Changes in Peripheral and Local Tumor Immunity After Neoadjuvant Chemotherapy Reshape Clinical Outcomes in Patients with Breast Cancer Margaret L
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Screening and Identification of Key Biomarkers in Clear Cell Renal Cell Carcinoma Based on Bioinformatics Analysis
bioRxiv preprint doi: https://doi.org/10.1101/2020.12.21.423889; this version posted December 23, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder.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. Screening and identification of key biomarkers in clear cell renal cell carcinoma based on bioinformatics analysis Basavaraj Vastrad1, Chanabasayya Vastrad*2 , Iranna Kotturshetti 1. Department of Biochemistry, Basaveshwar College of Pharmacy, Gadag, Karnataka 582103, India. 2. Biostatistics and Bioinformatics, Chanabasava Nilaya, Bharthinagar, Dharwad 580001, Karanataka, India. 3. Department of Ayurveda, Rajiv Gandhi Education Society`s Ayurvedic Medical College, Ron, Karnataka 562209, India. * Chanabasayya Vastrad [email protected] Ph: +919480073398 Chanabasava Nilaya, Bharthinagar, Dharwad 580001 , Karanataka, India bioRxiv preprint doi: https://doi.org/10.1101/2020.12.21.423889; this version posted December 23, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder.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. Abstract Clear cell renal cell carcinoma (ccRCC) is one of the most common types of malignancy of the urinary system. The pathogenesis and effective diagnosis of ccRCC have become popular topics for research in the previous decade. In the current study, an integrated bioinformatics analysis was performed to identify core genes associated in ccRCC. An expression dataset (GSE105261) was downloaded from the Gene Expression Omnibus database, and included 26 ccRCC and 9 normal kideny samples. Assessment of the microarray dataset led to the recognition of differentially expressed genes (DEGs), which was subsequently used for pathway and gene ontology (GO) enrichment analysis. -
Cd8a (Ly-2) Microbeads Mouse
CD8a (Ly-2) MicroBeads mouse Order no. 130-049-401 Contents 1.2 Background information 1. Description Mouse CD8a (Ly-2) MicroBeads were developed for positive + 1.1 Principle of the MACS® Separation selection or depletion of mouse CD8a T cells from single-cell suspensions of lymphoid and non-lymphoid tissues or from 1.2 Background information peripheral blood. The CD8a antigen is expressed on most 1.3 Applications thymocytes, almost all cytotoxic T cells and on subpopulations of dendritic cells. CD8a functions as an accessory molecule in 1.4 Reagent and instrument requirements the recognition of MHC class I/peptide complexes by the TCR 2. Protocol heterodimer on cytotoxic CD8a+ T cells. 2.1 Sample preparation 1.3 Applications 2.2 Magnetic labeling + 2.3 Magnetic separation ● Positive selection or depletion of CD8a T cells from lymphoid organs, non-lymphoid tissue, peripheral blood, or in vitro 2.4 Cell separation with the autoMACS® Pro Separator cultured cells. 3. Example of a separation using the CD8a (Ly-2) MicroBeads + ● Isolation of purified CD8 cells for in vitro and in vivo studies 1,2 4. References on protective immune responses against parasites or allergens3, and for adoptive transfer into immunodeficient4,5 and virus infected mice6. + Warnings ● Isolation of highly pure CD8 T cells from CNS of MHV infected 7 Reagents contain sodium azide. Under acidic conditions sodium mice for evaluation of their chemokine expression pattern. azide yields hydrazoic acid, which is extremely toxic. Azide compounds should be diluted with running water before discarding. 1.4 Reagent and instrument requirements These precautions are recommended to avoid deposits in plumbing ● Buffer: Prepare a solution containing phosphate-buffered where explosive conditions may develop. -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Single-Cell RNA Sequencing Demonstrates the Molecular and Cellular Reprogramming of Metastatic Lung Adenocarcinoma
ARTICLE https://doi.org/10.1038/s41467-020-16164-1 OPEN Single-cell RNA sequencing demonstrates the molecular and cellular reprogramming of metastatic lung adenocarcinoma Nayoung Kim 1,2,3,13, Hong Kwan Kim4,13, Kyungjong Lee 5,13, Yourae Hong 1,6, Jong Ho Cho4, Jung Won Choi7, Jung-Il Lee7, Yeon-Lim Suh8,BoMiKu9, Hye Hyeon Eum 1,2,3, Soyean Choi 1, Yoon-La Choi6,10,11, Je-Gun Joung1, Woong-Yang Park 1,2,6, Hyun Ae Jung12, Jong-Mu Sun12, Se-Hoon Lee12, ✉ ✉ Jin Seok Ahn12, Keunchil Park12, Myung-Ju Ahn 12 & Hae-Ock Lee 1,2,3,6 1234567890():,; Advanced metastatic cancer poses utmost clinical challenges and may present molecular and cellular features distinct from an early-stage cancer. Herein, we present single-cell tran- scriptome profiling of metastatic lung adenocarcinoma, the most prevalent histological lung cancer type diagnosed at stage IV in over 40% of all cases. From 208,506 cells populating the normal tissues or early to metastatic stage cancer in 44 patients, we identify a cancer cell subtype deviating from the normal differentiation trajectory and dominating the metastatic stage. In all stages, the stromal and immune cell dynamics reveal ontological and functional changes that create a pro-tumoral and immunosuppressive microenvironment. Normal resident myeloid cell populations are gradually replaced with monocyte-derived macrophages and dendritic cells, along with T-cell exhaustion. This extensive single-cell analysis enhances our understanding of molecular and cellular dynamics in metastatic lung cancer and reveals potential diagnostic and therapeutic targets in cancer-microenvironment interactions. 1 Samsung Genome Institute, Samsung Medical Center, Seoul 06351, Korea. -
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, -
CD29 Identifies IFN-Γ–Producing Human CD8+ T Cells With
+ CD29 identifies IFN-γ–producing human CD8 T cells with an increased cytotoxic potential Benoît P. Nicoleta,b, Aurélie Guislaina,b, Floris P. J. van Alphenc, Raquel Gomez-Eerlandd, Ton N. M. Schumacherd, Maartje van den Biggelaarc,e, and Monika C. Wolkersa,b,1 aDepartment of Hematopoiesis, Sanquin Research, 1066 CX Amsterdam, The Netherlands; bLandsteiner Laboratory, Oncode Institute, Amsterdam University Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; cDepartment of Research Facilities, Sanquin Research, 1066 CX Amsterdam, The Netherlands; dDivision of Molecular Oncology and Immunology, Oncode Institute, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands; and eDepartment of Molecular and Cellular Haemostasis, Sanquin Research, 1066 CX Amsterdam, The Netherlands Edited by Anjana Rao, La Jolla Institute for Allergy and Immunology, La Jolla, CA, and approved February 12, 2020 (received for review August 12, 2019) Cytotoxic CD8+ T cells can effectively kill target cells by producing therefore developed a protocol that allowed for efficient iso- cytokines, chemokines, and granzymes. Expression of these effector lation of RNA and protein from fluorescence-activated cell molecules is however highly divergent, and tools that identify and sorting (FACS)-sorted fixed T cells after intracellular cytokine + preselect CD8 T cells with a cytotoxic expression profile are lacking. staining. With this top-down approach, we performed an un- + Human CD8 T cells can be divided into IFN-γ– and IL-2–producing biased RNA-sequencing (RNA-seq) and mass spectrometry cells. Unbiased transcriptomics and proteomics analysis on cytokine- γ– – + + (MS) analyses on IFN- and IL-2 producing primary human producing fixed CD8 T cells revealed that IL-2 cells produce helper + + + CD8 Tcells. -
BTLA−HVEM Checkpoint Axis Regulates Hepatic Homeostasis and Inflammation in a Cona-Induced Hepatitis Model in Zebrafish
BTLA−HVEM Checkpoint Axis Regulates Hepatic Homeostasis and Inflammation in a ConA-Induced Hepatitis Model in Zebrafish This information is current as Wei Shi, Tong Shao, Jiang-yuan Li, Dong-dong Fan, Ai-fu of September 27, 2021. Lin, Li-xin Xiang and Jian-zhong Shao J Immunol published online 27 September 2019 http://www.jimmunol.org/content/early/2019/09/26/jimmun ol.1900458 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2019/09/26/jimmunol.190045 Material 8.DCSupplemental http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 27, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2019 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published September 27, 2019, doi:10.4049/jimmunol.1900458 The Journal of Immunology BTLA–HVEM Checkpoint Axis Regulates Hepatic Homeostasis and Inflammation in a ConA-Induced Hepatitis Model in Zebrafish Wei Shi,* Tong Shao,* Jiang-yuan Li,* Dong-dong Fan,* Ai-fu Lin,* Li-xin Xiang,* and Jian-zhong Shao*,† The BTLA2HVEM checkpoint axis plays extensive roles in immunomodulation and diseases, including cancer and autoimmune disorders. -
Roles of Activating Functions 1 and 2 of Estrogen Receptor Α in Lymphopoiesis
236 2 Journal of A Andersson et al. ERαAF-1 and ERαAF-2 in 236:2 99–109 Endocrinology ER-mediated immunomodulation RESEARCH Roles of activating functions 1 and 2 of estrogen receptor α in lymphopoiesis Annica Andersson1, Anna E Törnqvist2, Sofia Moverare-Skrtic2, Angelina I Bernardi1, Helen H Farman2, Pierre Chambon3, Cecilia Engdahl1,2, Marie K Lagerquist2, Sara H Windahl2, Hans Carlsten1, Claes Ohlsson2 and Ulrika Islander1 1Centre for Bone and Arthritis Research, Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden 2Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden 3Institut de Génétique et de Biologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique, National de la Sante et de la Recherche Medicale, ULP, Collège de France, Illkirch-Strasbourg, France Correspondence should be addressed to A Andersson: [email protected] Abstract Apart from the role of sex steroids in reproduction, sex steroids are also important Key Words regulators of the immune system. 17β-estradiol (E2) represses T and B cell development, f lymphopoiesis but augments B cell function, possibly explaining the different nature of immune f estrogen receptor alpha responses in men and women. Both E2 and selective estrogen receptors modulators f estradiol (SERM) act via estrogen receptors (ER). Activating functions (AF)-1 and 2 of the ER f selective estrogen bind to coregulators and thus influence target gene transcription and subsequent receptor modulators cellular response to ER activation. The importance of ERαAF-1 and AF-2 in the immunomodulatory effects of E2/SERM has previously not been reported. -
Human Lectins, Their Carbohydrate Affinities and Where to Find Them
biomolecules Review Human Lectins, Their Carbohydrate Affinities and Where to Review HumanFind Them Lectins, Their Carbohydrate Affinities and Where to FindCláudia ThemD. Raposo 1,*, André B. Canelas 2 and M. Teresa Barros 1 1, 2 1 Cláudia D. Raposo * , Andr1 é LAQVB. Canelas‐Requimte,and Department M. Teresa of Chemistry, Barros NOVA School of Science and Technology, Universidade NOVA de Lisboa, 2829‐516 Caparica, Portugal; [email protected] 12 GlanbiaLAQV-Requimte,‐AgriChemWhey, Department Lisheen of Chemistry, Mine, Killoran, NOVA Moyne, School E41 of ScienceR622 Co. and Tipperary, Technology, Ireland; canelas‐ [email protected] NOVA de Lisboa, 2829-516 Caparica, Portugal; [email protected] 2* Correspondence:Glanbia-AgriChemWhey, [email protected]; Lisheen Mine, Tel.: Killoran, +351‐212948550 Moyne, E41 R622 Tipperary, Ireland; [email protected] * Correspondence: [email protected]; Tel.: +351-212948550 Abstract: Lectins are a class of proteins responsible for several biological roles such as cell‐cell in‐ Abstract:teractions,Lectins signaling are pathways, a class of and proteins several responsible innate immune for several responses biological against roles pathogens. such as Since cell-cell lec‐ interactions,tins are able signalingto bind to pathways, carbohydrates, and several they can innate be a immuneviable target responses for targeted against drug pathogens. delivery Since sys‐ lectinstems. In are fact, able several to bind lectins to carbohydrates, were approved they by canFood be and a viable Drug targetAdministration for targeted for drugthat purpose. delivery systems.Information In fact, about several specific lectins carbohydrate were approved recognition by Food by andlectin Drug receptors Administration was gathered for that herein, purpose. plus Informationthe specific organs about specific where those carbohydrate lectins can recognition be found by within lectin the receptors human was body. -
University of California Santa Cruz Sample
UNIVERSITY OF CALIFORNIA SANTA CRUZ SAMPLE-SPECIFIC CANCER PATHWAY ANALYSIS USING PARADIGM A dissertation submitted in partial satisfaction of the requirements for the degree of DOCTOR OF PHILOSOPHY in BIOMOLECULAR ENGINEERING AND BIOINFORMATICS by Stephen C. Benz June 2012 The Dissertation of Stephen C. Benz is approved: Professor David Haussler, Chair Professor Joshua Stuart Professor Nader Pourmand Dean Tyrus Miller Vice Provost and Dean of Graduate Studies Copyright c by Stephen C. Benz 2012 Table of Contents List of Figures v List of Tables xi Abstract xii Dedication xiv Acknowledgments xv 1 Introduction 1 1.1 Identifying Genomic Alterations . 2 1.2 Pathway Analysis . 5 2 Methods to Integrate Cancer Genomics Data 10 2.1 UCSC Cancer Genomics Browser . 11 2.2 BioIntegrator . 16 3 Pathway Analysis Using PARADIGM 20 3.1 Method . 21 3.2 Comparisons . 26 3.2.1 Distinguishing True Networks From Decoys . 27 3.2.2 Tumor versus Normal - Pathways associated with Ovarian Cancer 29 3.2.3 Differentially Regulated Pathways in ER+ve vs ER-ve breast can- cers . 36 3.2.4 Therapy response prediction using pathways (Platinum Free In- terval in Ovarian Cancer) . 38 3.3 Unsupervised Stratification of Cancer Patients by Pathway Activities . 42 4 SuperPathway - A Global Pathway Model for Cancer 51 4.1 SuperPathway in Ovarian Cancer . 55 4.2 SuperPathway in Breast Cancer . 61 iii 4.2.1 Chin-Naderi Cohort . 61 4.2.2 TCGA Breast Cancer . 63 4.3 Cross-Cancer SuperPathway . 67 5 Pathway Analysis of Drug Effects 74 5.1 SuperPathway on Breast Cell Lines . -