • Chromatin Module Inference on Cellular Trajectories Identifies Key Transition Points and Poised Epigenetic States in Diverse Developmental Processes
    Downloaded from genome.cshlp.org on October 5, 2021 - Published by Cold Spring Harbor Laboratory Press Chromatin module inference on cellular trajectories identifies key transition points and poised epigenetic states in diverse developmental processes Sushmita Roy1, 3, * and Rupa Sridharan2, 3, * 1. Department of Biostatistics and Medical Informatics, University of Wisconsin-Madison, Madison, WI 53715, USA 2. Department of Cell and Regenerative Biology, University of Wisconsin, Madison WI 53715, USA 3. Wisconsin Institute for Discovery, 330 N. Orchard Street, Madison, WI 53715, USA *Corresponding author [email protected] [email protected] Downloaded from genome.cshlp.org on October 5, 2021 - Published by Cold Spring Harbor Laboratory Press Abstract Changes in chromatin state play important roles in cell fate transitions. Current computational approaches to analyze chromatin modifications across multiple cell types do not model how the cell types are related on a lineage or over time. To overcome this limitation, we have developed a method called CMINT (Chromatin Module INference on Trees), a probabilistic clustering approach to systematically capture chromatin state dynamics across multiple cell types. Compared to existing approaches, CMINT can handle complex lineage topologies, capture higher quality clusters, and reliably detect chromatin transitions between cell types. We applied CMINT to gain novel insights in two complex processes: reprogramming to induced pluripotent stem cells (iPSCs) and hematopoiesis. In reprogramming, chromatin changes could occur without large gene expression changes; different combinations of activating marks were associated with specific reprogramming factors; there was an order of acquisition of chromatin marks at pluripotency loci; and multivalent states, comprising previously undetermined combinations of activating and repressive histone modifications were enriched for CTCF.
    [Show full text]
  • Analysis of Genomic Regions of Increased Gene Expression (RIDGE)S in Immune Activation
    Analysis of genomic Regions of IncreaseD Gene Expression (RIDGE)s in immune activation Lena Hansson Doctor of Philosophy Institute for Adaptive and Neural Computation School of Informatics and Division of Pathway Medicine Medical School University of Edinburgh 2009 Abstract A RIDGE (Region of IncreaseD Gene Expression), as defined by previous studies, is a con- secutive set of active genes on a chromosome that span a region around 110 kbp long. This study investigated RIDGE formation by focusing on the well-defined, immunological impor- tant MHC locus. Macrophages were assayed for gene expression levels using the Affymetrix MG-U74Av2 chip are were either 1) uninfected, 2) primed with IFN-g, 3) viral activated with mCMV, or 4) both primed and viral activated. Gene expression data from these conditions was studied using data structures and new software developed for the visualisation and handling of structured functional genomic data. Specifically, the data was used to study RIDGE structures and investigate whether physically linked genes were also functionally related, and exhibited co-expression and potentially co-regulation. A greater number of RIDGEs with a greater number of members than expected by chance were found. Observed RIDGEs featured functional associations between RIDGE members (mainly explored via GO, UniProt, and Ingenuity), shared upstream control elements (via PROMO, TRANSFAC, and ClustalW), and similar gene expression profiles. Furthermore RIDGE formation cannot be explained by sequence duplication events alone. When the analysis was extended to the entire mouse genome, it became apparent that known genomic loci (for example the protocadherin loci) were more likely to contain more and longer RIDGEs.
    [Show full text]
  • A CATH Domain Functional Family Based Approach to Identify
    bioRxiv preprint doi: https://doi.org/10.1101/399014; this version posted August 25, 2018. 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 A CATH domain functional family based approach to identify putative cancer driver genes and driver mutations Paul Ashford1,+, Camilla S.M. Pang1,+, Aurelio A. Moya-García1,2, Tolulope Adeyelu1 & Christine A. Orengo1,* +These authors contributed equally to this work. 1University College London, Institute of Structural and Molecular Biology, London, UK. 2Laboratorio de Biología Molecular del Cáncer, Centro de Investigaciones Médico-Sanitarias (CIMES), Universidad de Málaga, Málaga, Spain Correspondence and requests for materials should be addressed to Christine Orengo (email: [email protected]). Tumour sequencing identifies highly recurrent point mutations in cancer driver genes, but rare functional mutations are hard to distinguish from large numbers of passengers. We developed a novel computational platform applying a multi-modal approach to filter out passengers and more robustly identify putative driver genes. The primary filter identifies enrichment of cancer mutations in CATH functional families (CATH-FunFams) – structurally and functionally coherent sets of evolutionary related domains. Using structural representatives from CATH-FunFams, we subsequently seek enrichment of mutations in 3D and show that these mutation clusters have a very significant tendency to lie close to known functional sites or conserved sites predicted using CATH-FunFams. Our third filter identifies enrichment of putative driver genes in functionally coherent protein network modules confirmed by literature analysis to be cancer associated.
    [Show full text]
  • Biomedical Informatics
    BIOMEDICAL INFORMATICS Abstract GENE LIST AUTOMATICALLY DERIVED FOR YOU (GLAD4U): DERIVING AND PRIORITIZING GENE LISTS FROM PUBMED LITERATURE JEROME JOURQUIN Thesis under the direction of Professor Bing Zhang Answering questions such as ―Which genes are related to breast cancer?‖ usually requires retrieving relevant publications through the PubMed search engine, reading these publications, and manually creating gene lists. This process is both time-consuming and prone to errors. We report GLAD4U (Gene List Automatically Derived For You), a novel, free web-based gene retrieval and prioritization tool. The quality of gene lists created by GLAD4U for three Gene Ontology terms and three disease terms was assessed using ―gold standard‖ lists curated in public databases. We also compared the performance of GLAD4U with that of another gene prioritization software, EBIMed. GLAD4U has a high overall recall. Although precision is generally low, its prioritization methods successfully rank truly relevant genes at the top of generated lists to facilitate efficient browsing. GLAD4U is simple to use, and its interface can be found at: http://bioinfo.vanderbilt.edu/glad4u. Approved ___________________________________________ Date _____________ GENE LIST AUTOMATICALLY DERIVED FOR YOU (GLAD4U): DERIVING AND PRIORITIZING GENE LISTS FROM PUBMED LITERATURE By Jérôme Jourquin Thesis Submitted to the Faculty of the Graduate School of Vanderbilt University in partial fulfillment of the requirements for the degree of MASTER OF SCIENCE in Biomedical Informatics May, 2010 Nashville, Tennessee Approved: Professor Bing Zhang Professor Hua Xu Professor Daniel R. Masys ACKNOWLEDGEMENTS I would like to express profound gratitude to my advisor, Dr. Bing Zhang, for his invaluable support, supervision and suggestions throughout this research work.
    [Show full text]
  • Supplementary Methods
    Supplementary Methods Patient Cohorts and Clinicopathological Review AOCS and Clinical Cohort AOCS is a population-based, case control study of ovarian cancer which recruited eligible women aged 18-79 years with newly diagnosed epithelial ovarian cancer (including primary peritoneal and fallopian tube cancer) through 20 gynaecologic oncology units across all Australian states, between January 2002 and June 2006. Women who were unable to provide informed consent due to illness, language difficulties or mental incapacity were excluded, as were those whose diagnosis was not histopathologically confirmed. Detailed clinical and follow-up data was obtained from medical records at predefined intervals: post surgery, post primary chemotherapy, at 6-monthly intervals to 5 years and annually thereafter. All treatment details and clinical assessments were recorded on case report forms using Good Clinical Practice (GCP) guidelines (ICH E6: Good Clinical Practice: Consolidated Guidance. 1996; http://www.fda.gov/oc/gcp/guidance.html), and included chemotherapy regimen, imaging details and pre- and post-treatment serum CA125 levels. The CA125 assay type and upper limit of normal for each measurement were recorded and assignment of relapse date was based on Gynecologic Cancer Intergroup (GCIG) criteria1. Clinical details for the cases from The Royal Brisbane Hospital, and Westmead Hospital were obtained retrospectively from medical records. The majority of patients with invasive ovarian cancer (n= 267) underwent laparotomy for diagnosis, staging and debulking and subsequently received first-line platinum/taxane based chemotherapy. In most cases, tumor examined was excised at the time of primary surgery, prior to the administration of chemotherapy. Eighteen patients who had neoadjuvant, platinum based chemotherapy were also included in the study as were 18 patients with low malignant potential disease.
    [Show full text]