SOCS6 Rabbit Pab

Total Page：16

File Type：pdf, Size：1020Kb

Leader in Biomolecular Solutions for Life Science SOCS6 Rabbit pAb Catalog No.: A9957 Basic Information Background Catalog No. The protein encoded by this gene contains a SH2 domain and a CIS homolog domain. A9957 The protein thus belongs to the cytokine-induced STAT inhibitor (CIS), also known as suppressor of cytokine signaling (SOCS) or STAT-induced STAT inhibitor (SSI), protein Observed MW family. CIS family members are known to be cytokine-inducible negative regulators of 70kDa cytokine signaling. The expression of this gene can be induced by GM-CSF and EPO in hematopoietic cells. A high expression level of this gene was found in factor- Calculated MW independent chronic myelogenous leukemia (CML) and erythroleukemia (HEL) cell lines. 59kDa Category Primary antibody Applications WB, IHC Cross-Reactivity Human, Mouse Recommended Dilutions Immunogen Information WB 1:500 - 1:2000 Gene ID Swiss Prot 9306 O14544 IHC 1:50 - 1:200 Immunogen Recombinant fusion protein containing a sequence corresponding to amino acids 1-210 of human SOCS6 (NP_004223.2). Synonyms SOCS6;CIS-4;CIS4;HSPC060;SOCS-4;SOCS-6;SOCS4;SSI4;STAI4;STATI4 Contact Product Information www.abclonal.com Source Isotype Purification Rabbit IgG Affinity purification Storage Store at -20℃. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide,50% glycerol,pH7.3. Validation Data Western blot analysis of extracts of various cell lines, using SOCS6 antibody (A9957) at 1:1000 dilution. Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (AS014) at 1:10000 dilution. Lysates/proteins: 25ug per lane. Blocking buffer: 3% nonfat dry milk in TBST. Detection: ECL Basic Kit (RM00020). Exposure time: 30s. Immunohistochemistry of paraffin- Immunohistochemistry of paraffin- Immunohistochemistry of paraffin- embedded human mammary cancer using embedded human liver cancer using embedded human lung cancer using SOCS6 antibody (A9957) at dilution of SOCS6 antibody (A9957) at dilution of SOCS6 antibody (A9957) at dilution of 1:100 (40x lens). 1:100 (40x lens). 1:100 (40x lens). Antibody | Protein | ELISA Kits | Enzyme | NGS | Service For research use only. Not for therapeutic or diagnostic purposes. Please visit http://abclonal.com for a complete listing of recommended products..

Copy Link

Recommended publications

Supplementary Material DNA Methylation in Inflammatory Pathways Modifies the Association Between BMI and Adult-Onset Non- Atopic
Supplementary Material DNA Methylation in Inflammatory Pathways Modifies the Association between BMI and Adult-Onset Non- Atopic Asthma Ayoung Jeong 1,2, Medea Imboden 1,2, Akram Ghantous 3, Alexei Novoloaca 3, Anne-Elie Carsin 4,5,6, Manolis Kogevinas 4,5,6, Christian Schindler 1,2, Gianfranco Lovison 7, Zdenko Herceg 3, Cyrille Cuenin 3, Roel Vermeulen 8, Deborah Jarvis 9, André F. S. Amaral 9, Florian Kronenberg 10, Paolo Vineis 11,12 and Nicole Probst-Hensch 1,2,* 1 Swiss Tropical and Public Health Institute, 4051 Basel, Switzerland; [email protected] (A.J.); [email protected] (M.I.); [email protected] (C.S.) 2 Department of Public Health, University of Basel, 4001 Basel, Switzerland 3 International Agency for Research on Cancer, 69372 Lyon, France; [email protected] (A.G.); [email protected] (A.N.); [email protected] (Z.H.); [email protected] (C.C.) 4 ISGlobal, Barcelona Institute for Global Health, 08003 Barcelona, Spain; [email protected] (A.-E.C.); [email protected] (M.K.) 5 Universitat Pompeu Fabra (UPF), 08002 Barcelona, Spain 6 CIBER Epidemiología y Salud Pública (CIBERESP), 08005 Barcelona, Spain 7 Department of Economics, Business and Statistics, University of Palermo, 90128 Palermo, Italy; [email protected] 8 Environmental Epidemiology Division, Utrecht University, Institute for Risk Assessment Sciences, 3584CM Utrecht, Netherlands; [email protected] 9 Population Health and Occupational Disease, National Heart and Lung Institute, Imperial College, SW3 6LR London, UK; [email protected] (D.J.); [email protected] (A.F.S.A.) 10 Division of Genetic Epidemiology, Medical University of Innsbruck, 6020 Innsbruck, Austria; [email protected] 11 MRC-PHE Centre for Environment and Health, School of Public Health, Imperial College London, W2 1PG London, UK; [email protected] 12 Italian Institute for Genomic Medicine (IIGM), 10126 Turin, Italy * Correspondence: [email protected]; Tel.: +41-61-284-8378 Int.
[Show full text]
Expression of SOCS1 and SOCS3 Genes Is Differentially Regulated in Breast Cancer Cells in Response to Proinﬂammatory Cytokine and Growth Factor Signals
Oncogene (2007) 26, 1941–1948 & 2007 Nature Publishing Group All rights reserved 0950-9232/07 $30.00 www.nature.com/onc ORIGINAL ARTICLE Expression of SOCS1 and SOCS3 genes is differentially regulated in breast cancer cells in response to proinﬂammatory cytokine and growth factor signals MK Evans1, C-R Yu2, A Lohani1, RM Mahdi2, X Liu2, AR Trzeciak1 and CE Egwuagu2 1Laboratory of Cellular and Molecular Biology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA and 2Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD, USA DNA-hypermethylation of SOCS genes in breast, ova- Keywords: breast-cancer cells; SOCS; breast cancer; STAT; rian, squamous cell and hepatocellular carcinoma has led BRCA1; DNA hypermethylation; interferon to speculation that silencing of SOCS1 and SOCS3 genes might promote oncogenic transformation of epithelial tissues. To examine whether transcriptional silencing of SOCS genes is a common feature of human carcinoma, we have investigated regulation of SOCS genes expression by Introduction IFNc, IGF-1 and ionizing radiation, in a normal human mammary epithelial cell line (AG11134), two breast- Development of the mammary gland is regulated by cancer cell lines (MCF-7, HCC1937) and three prostate factors that coordinate proliferation, differentiation, cancer cell lines. Compared to normal breast cells, we maturation and apoptosis of mammary epithelial cells. observe a high level constitutive expression of SOCS2, Exquisite control of the initiation, strength and duration SOCS3, SOCS5, SOCS6, SOCS7, CIS and/or SOCS1 of signals from the diverse array of cytokines and genes in the human cancer cells. In MCF-7 and HCC1937 growth factors in mammalian breast is essential to the breast-cancer cells, transcription of SOCS1 is dramati- timely initiation of the menstrual cycle, lactation or cally up-regulated by IFNc and/or ionizing-radiation breast lobule involution (Medina, 2005).
[Show full text]
Structural Insights Into Substrate Recognition by the SOCS2 E3 Ubiquitin Ligase
bioRxiv preprint doi: https://doi.org/10.1101/470187; this version posted March 15, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 Title 2 Structural insights into substrate recognition by the SOCS2 E3 ubiquitin ligase 3 4 Authors 5 Wei-Wei Kung*, Sarath Ramachandran*, Nikolai Makukhin*, Elvira Bruno, Alessio Ciulli 6 *These authors contributed equally to this work 7 8 Address 9 Division of Biological Chemistry and Drug Discovery, School of Life Sciences, University of 10 Dundee, James Black Centre, Dow Street, Dundee, DD1 5EH, United Kingdom 11 12 Abstract 13 The suppressor of cytokine signaling 2 (SOCS2) acts as substrate recognition subunit of a 14 Cullin5 E3 ubiquitin ligase complex. SOCS2 binds to phosphotyrosine-modified epitopes 15 as degrons for ubiquitination and proteasomal degradation, yet the molecular basis of 16 substrate recognition has remained elusive. We solved co-crystal structures of SOCS2- 17 ElonginB-ElonginC in complex with phosphorylated peptides from substrates growth 18 hormone receptor (GHR-pY595) and erythropoietin receptor (EpoR-pY426) at 1.98 Å and 19 2.69 Å, respectively. Both peptides bind in an extended conformation recapitulating the 20 canonical SH2 domain-pY pose, yet capture different conformations of the EF loop via 21 specific hydrophobic interactions. The flexible BG loop, for the first time fully defined in the 22 electron density, does not contact the substrate degrons directly. Cancer-associated SNPs 23 located around the pY pocket weaken substrate-binding affinity in biophysical assays.
[Show full text]
The Emerging Role of Suppressors of Cytokine Signaling (SOCS) in the Development and Progression of Leukemia
cancers Review The Emerging Role of Suppressors of Cytokine Signaling (SOCS) in the Development and Progression of Leukemia Esra’a Keewan 1,2 and Ksenia Matlawska-Wasowska 1,2,* 1 Department of Pediatrics, Division of Hematology and Oncology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA; [email protected] 2 Comprehensive Cancer Center, University of New Mexico, Albuquerque, NM 87131, USA * Correspondence: [email protected]; Tel.: +1-505-272-6177 Simple Summary: The suppressors of cytokine signaling (SOCS) are known cytokine-inducible negative regulators of JAK/STAT and other cell signaling pathways. Deregulation of SOCS expression is linked to various tumor types and inﬂammatory diseases. While SOCS play a crucial role in the regulation of immune cell function, their roles in hematological malignancies have not been elucidated thus far. In this review, we summarize the current knowledge on the roles of SOCS in leukemia development and progression. We delineate the paradoxical activities of SOCS in different leukemia types and the regulatory mechanisms underlying SOCS deregulation in leukemia. Lastly, we discuss the possible implications of SOCS deregulation for leukemia diagnosis and prognosis. This paper provides new insights into the roles of SOCS in the pathobiology of leukemia and leukemia research. Abstract: Cytokines are pleiotropic signaling molecules that execute an essential role in cell-to-cell communication through binding to cell surface receptors. Receptor binding activates intracellular Citation: Keewan, E.; signaling cascades in the target cell that bring about a wide range of cellular responses, including Matlawska-Wasowska, K. The induction of cell proliferation, migration, differentiation, and apoptosis.
[Show full text]
Potential Implications for SOCS in Chronic Wound Healing
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 38: 1349-1358, 2016 Expression of the SOCS family in human chronic wound tissues: Potential implications for SOCS in chronic wound healing YI FENG1, ANDREW J. SANDERS1, FIONA RUGE1,2, CERI-ANN MORRIS2, KEITH G. HARDING2 and WEN G. JIANG1 1Cardiff China Medical Research Collaborative and 2Wound Healing Research Unit, Cardiff University School of Medicine, Cardiff University, Cardiff CF14 4XN, UK Received April 12, 2016; Accepted August 2, 2016 DOI: 10.3892/ijmm.2016.2733 Abstract. Cytokines play important roles in the wound an imbalance between proteinases and their inhibitors, and healing process through various signalling pathways. The the presence of senescent cells is of importance in chronic JAK-STAT pathway is utilised by most cytokines for signal wounds (1). A variety of treatments, such as dressings, appli- transduction and is regulated by a variety of molecules, cation of topical growth factors, autologous skin grafting and including suppressor of cytokine signalling (SOCS) proteins. bioengineered skin equivalents have been applied to deal SOCS are associated with inflammatory diseases and have with certain types of chronic wounds in addition to the basic an impact on cytokines, growth factors and key cell types treatments (1). However, the specific mechanisms of each trea- involved in the wound-healing process. SOCS, a negative ment remain unclear and are under investigation. Therefore, regulator of cytokine signalling, may hold the potential more insight into the mechanisms responsible are required to regulate cytokine-induced signalling in the chronic to gain a better understanding of the wound-healing process. wound-healing process. Wound edge tissues were collected Further clarification of this complex system may contribute to from chronic venous leg ulcer patients and classified as non- the emergence of a prognositc marker to predict the healing healing and healing wounds.
[Show full text]
Negative Regulation of Cytokine Signaling in Immunity
Downloaded from http://cshperspectives.cshlp.org/ on September 27, 2021 - Published by Cold Spring Harbor Laboratory Press Negative Regulation of Cytokine Signaling in Immunity Akihiko Yoshimura, Minako Ito, Shunsuke Chikuma, Takashi Akanuma, and Hiroko Nakatsukasa Department of Microbiology and Immunology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan Correspondence: [email protected] Cytokines are key modulators of immunity. Most cytokines use the Janus kinase and signal transducers and activators of transcription (JAK-STAT) pathway to promote gene tran- scriptional regulation, but their signals must be attenuated by multiple mechanisms. These include the suppressors of cytokine signaling (SOCS) family of proteins, which represent a main negative regulation mechanism for the JAK-STAT pathway. Cytokine-inducible Src homology 2 (SH2)-containing protein (CIS), SOCS1, and SOCS3 proteins regulate cytokine signals that control the polarization of CD4þ T cells and the maturation of CD8þ T cells. SOCS proteins also regulate innate immune cells and are involved in tumorigenesis. This review summarizes recent progress on CIS, SOCS1, and SOCS3 in T cells and tumor immunity. here are four types of the cytokine receptors: (ERK) pathway (see Fig. 1). Any receptor that T(1) receptors that activate nuclear factor activates intracellular signaling pathways has (NF)-kB and mitogen-activated protein (MAP) multiple negative feedback systems, which en- kinases (mainly p38 and c-Jun amino-terminal sures transient activation of the pathway and kinase [JNK]), such as receptors for the tumor downstream transcription factors. Typical neg- necrosis factor (TNF)-a family, the interleukin ative regulators are shown in Figure 1. Lack of (IL)-1 family, including IL-1b, IL-18, and IL- such negative regulators results in autoimmune 33, and the IL-17 family; (2) receptors that diseases, autoinﬂammatory diseases, and some- activate the Janus kinase and signal transducers times-fatal disorders, including cancer.
[Show full text]
The Role of Suppressor of Cytokine Signaling 1 and 3 in Human Cytomegalovirus Replication
Zurich Open Repository and Archive University of Zurich Main Library Strickhofstrasse 39 CH-8057 Zurich www.zora.uzh.ch Year: 2012 The Role of Suppressor of Cytokine Signaling 1 and 3 in Human Cytomegalovirus Replication Sonzogni, O Posted at the Zurich Open Repository and Archive, University of Zurich ZORA URL: https://doi.org/10.5167/uzh-71661 Dissertation Published Version Originally published at: Sonzogni, O. The Role of Suppressor of Cytokine Signaling 1 and 3 in Human Cytomegalovirus Replica- tion. 2012, University of Zurich, Faculty of Science. The Role of Suppressor of Cytokine Signaling 1 and 3 in Human Cytomegalovirus Replication Dissertation zur Erlangung der naturwissenschaftlichen Doktorwürde (Dr. sc. nat.) vorgelegt der Mathematisch-naturwissenschaftlichen Fakultät der Universität Zürich von Olmo Sonzogni von Moleno, TI Promotionskomitee: Prof. Dr. Nicolas J. Müller (Leitung der Dissertation) Prof. Dr. Christoph Renner (Vorsitz) Prof. Dr. Amedeo Caflisch Zürich, 2012 To my parents Dissertation Table of contents 1. Summary......................................................................................................................9 2. Zusammenfassung ...................................................................................................11 3. Introduction ...............................................................................................................13 3.1 Human cytomegalovirus .........................................................................................13 3.1.1 Epidemiology and
[Show full text]
Suppressor of Cytokine Signaling 2 Is a Feedback Inhibitor of TLR
Suppressor of Cytokine Signaling 2 Is a Feedback Inhibitor of TLR-Induced Activation in Human Monocyte-Derived Dendritic Cells This information is current as of September 27, 2021. Gernot Posselt, Harald Schwarz, Albert Duschl and Jutta Horejs-Hoeck J Immunol 2011; 187:2875-2884; Prepublished online 15 August 2011; doi: 10.4049/jimmunol.1003348 Downloaded from http://www.jimmunol.org/content/187/6/2875 Supplementary http://www.jimmunol.org/content/suppl/2011/08/15/jimmunol.100334 http://www.jimmunol.org/ Material 8.DC1 References This article cites 51 articles, 24 of which you can access for free at: http://www.jimmunol.org/content/187/6/2875.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on September 27, 2021 • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *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 © 2011 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Suppressor of Cytokine Signaling 2 Is a Feedback Inhibitor of TLR-Induced Activation in Human Monocyte-Derived Dendritic Cells Gernot Posselt, Harald Schwarz, Albert Duschl, and Jutta Horejs-Hoeck Dendritic cells (DCs) are key players in initiating and directing the immune response.
[Show full text]
SOCS6 Promotes Radiosensitivity and Decreases Cancer Cell Stemness in Esophageal Squamous Cell Carcinoma by Regulating C-Kit
Sun et al. Cancer Cell Int (2021) 21:165 https://doi.org/10.1186/s12935-021-01859-2 Cancer Cell International PRIMARY RESEARCH Open Access SOCS6 promotes radiosensitivity and decreases cancer cell stemness in esophageal squamous cell carcinoma by regulating c-Kit ubiquitylation Xuanzi Sun1, Yuchen Sun1, Jing Li1, Xu Zhao1, Xiaobo Shi1, Tuotuo Gong1, Shupei Pan2, Zhongqiang Zheng3 and Xiaozhi Zhang1* Abstract Background: Radiotherapy is a major treatment for esophageal squamous cell carcinoma (ESCC). However, HPV infection related radioresistance caused poor prognosis of ESCC. The function of SOCS6, which has been shown to be a tumor suppressor in several cancers, has not been fully investigated up till now. In this manuscript, we aim to further investigate the role of SOCS6 in regulating ESCC radioresistance. Methods: Fifty-seven ESCC patients were enrolled for survival analysis. SOCS6 was stably overexpressed in HPV + ESCC and ESCC cells, and cells were treated with radiation and then subjected to colony formation assays. Expression of DNA damage repair regulating proteins were examined by Western blotting. Cell growth, cell migration and cispl- atin sensitivity were then analyzed. Sphere formation assays and fow cytometry were used to investigate changes in cancer stem cell (CSC) properties. Immunofuorescent staining and confocal microscopy were used to locate SOCS6 and c-Kit. Ubiquitylation level of c-Kit were analyzed after immunoprecipitation. Then, coimmunoprecipitation (CoIP) of SOCS6 and c-Kit were performed. In vivo, xenograft animal models were treated with radiation to examine the radiosensitivity. Results: SOCS6 is correlated with better prognosis in ESCC patients. Radioresistance is impaired by SOCS6 upregula- tion, which inhibited cell growth, migration and increased sensitivity to cisplatin.
[Show full text]
Role of the JAK/STAT Pathway in Cervical Cancer: Its Relationship with HPV E6/E7 Oncoproteins
cells Review Role of the JAK/STAT Pathway in Cervical Cancer: Its Relationship with HPV E6/E7 Oncoproteins Adriana Gutiérrez-Hoya 1,2 and Isabel Soto-Cruz 1,* 1 Molecular Oncology Laboratory, Cell Differentiation and Cancer Research Unit, FES Zaragoza, National University of Mexico, Batalla 5 de Mayo s/n Col. Ejército de Oriente, Mexico City 09230, Mexico; [email protected] 2 Cátedra CONACYT, CONACYT, Avenida Insurgentes Sur 1582, Col. Crédito Constructor Del. Benito Juárez, Mexico City 03940, Mexico * Correspondence: [email protected]; Tel.: +52-55-56230796 Received: 31 August 2020; Accepted: 12 October 2020; Published: 15 October 2020 Abstract: The janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway is associated with the regulation of essential cellular mechanisms, such as proliferation, invasion, survival, inflammation, and immunity. Aberrant JAK/STAT signaling contributes to cancer progression and metastatic development. STAT proteins play an essential role in the development of cervical cancer, and the inhibition of the JAK/STAT pathway may be essential for enhancing tumor cell death. Persistent activation of different STATs is present in a variety of cancers, including cervical cancer, and their overactivation may be associated with a poor prognosis and poor overall survival. The oncoproteins E6 and E7 play a critical role in the progression of cervical cancer and may mediate the activation of the JAK/STAT pathway. Inhibition of STAT proteins appears to show promise for establishing new targets in cancer treatment. The present review summarizes the knowledge about the participation of the different components of the JAK/STAT pathway and the participation of the human papillomavirus (HPV) associated with the process of cellular malignancy.
[Show full text]
Supplementary Information
Supplementary Information Material and Methods RNA/DNA extraction and real time PCR AllPrep extraction kit (Qiagen, Hilden, Germany) was used to extract RNA and DNA. cDNA was obtained by reverse transcription using the high capacity cDNA reverse transcription kit (Applied Biosystems). RNA quality was checked by The Experion™ automated electrophoresis system (Bio- Rad Laboratories, Inc.) and RNA quality from all primary samples was of average quality. The expression of SOCSs as well as known marker genes was assessed by quantitative RT-PCR using TaqMan technology. TaqMan® chemistry-based primer/probe sets are recommended for use with RNA from microdissected samples, due to their improved specificity over primer only-based detection chemistries (e.g. SYBR) (Erickson et al, 2009). Reference numbers from Applied Biosystems are for SOCS1: Hs00864158_g1, SOCS2: HS 00919620_m1, SOCS3: Hs01000485_g1, SOCS6: Hs04272776_m1, osteopontin/SPP1,: Hs00959010_m1, CDX1: Hs00950423_g1, KIAA1199: Hs01552124_m1, GR: Hs00353740_m1 and HPRT: Hs02800695_m1. Briefly, TaqMan® Universal PCR Master Mix (Applied Biosystems) was used and the reaction was run on a cycler 7500 FAST Real time PCR Detection System (Applied Biosystems) with the following settings: 50°C 2 min, 95°C 10 min and 40x (15 sec 45°C and 1 min at 60°). Expression levels of the gene of interest were normalized against the house-keeping gene HPRT (Erickson et al, 2009). Absolute quantification analysis was used and the resulting expression data were presented as relative ratios to HPRT. Supplementary Figure 1 A *** *** *** 2.0 1.5 *** 1.0 *** *** * 0.5 *** log2 foldchangelog2 0.0 -0.5 SOCS1 SOCS2 SOCS3 SOCS4 SOCS5 SOCS6 SOCS7 CISH SPP1 CDX1 KIAA1199 B 2 SOCS2 SOCS6 SPP1 1 0 log2 log2 fold change 1 - 2 - adenoma CRC.A CRC.B CRC.C CRC.D Supporting Information Figure 1.
[Show full text]
Identification of the Presence and Activity of the JAK-STAT Pathway In
Identification of the Presence and Activity of the JAK-STAT Pathway in Canine Tumors Erin A. Fagan Thesis submitted to the faculty of the Virginia Polytechnic Institute and State University in partial fulfillment of the requirements for the degree of Master of Science In Biomedical and Veterinary Sciences Nikolaos Dervisis Shawna Klahn Tanya LeRoith April 13th 2017 Keywords: JAK-STAT, canine, hemangiosarcoma, mast cell tumor, thyroid carcinoma, apocrine gland anal sac adenocarcinoma, neoplasia ABSTRACT (Academic) Background: The JAK-STAT pathway is a cellular signaling pathway, which acts normally in humans and animals in the control of multiple important functions. Dysregulation of this pathway has been identified in human cancers, as well as a limited number of veterinary cancers. Objectives: The aims of this study were to identify the presence and tentative activity of components of the JAK-STAT pathway in selected canine tumors. Methods: Formalin-fixed, paraffin-embedded samples from mast cell tumors (MCT), hemangiosarcomas (HSA), thyroid carcinomas, and apocrine gland anal sac adenocarcinomas (AGASACA) were obtained from the Diagnostic Histopathology Laboratory at the Virginia Maryland College of Veterinary Medicine. Immunohistochemistry was performed to evaluate protein levels of JAK1, phospho-JAK1, JAK2, phospho-JAK2, STAT3, and phospho-STAT3. Signalment, treatment information, and survival information was obtained from the medical record for each case. Results: Tumor samples were scored for percent positive neoplastic cells. Positive staining was seen for all antibodies in all tumor types, with expression of JAK1, STAT3, and pSTAT3 being highest overall for all tumor types. Significant associations were seen between JAK1 and survival time in MCT (p = 0.03), pJAK1 and survival time in HSA (p = 0.009) and MCT (p = 0.04), and pSTAT3 and metastasis in MCT (p = 0.0008).
[Show full text]