DOCSLIB.ORG

TNFSF12 Antibody Cat

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
TNFSF12 Antibody Cat TNFSF12 Antibody Cat. No.: 25-364 TNFSF12 Antibody Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human Antibody produced in rabbits immunized with a synthetic peptide corresponding a region IMMUNOGEN: of human TNFSF12. TESTED APPLICATIONS: ELISA, WB TNFSF12 antibody can be used for detection of TNFSF12 by ELISA at 1:1562500. TNFSF12 APPLICATIONS: antibody can be used for detection of TNFSF12 by western blot at 1 μg/mL, and HRP conjugated secondary antibody should be diluted 1:50,000 - 100,000. POSITIVE CONTROL: 1) 721_B Cell Lysate PREDICTED MOLECULAR 17 kDa WEIGHT: Properties PURIFICATION: Antibody is purified by peptide affinity chromatography method. CLONALITY: Polyclonal CONJUGATE: Unconjugated PHYSICAL STATE: Liquid September 27, 2021 1 https://www.prosci-inc.com/tnfsf12-antibody-25-364.html Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% BUFFER: sucrose. CONCENTRATION: batch dependent For short periods of storage (days) store at 4˚C. For longer periods of storage, store STORAGE CONDITIONS: TNFSF12 antibody at -20˚C. As with any antibody avoid repeat freeze-thaw cycles. Additional Info OFFICIAL SYMBOL: TNFSF12 ALTERNATE NAMES: TNFSF12, APO3L, DR3LG, MGC129581, MGC20669, TWEAK ACCESSION NO.: NP_003800 PROTEIN GI NO.: 4507597 GENE ID: 8742 USER NOTE: Optimal dilutions for each application to be determined by the researcher. Background and References TNFSF12 is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein is a ligand for the FN14/TWEAKR receptor. This cytokine has overlapping signaling functions with TNF, but displays a much wider tissue distribution. This cytokine can induce apoptosis via multiple pathways of cell death in a cell type-specific manner. This cytokine is also found to promote proliferation and migration of endothelial cells, and thus acts as a regulator of angiogenesis. Two alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported. The protein encoded by this gene is a BACKGROUND: cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein is a ligand for the FN14/TWEAKR receptor. This cytokine has overlapping signaling functions with TNF, but displays a much wider tissue distribution. This cytokine can induce apoptosis via multiple pathways of cell death in a cell type-specific manner. This cytokine is also found to promote proliferation and migration of endothelial cells, and thus acts as a regulator of angiogenesis. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Entrez Gene record to access additional publications. REFERENCES: 1) Park, M.C., (2008) Scand. J. Rheumatol. 37 (3), 173-178. ANTIBODIES FOR RESEARCH USE ONLY. For additional information, visit ProSci's Terms & Conditions Page. September 27, 2021 2 https://www.prosci-inc.com/tnfsf12-antibody-25-364.html.
Load more

Recommended publications
  • The TNF and TNF Receptor Review Superfamilies: Integrating Mammalian Biology
    Cell, Vol. 104, 487±501, February 23, 2001, Copyright 2001 by Cell Press The TNF and TNF Receptor Review Superfamilies: Integrating Mammalian Biology Richard M. Locksley,*²³k Nigel Killeen,²k The receptors and ligands in this superfamily have and Michael J. Lenardo§k unique structural attributes that couple them directly to *Department of Medicine signaling pathways for cell proliferation, survival, and ² Department of Microbiology and Immunology differentiation. Thus, they have assumed prominent ³ Howard Hughes Medical Institute roles in the generation of tissues and transient microen- University of California, San Francisco vironments. Most TNF/TNFR SFPs are expressed in the San Francisco, California 94143 immune system, where their rapid and potent signaling § Laboratory of Immunology capabilities are crucial in coordinating the proliferation National Institute of Allergy and Infectious Diseases and protective functions of pathogen-reactive cells. National Institutes of Health Here, we review the organization of the TNF/TNFR SF Bethesda, Maryland 20892 and how these proteins have been adapted for pro- cesses as seemingly disparate as host defense and or- ganogenesis. In interpreting this large and highly active Introduction area of research, we have focused on common themes that unite the actions of these genes in different tissues. Three decades ago, lymphotoxin (LT) and tumor necro- We also discuss the evolutionary success of this super- sis factor (TNF) were identified as products of lympho- familyÐsuccess that we infer from its expansion across cytes and macrophages that caused the lysis of certain the mammalian genome and from its many indispens- types of cells, especially tumor cells (Granger et al., able roles in mammalian biology.
    [Show full text]
  • 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.
    [Show full text]
  • Mouse TWEAK/TNFSF12 Antibody Antigen Affinity-Purified Polyclonal Goat Igg Catalog Number: AF1237
    Mouse TWEAK/TNFSF12 Antibody Antigen Affinity-purified Polyclonal Goat IgG Catalog Number: AF1237 DESCRIPTION Species Reactivity Mouse Specificity Detects TWEAK/TNFSF12 in direct ELISAs and Western blots. In direct ELISAs, approximately 30% cross­reactivity with recombinant human TWEAK is observed and less than 1% cross­reactivity with recombinant mouse (rm) BAFF, rmFas Ligand, rmOX40 Ligand, rmTNF­α, and rmTRAIL is observed. Source Polyclonal Goat IgG Purification Antigen Affinity­purified Immunogen E. coli­derived recombinant mouse TWEAK/TNFSF12 Arg105­His249 Accession # O54907 Endotoxin Level <0.10 EU per 1 μg of the antibody by the LAL method. Formulation Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. See Certificate of Analysis for details. APPLICATIONS Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website. Recommended Sample Concentration Western Blot 0.1 µg/mL Recombinant Mouse TWEAK/TNFSF12 (Catalog # 1237­TW) Neutralization Measured by its ability to neutralize TWEAK/TNFSF12­induced inhibition of proliferation in the HT­29 human colon adenocarcinoma cell line. Yu, K. Y. et al. (1999) J. Biol. Chem. 274:13733; Harrop, J. A. et al. (1998) J. Biol. Chem. 273:27548The Neutralization Dose (ND ) is typically 4­16 µg/mL in the presence of 2 µg/mL Recombinant 50 Mouse TWEAK/TNFSF12. DATA Neutralization TWEAK/TNFSF12 Inhibition of Cell Proliferation and Neutralization by Mouse TWEAK/TNFSF12 Antibody. Recombinant Mouse TWEAK/TNFSF12 (Catalog # 1237­TW) inhibits proliferation in the the HT­29 human colon adenocarcinoma cell line in a dose­dependent manner (orange line).
    [Show full text]
  • Supplementary Material
    Supplementary Material Table S1: Significant downregulated KEGGs pathways identified by DAVID following exposure to five cinnamon- based phenylpropanoids (p < 0.05). p-value Term: Genes (Benjamini) Cytokine-cytokine receptor interaction: FASLG, TNFSF14, CXCL11, IL11, FLT3LG, CCL3L1, CCL3L3, CXCR6, XCR1, 2.43 × 105 RTEL1, CSF2RA, TNFRSF17, TNFRSF14, CCNL2, VEGFB, AMH, TNFRSF10B, INHBE, IFNB1, CCR3, VEGFA, CCR2, IL12A, CCL1, CCL3, CXCL5, TNFRSF25, CCR1, CSF1, CX3CL1, CCL7, CCL24, TNFRSF1B, IL12RB1, CCL21, FIGF, EPO, IL4, IL18R1, FLT1, TGFBR1, EDA2R, HGF, TNFSF8, KDR, LEP, GH2, CCL13, EPOR, XCL1, IFNA16, XCL2 Neuroactive ligand-receptor interaction: OPRM1, THRA, GRIK1, DRD2, GRIK2, TACR2, TACR1, GABRB1, LPAR4, 9.68 × 105 GRIK5, FPR1, PRSS1, GNRHR, FPR2, EDNRA, AGTR2, LTB4R, PRSS2, CNR1, S1PR4, CALCRL, TAAR5, GABRE, PTGER1, GABRG3, C5AR1, PTGER3, PTGER4, GABRA6, GABRA5, GRM1, PLG, LEP, CRHR1, GH2, GRM3, SSTR2, Chlorogenic acid Chlorogenic CHRM3, GRIA1, MC2R, P2RX2, TBXA2R, GHSR, HTR2C, TSHR, LHB, GLP1R, OPRD1 Hematopoietic cell lineage: IL4, CR1, CD8B, CSF1, FCER2, GYPA, ITGA2, IL11, GP9, FLT3LG, CD38, CD19, DNTT, 9.29 × 104 GP1BB, CD22, EPOR, CSF2RA, CD14, THPO, EPO, HLA-DRA, ITGA2B Cytokine-cytokine receptor interaction: IL6ST, IL21R, IL19, TNFSF15, CXCR3, IL15, CXCL11, TGFB1, IL11, FLT3LG, CXCL10, CCR10, XCR1, RTEL1, CSF2RA, IL21, CCNL2, VEGFB, CCR8, AMH, TNFRSF10C, IFNB1, PDGFRA, EDA, CXCL5, TNFRSF25, CSF1, IFNW1, CNTFR, CX3CL1, CCL5, TNFRSF4, CCL4, CCL27, CCL24, CCL25, CCL23, IFNA6, IFNA5, FIGF, EPO, AMHR2, IL2RA, FLT4, TGFBR2, EDA2R,
    [Show full text]
  • Gene List HTG Edgeseq Immuno-Oncology Assay
    Gene List HTG EdgeSeq Immuno-Oncology Assay Adhesion ADGRE5 CLEC4A CLEC7A IBSP ICAM4 ITGA5 ITGB1 L1CAM MBL2 SELE ALCAM CLEC4C DST ICAM1 ITGA1 ITGA6 ITGB2 LGALS1 MUC1 SVIL CDH1 CLEC5A EPCAM ICAM2 ITGA2 ITGAL ITGB3 LGALS3 NCAM1 THBS1 CDH5 CLEC6A FN1 ICAM3 ITGA4 ITGAM ITGB4 LGALS9 PVR THY1 Apoptosis APAF1 BCL2 BID CARD11 CASP10 CASP8 FADD NOD1 SSX1 TP53 TRAF3 BCL10 BCL2L1 BIRC5 CASP1 CASP3 DDX58 NLRP3 NOD2 TIMP1 TRAF2 TRAF6 B-Cell Function BLNK BTLA CD22 CD79A FAS FCER2 IKBKG PAX5 SLAMF1 SLAMF7 SPN BTK CD19 CD24 EBF4 FASLG IKBKB MS4A1 RAG1 SLAMF6 SPI1 Cell Cycle ABL1 ATF1 ATM BATF CCND1 CDK1 CDKN1B NCL RELA SSX1 TBX21 TP53 ABL2 ATF2 AXL BAX CCND3 CDKN1A EGR1 REL RELB TBK1 TIMP1 TTK Cell Signaling ADORA2A DUSP4 HES1 IGF2R LYN MAPK1 MUC1 NOTCH1 RIPK2 SMAD3 STAT5B AKT3 DUSP6 HES5 IKZF1 MAF MAPK11 MYC PIK3CD RNF4 SOCS1 STAT6 BCL6 ELK1 HEY1 IKZF2 MAP2K1 MAPK14 NFATC1 PIK3CG RORC SOCS3 SYK CEBPB EP300 HEY2 IKZF3 MAP2K2 MAPK3 NFATC3 POU2F2 RUNX1 SPINK5 TAL1 CIITA ETS1 HEYL JAK1 MAP2K4 MAPK8 NFATC4 PRKCD RUNX3 STAT1 TCF7 CREB1 FLT3 HMGB1 JAK2 MAP2K7 MAPKAPK2 NFKB1 PRKCE S100B STAT2 TYK2 CREB5 FOS HRAS JAK3 MAP3K1 MEF2C NFKB2 PTEN SEMA4D STAT3 CREBBP GATA3 IGF1R KIT MAP3K5 MTDH NFKBIA PYCARD SMAD2 STAT4 Chemokine CCL1 CCL16 CCL20 CCL25 CCL4 CCR2 CCR7 CX3CL1 CXCL12 CXCL3 CXCR1 CXCR6 CCL11 CCL17 CCL21 CCL26 CCL5 CCR3 CCR9 CX3CR1 CXCL13 CXCL5 CXCR2 MST1R CCL13 CCL18 CCL22 CCL27 CCL7 CCR4 CCRL2 CXCL1 CXCL14 CXCL6 CXCR3 PPBP CCL14 CCL19 CCL23 CCL28 CCL8 CCR5 CKLF CXCL10 CXCL16 CXCL8 CXCR4 XCL2 CCL15 CCL2 CCL24 CCL3 CCR1 CCR6 CMKLR1 CXCL11 CXCL2 CXCL9 CXCR5
    [Show full text]
  • Intratumoral Injection of SYNB1891, a Synthetic Biotic Medicine Designed
    Intratumoral injection of SYNB1891 A Synthetic Biotic medicine designed to activate the innate immune system. Therapy demonstrates target engagement in humans including intratumoral STING activation. Janku F, MD Anderson Cancer Center; Luke JJ, UPMC Hillman Cancer Center; Brennan AM, Synlogic; Riese RJ, Synlogic; Varterasian M, Pharmaceutical Consultant; Kuhn K, Synlogic; Sokolovska A, Synlogic; Strauss J, Mary Crowley Cancer Research Presented by Filip Janku, MD, PhD Study supported by Synlogic, Inc American Association for Cancer Research (AACR) April 2021 Introduction and Methods SYNB1891 Strain Phase 1 First-in-Human Clinical Trial • Live, modified strain of the probiotic E. coli • Enrolling patients with refractory advanced solid Nissle engineered to produce cyclic tumors or lymphoma dinucleotides (CDN) under hypoxia leading to stimulator of interferon genes (STING)- • Intratumoral (IT) injection of SYNB1891 on Days activation 1, 8 and 15 of the first 21-day cycle and then on Day 1 of each subsequent cycle. • Preferentially taken up by phagocytic antigen- presenting cells in tumors, activating • Dose escalation planned across 7 cohorts (1x106 complementary innate immune pathways – 1x109 live cells) with Arm 1 consisting of (direct CDN STING activation; cGAS-mediated SYNB1891 as monotherapy, and Arm 2 in STING activation and TLR4/MyD88 activation by combination with atezolizumab the bacterial chassis) SYNB1891 was safe and well-tolerated in heterogenous population Nov 2020: Interim Analysis IA Updated through 15 Mar 2021 15 Mar 2021:
    [Show full text]
  • Development and Validation of a Protein-Based Risk Score for Cardiovascular Outcomes Among Patients with Stable Coronary Heart Disease
    Supplementary Online Content Ganz P, Heidecker B, Hveem K, et al. Development and validation of a protein-based risk score for cardiovascular outcomes among patients with stable coronary heart disease. JAMA. doi: 10.1001/jama.2016.5951 eTable 1. List of 1130 Proteins Measured by Somalogic’s Modified Aptamer-Based Proteomic Assay eTable 2. Coefficients for Weibull Recalibration Model Applied to 9-Protein Model eFigure 1. Median Protein Levels in Derivation and Validation Cohort eTable 3. Coefficients for the Recalibration Model Applied to Refit Framingham eFigure 2. Calibration Plots for the Refit Framingham Model eTable 4. List of 200 Proteins Associated With the Risk of MI, Stroke, Heart Failure, and Death eFigure 3. Hazard Ratios of Lasso Selected Proteins for Primary End Point of MI, Stroke, Heart Failure, and Death eFigure 4. 9-Protein Prognostic Model Hazard Ratios Adjusted for Framingham Variables eFigure 5. 9-Protein Risk Scores by Event Type This supplementary material has been provided by the authors to give readers additional information about their work. Downloaded From: https://jamanetwork.com/ on 10/02/2021 Supplemental Material Table of Contents 1 Study Design and Data Processing ......................................................................................................... 3 2 Table of 1130 Proteins Measured .......................................................................................................... 4 3 Variable Selection and Statistical Modeling ........................................................................................
    [Show full text]
  • Supplementary Table 1: Differentially Methylated Genes and Functions of the Genes Before/After Treatment with A) Doxorubicin and B) FUMI and in C) Responders Vs
    Supplementary Table 1: Differentially methylated genes and functions of the genes before/after treatment with a) doxorubicin and b) FUMI and in c) responders vs. non- responders for doxorubicin and d) FUMI Differentially methylated genes before/after treatment a. Doxo GENE FUNCTION CCL5, CCL8, CCL15, CCL21, CCR1, CD33, IL5, immunoregulatory and inflammatory processes IL8, IL24, IL26, TNFSF11 CCNA1, CCND2, CDKN2A cell cycle regulators ESR1, FGF2, FGF14, FGF18 growth factors WT1, RASSF5, RASSF6 tumor suppressor b. FUMI GENE FUNCTION CCL7, CCL15, CD28, CD33, CD40, CD69, TNFSF18 immunoregulatory and inflammatory processes CCND2, CDKN2A cell cycle regulators IGF2BP1, IGFBP3 growth factors HOXB4, HOXB6, HOXC8 regulation of cell transcription WT1, RASSF6 tumor suppressor Differentially methylated genes in responders vs. non-responders c. Doxo GENE FUNCTION CBR1, CCL4, CCL8, CCR1, CCR7, CD1A, CD1B, immunoregulatory and inflammatory processes CD1D, CD1E, CD33, CD40, IL5, IL8, IL20, IL22, TLR4 CCNA1, CCND2, CDKN2A cell cycle regulators ESR2, ERBB3, FGF11, FGF12, FGF14, FGF17 growth factors WNT4, WNT16, WNT10A implicated in oncogenesis TNFSF12, TNFSF15 apoptosis FOXL1, FOXL2, FOSL1,HOXA2, HOXA7, HOXA11, HOXA13, HOXB4, HOXB6, HOXB8, HOXB9, HOXC8, regulation of cell transcription HOXD8, HOXD9, HOXD11 GSTP1, MGMT DNA repair APC, WT1 tumor suppressor d. FUMI GENE FUNCTION CCL1, CCL3, CCL5,CCL14, CD1B, CD33, CD40, CD69, immunoregulatory and inflammatory IL20, IL32 processes CCNA1, CCND2, CDKN2A cell cycle regulators IGF2BP1, IGFBP3, IGFBP7, EGFR, ESR2,RARB2
    [Show full text]
  • Cytokine Biosignature of Active and Latent Mycobacterium Tuberculosis Infection in Children
    pathogens Article Cytokine Biosignature of Active and Latent Mycobacterium Tuberculosis Infection in Children Magdalena Druszczynska 1,* , Michal Seweryn 2, Sebastian Wawrocki 1 , Magdalena Kowalewska-Pietrzak 3, Anna Pankowska 3 and Wieslawa Rudnicka 1 1 Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Im-munology, Faculty of Biology and Environmental Protection, University of Lodz, Banacha 12/16, 90-237 Lodz, Poland; [email protected] (S.W.); [email protected] (W.R.) 2 Biobank Lab, Department of Molecular Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, Banacha 12/16, 90-237 Lodz, Poland; [email protected] 3 Regional Specialized Hospital of Tuberculosis, Lung Diseases and Rehabilitation in Lodz, Okolna 181, 91-520 Lodz, Poland; [email protected] (M.K.-P.); [email protected] (A.P.) * Correspondence: [email protected]; Tel.: +48-42-635-44-70 Abstract: None of the currently used diagnostic tools are efficient enough in diagnosing Mycobac- terium tuberculosis (M.tb) infection in children. The study was aimed to identify cytokine biosigna- tures characterizing active and latent tuberculosis (TB) in children. Using a multiplex bead-based technology, we analyzed the levels of 53 Th17-related cytokines and inflammatory mediators in sera from 216 BCG-vaccinated children diagnosed with active TB (TB) or latent TB (LTBI) as well as uninfected controls (HC). Children with active TB, compared to HC children, showed reduced serum levels of IL-17A, MMP-2, OPN, PTX-3, and markedly elevated concentrations of APRIL/TNFSF13. Citation: Druszczynska, M.; IL-21, sCD40L, MMP-2, and IL-8 were significantly differentially expressed in the comparisons Seweryn, M.; Wawrocki, S.; between groups: (1) HC versus TB and LTBI (jointly), and (2) TB versus LTBI.
    [Show full text]
  • Cx3cr1 Mediates the Development of Monocyte-Derived Dendritic Cells During Hepatic Inflammation
    CX3CR1 MEDIATES THE DEVELOPMENT OF MONOCYTE-DERIVED DENDRITIC CELLS DURING HEPATIC INFLAMMATION. Supplementary material Supplementary Figure 1: Liver CD45+ myeloid cells were pre-gated for Ly6G negative cells for excluding granulocytes and HDCs subsequently analyzed among the cells that were CD11c+ and had high expression of MHCII. Supplementary Table 1 low/- high + Changes in gene expression between CX3CR1 and CX3CR1 CD11b myeloid hepatic dendritic cells (HDCs) from CCl4-treated mice high Genes up-regulated in CX3CR1 HDCs Gene Fold changes P value Full name App 4,01702 5,89E-05 amyloid beta (A4) precursor protein C1qa 9,75881 1,69E-22 complement component 1, q subcomponent, alpha polypeptide C1qb 9,19882 3,62E-20 complement component 1, q subcomponent, beta polypeptide Ccl12 2,51899 0,011769 chemokine (C-C motif) ligand 12 Ccl2 6,53486 6,37E-11 chemokine (C-C motif) ligand 2 Ccl3 4,99649 5,84E-07 chemokine (C-C motif) ligand 3 Ccl4 4,42552 9,62E-06 chemokine (C-C motif) ligand 4 Ccl6 3,9311 8,46E-05 chemokine (C-C motif) ligand 6 Ccl7 2,60184 0,009272 chemokine (C-C motif) ligand 7 Ccl9 4,17294 3,01E-05 chemokine (C-C motif) ligand 9 Ccr2 3,35195 0,000802 chemokine (C-C motif) receptor 2 Ccr5 3,23358 0,001222 chemokine (C-C motif) receptor 5 Cd14 6,13325 8,61E-10 CD14 antigen Cd36 2,94367 0,003243 CD36 antigen Cd44 4,89958 9,60E-07 CD44 antigen Cd81 6,49623 8,24E-11 CD81 antigen Cd9 3,06253 0,002195 CD9 antigen Cdkn1a 4,65279 3,27E-06 cyclin-dependent kinase inhibitor 1A (P21) Cebpb 6,6083 3,89E-11 CCAAT/enhancer binding protein (C/EBP),
    [Show full text]
  • Figure S1. Reverse Transcription‑Quantitative PCR Analysis of ETV5 Mrna Expression Levels in Parental and ETV5 Stable Transfectants
    Figure S1. Reverse transcription‑quantitative PCR analysis of ETV5 mRNA expression levels in parental and ETV5 stable transfectants. (A) Hec1a and Hec1a‑ETV5 EC cell lines; (B) Ishikawa and Ishikawa‑ETV5 EC cell lines. **P<0.005, unpaired Student's t‑test. EC, endometrial cancer; ETV5, ETS variant transcription factor 5. Figure S2. Survival analysis of sample clusters 1‑4. Kaplan Meier graphs for (A) recurrence‑free and (B) overall survival. Survival curves were constructed using the Kaplan‑Meier method, and differences between sample cluster curves were analyzed by log‑rank test. Figure S3. ROC analysis of hub genes. For each gene, ROC curve (left) and mRNA expression levels (right) in control (n=35) and tumor (n=545) samples from The Cancer Genome Atlas Uterine Corpus Endometrioid Cancer cohort are shown. mRNA levels are expressed as Log2(x+1), where ‘x’ is the RSEM normalized expression value. ROC, receiver operating characteristic. Table SI. Clinicopathological characteristics of the GSE17025 dataset. Characteristic n % Atrophic endometrium 12 (postmenopausal) (Control group) Tumor stage I 91 100 Histology Endometrioid adenocarcinoma 79 86.81 Papillary serous 12 13.19 Histological grade Grade 1 30 32.97 Grade 2 36 39.56 Grade 3 25 27.47 Myometrial invasiona Superficial (<50%) 67 74.44 Deep (>50%) 23 25.56 aMyometrial invasion information was available for 90 of 91 tumor samples. Table SII. Clinicopathological characteristics of The Cancer Genome Atlas Uterine Corpus Endometrioid Cancer dataset. Characteristic n % Solid tissue normal 16 Tumor samples Stagea I 226 68.278 II 19 5.740 III 70 21.148 IV 16 4.834 Histology Endometrioid 271 81.381 Mixed 10 3.003 Serous 52 15.616 Histological grade Grade 1 78 23.423 Grade 2 91 27.327 Grade 3 164 49.249 Molecular subtypeb POLE 17 7.328 MSI 65 28.017 CN Low 90 38.793 CN High 60 25.862 CN, copy number; MSI, microsatellite instability; POLE, DNA polymerase ε.
    [Show full text]
  • KRAS Mutations Are Negatively Correlated with Immunity in Colon Cancer
    www.aging-us.com AGING 2021, Vol. 13, No. 1 Research Paper KRAS mutations are negatively correlated with immunity in colon cancer Xiaorui Fu1,2,*, Xinyi Wang1,2,*, Jinzhong Duanmu1, Taiyuan Li1, Qunguang Jiang1 1Department of Gastrointestinal Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, People's Republic of China 2Queen Mary College, Medical Department, Nanchang University, Nanchang, Jiangxi, People's Republic of China *Equal contribution Correspondence to: Qunguang Jiang; email: [email protected] Keywords: KRAS mutations, immunity, colon cancer, tumor-infiltrating immune cells, inflammation Received: March 27, 2020 Accepted: October 8, 2020 Published: November 26, 2020 Copyright: © 2020 Fu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT The heterogeneity of colon cancer tumors suggests that therapeutics targeting specific molecules may be effective in only a few patients. It is therefore necessary to explore gene mutations in colon cancer. In this study, we obtained colon cancer samples from The Cancer Genome Atlas, and the International Cancer Genome Consortium. We evaluated the landscape of somatic mutations in colon cancer and found that KRAS mutations, particularly rs121913529, were frequent and had prognostic value. Using ESTIMATE analysis, we observed that the KRAS-mutated group had higher tumor purity, lower immune score, and lower stromal score than the wild- type group. Through single-sample Gene Set Enrichment Analysis and Gene Set Enrichment Analysis, we found that KRAS mutations negatively correlated with enrichment levels of tumor infiltrating lymphocytes, inflammation, and cytolytic activities.
    [Show full text]