Tumor Markers
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Ptvg-HP Vaccine Protocol
Version 10/7/2015 Randomized Phase II Trial of a DNA Vaccine Encoding Prostatic Acid Phosphatase (pTVG-HP) versus GM-CSF Adjuvant in Patients with Non-Metastatic Prostate Cancer CO 08801 Investigational Agent: BB IND 12109 - pTVG-HP DNA encoding human prostatic acid phosphatase Study Sponsors: 56 patients – treated at UWCCC and UCSF Department of Defense Prostate Cancer Research Program federal grant 50 patients in biomarker cohort – treated at UWCCC, UCSF and JHU Madison Vaccines Inc. (MVI) corporate sponsor STUDY SITE INFORMATION Study Sites: University of Wisconsin Carbone Cancer Center (UWCCC) 1111 Highland Avenue Madison, WI 53705 University of California San Francisco (UCSF) Johns Hopkins School of Medicine (JHU) Study Principal Investigator: Douglas G. McNeel, M.D., Ph.D. UWCCC 7007 Wisconsin Institutes for Medical Research 1111 Highland Ave. Madison, WI 53705 Tel: (608) 263-4198 Fax: (608) 265-0614 [email protected] UWCCC Local Principal Investigator : Glenn Liu, MD UWCCC 7051 Wisconsin Institutes for Medical Research 1111 Highland Ave. Madison, WI 53705 Tel : (608) 265-8689 Fax : (608) 265-5146 [email protected] Medical Monitor: Mark Albertini, M.D. UWCCC 600 Highland Ave. K6/5 CSC Madison, WI 53792 Tel: (608) 265-8131 Fax: (608) 265-8133 [email protected] Other UWCCC Investigators: Joshua Lang, M.D. – Clinical Investigator Christos Kyriakopolous, M.D. – Clinical Investigator Robert Jeraj, Ph.D. – Medical Physics, Quantitative Total Bone Imaging Scott Perlman, M.D. – Nuclear Medicine UCSF Principal Investigator: Lawrence Fong, M.D. JHU Principal Investigator: Emmanuel Antonarakis, MD Study Coordinator: Mary Jane Staab, R.N. B.S.N. UWCCC 600 Highland Ave. -
The Rac Gtpase in Cancer: from Old Concepts to New Paradigms Marcelo G
Published OnlineFirst August 14, 2017; DOI: 10.1158/0008-5472.CAN-17-1456 Cancer Review Research The Rac GTPase in Cancer: From Old Concepts to New Paradigms Marcelo G. Kazanietz1 and Maria J. Caloca2 Abstract Rho family GTPases are critical regulators of cellular func- mislocalization of Rac signaling components. The unexpected tions that play important roles in cancer progression. Aberrant pro-oncogenic functions of Rac GTPase-activating proteins also activity of Rho small G-proteins, particularly Rac1 and their challenged the dogma that these negative Rac regulators solely regulators, is a hallmark of cancer and contributes to the act as tumor suppressors. The potential contribution of Rac tumorigenic and metastatic phenotypes of cancer cells. This hyperactivation to resistance to anticancer agents, including review examines the multiple mechanisms leading to Rac1 targeted therapies, as well as to the suppression of antitumor hyperactivation, particularly focusing on emerging paradigms immune response, highlights the critical need to develop ther- that involve gain-of-function mutations in Rac and guanine apeutic strategies to target the Rac pathway in a clinical setting. nucleotide exchange factors, defects in Rac1 degradation, and Cancer Res; 77(20); 5445–51. Ó2017 AACR. Introduction directed toward targeting Rho-regulated pathways for battling cancer. Exactly 25 years ago, two seminal papers by Alan Hall and Nearly all Rho GTPases act as molecular switches that cycle colleagues illuminated us with one of the most influential dis- between GDP-bound (inactive) and GTP-bound (active) forms. coveries in cancer signaling: the association of Ras-related small Activation is promoted by guanine nucleotide exchange factors GTPases of the Rho family with actin cytoskeleton reorganization (GEF) responsible for GDP dissociation, a process that normally (1, 2). -
A GTP-State Specific Cyclic Peptide Inhibitor of the Gtpase Gαs
bioRxiv preprint doi: https://doi.org/10.1101/2020.04.25.054080; this version posted April 27, 2020. 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-NC-ND 4.0 International license. A GTP-state specific cyclic peptide inhibitor of the GTPase Gαs Shizhong A. Dai1,2†, Qi Hu1,2†, Rong Gao3†, Andre Lazar1,4†, Ziyang Zhang1,2, Mark von Zastrow1,4, Hiroaki Suga3*, Kevan M. Shokat1,2* 5 1Department of Cellular and Molecular Pharmacology, University of California San Francisco, San Francisco, CA, 94158, USA 2Howard Hughes Medical Institute 3Department of Chemistry, Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan 10 4Department of Psychiatry, University of California, San Francisco, San Francisco, CA, 94158, USA *Correspondence to: [email protected], [email protected] †These authors contributed equally. 15 20 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.04.25.054080; this version posted April 27, 2020. 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-NC-ND 4.0 International license. Abstract: The G protein-coupled receptor (GPCR) cascade leading to production of the second messenger cAMP is replete with pharmacologically targetable receptors and enzymes with the exception of the stimulatory G protein α subunit, Gαs. -
Clinical Utility of Recently Identified Diagnostic, Prognostic, And
Modern Pathology (2017) 30, 1338–1366 1338 © 2017 USCAP, Inc All rights reserved 0893-3952/17 $32.00 Clinical utility of recently identified diagnostic, prognostic, and predictive molecular biomarkers in mature B-cell neoplasms Arantza Onaindia1, L Jeffrey Medeiros2 and Keyur P Patel2 1Instituto de Investigacion Marques de Valdecilla (IDIVAL)/Hospital Universitario Marques de Valdecilla, Santander, Spain and 2Department of Hematopathology, MD Anderson Cancer Center, Houston, TX, USA Genomic profiling studies have provided new insights into the pathogenesis of mature B-cell neoplasms and have identified markers with prognostic impact. Recurrent mutations in tumor-suppressor genes (TP53, BIRC3, ATM), and common signaling pathways, such as the B-cell receptor (CD79A, CD79B, CARD11, TCF3, ID3), Toll- like receptor (MYD88), NOTCH (NOTCH1/2), nuclear factor-κB, and mitogen activated kinase signaling, have been identified in B-cell neoplasms. Chronic lymphocytic leukemia/small lymphocytic lymphoma, diffuse large B-cell lymphoma, follicular lymphoma, mantle cell lymphoma, Burkitt lymphoma, Waldenström macroglobulinemia, hairy cell leukemia, and marginal zone lymphomas of splenic, nodal, and extranodal types represent examples of B-cell neoplasms in which novel molecular biomarkers have been discovered in recent years. In addition, ongoing retrospective correlative and prospective outcome studies have resulted in an enhanced understanding of the clinical utility of novel biomarkers. This progress is reflected in the 2016 update of the World Health Organization classification of lymphoid neoplasms, which lists as many as 41 mature B-cell neoplasms (including provisional categories). Consequently, molecular genetic studies are increasingly being applied for the clinical workup of many of these neoplasms. In this review, we focus on the diagnostic, prognostic, and/or therapeutic utility of molecular biomarkers in mature B-cell neoplasms. -
LEUKOCYTE SURFACE ORIGIN of HUMAN At-ACID GLYCOPROTEIN (OROSOMUCOID)*
LEUKOCYTE SURFACE ORIGIN OF HUMAN at-ACID GLYCOPROTEIN (OROSOMUCOID)* BY CARL G. GAHMBERG AND LEIF C. ANDERSSON (From the Department of Bacteriology and Immunology, and the Transplantation Laboratory, Department of Surgery IV, University of Helsinki, Helsinki 29, Finland) Human al-acid glycoprotein (orosomucoid) (o~I-AG)1 constitutes the main component of the seromucoid fraction of human plasma. It belongs to the acute phase proteins, which increase under conditions such as inflammation, pregnancy, and cancer (1, 2). al-AG has previously been found to be synthesized in liver (3), and after removal of terminal sialic acids, it is cleared from the circulation by binding to a receptor protein on liver cell plasma membranes (4). The structure of al-AG is well known. It is composed of a single polypeptide chain and contains 245% carbohydrate including a large amount of sialic acid. The carbohydrate is located in the first half of the peptide chain linked to asparagine residues (5, 6). The function of al-AG is unclear. However, Schmid et al. (5) and Ikenaka et al. (7) and reported that the amino acid sequence of the protein shows a significant homology with human IgG. This finding and the striking increase in inflammatory and lymphopro- liferative disorders made us consider the possibility that leukocytes could be directly involved in the synthesis and release of a~-AG. We report here the presence of a membrane form of al-AG, with an apparent tool wt of 52,000, on normal human lymphocytes, granulocytes, and monocytes. By the use of internal labeling with [3H]leucine in vitro, we demonstrate that the membrane protein is synthesized by lymphocytes. -
Endocrinology Test List Endocrinology Test List
For Endocrinologists Endocrinology Test List Endocrinology Test List Extensive Capabilities Managing patients with endocrine disorders is complex. Having access to the right test for the right patient is key. With a legacy of expertise in endocrine laboratory diagnostics, Quest Diagnostics offers an extensive menu of laboratory tests across the spectrum of endocrine disorders. This test list highlights the extensive menu of laboratory diagnostic tests we offer, including highly specialized tests and those performed using highly specific and sensitive mass spectrometry detection. It is conveniently organized by glandular function or common endocrine disorder, making it easy for you to identify the tests you need to care for the patients you treat. Comprehensive Care Quest Diagnostics Nichols Institute has been pioneering state-of-the-art endocrine testing for over four decades. Our commitment to innovative diagnostics and our dedication to quality and service means we deliver solutions that enable you to make informed clinical decisions for comprehensive patient management. We strive to remain at the forefront of innovation in endocrine testing so you can deliver the highest level of patient care. Abbreviations and Footnotes NDM, neonatal diabetes mellitus; MODY, maturity-onset diabetes of the young; CH, congenital hyperinsulinism; MSUD, maple syrup urine disease; IHH, idiopathic hypogonadotropic hypogonadism; BBS, Bardet-Biedl syndrome; OI, osteogenesis imperfecta; PKD, polycystic kidney disease; OPPG, osteoporosis-pseudoglioma syndrome; CPHD, combined pituitary hormone deficiency; GHD, growth hormone deficiency. The tests highlighted in green are performed using highly specific and sensitive mass spectrometry detection. Panels that include a test(s) performed using mass spectrometry are highlighted in yellow. For tests highlighted in blue, refer to the Athena Diagnostics website (athenadiagnostics.com/content/test-catalog) for test information. -
Differential Gene Expression in Oligodendrocyte Progenitor Cells, Oligodendrocytes and Type II Astrocytes
Tohoku J. Exp. Med., 2011,Differential 223, 161-176 Gene Expression in OPCs, Oligodendrocytes and Type II Astrocytes 161 Differential Gene Expression in Oligodendrocyte Progenitor Cells, Oligodendrocytes and Type II Astrocytes Jian-Guo Hu,1,2,* Yan-Xia Wang,3,* Jian-Sheng Zhou,2 Chang-Jie Chen,4 Feng-Chao Wang,1 Xing-Wu Li1 and He-Zuo Lü1,2 1Department of Clinical Laboratory Science, The First Affiliated Hospital of Bengbu Medical College, Bengbu, P.R. China 2Anhui Key Laboratory of Tissue Transplantation, Bengbu Medical College, Bengbu, P.R. China 3Department of Neurobiology, Shanghai Jiaotong University School of Medicine, Shanghai, P.R. China 4Department of Laboratory Medicine, Bengbu Medical College, Bengbu, P.R. China Oligodendrocyte precursor cells (OPCs) are bipotential progenitor cells that can differentiate into myelin-forming oligodendrocytes or functionally undetermined type II astrocytes. Transplantation of OPCs is an attractive therapy for demyelinating diseases. However, due to their bipotential differentiation potential, the majority of OPCs differentiate into astrocytes at transplanted sites. It is therefore important to understand the molecular mechanisms that regulate the transition from OPCs to oligodendrocytes or astrocytes. In this study, we isolated OPCs from the spinal cords of rat embryos (16 days old) and induced them to differentiate into oligodendrocytes or type II astrocytes in the absence or presence of 10% fetal bovine serum, respectively. RNAs were extracted from each cell population and hybridized to GeneChip with 28,700 rat genes. Using the criterion of fold change > 4 in the expression level, we identified 83 genes that were up-regulated and 89 genes that were down-regulated in oligodendrocytes, and 92 genes that were up-regulated and 86 that were down-regulated in type II astrocytes compared with OPCs. -
Thyroglobulin (Tg) Assays
Thyroglobulin (Tg) Assays ABOUT DTC patients is limited. In the US, a Tg-RIA with a functional sensitivity (9, 10) The Laboratory Services Committee of the American Thyroid of 0.5 µg/L is available for clinical purposes. Although the functional Association® (ATA) conducted a survey of ATA® members to identify sensitivity of this assay is still suboptimal, it has been extensively used as areas of member interest for education in pathology and laboratory a “gold standard” in studies evaluating the effect of TgAb interference in (4, 11, 12, 13) medicine. In response to the results of the survey, the Lab Service Tg IMA. This assay is promoted as being more resistant to TgAb Committee developed a series of educational materials to share with the interferences due to the use of polyclonal antibodies that could recognize 9 ATA® membership. The topics below were ranked as high educational Tg epitopes even when bound to TgAb. However, interferences in Tg-RIA priorities amongst the membership. results have been reported. Early studies reported that TgAb caused an overestimation of Tg by RIA.14 Others have reported underestimation of MEASUREMENT OF SERUM THYROGLOBULIN Tg by RIA in the presence of TgAb.(15,16) Thyroglobulin (Tg) measurement is an integral part of the follow up IMMUNOMETRIC ASSAYS and management of patients with differentiated thyroid cancer (DTC). Tg-IMA are based on a two-site reaction that involves Tg capture by Although, measurement of Tg for initial evaluation of suspicious thyroid a solid-phase antibody followed by addition of a labeled antibody that nodules is not recommended, serum Tg measurements are used targets different epitopes on the captured Tg. -
Screening for Tumor Suppressors: Loss of Ephrin PNAS PLUS Receptor A2 Cooperates with Oncogenic Kras in Promoting Lung Adenocarcinoma
Screening for tumor suppressors: Loss of ephrin PNAS PLUS receptor A2 cooperates with oncogenic KRas in promoting lung adenocarcinoma Narayana Yeddulaa, Yifeng Xiaa, Eugene Kea, Joep Beumera,b, and Inder M. Vermaa,1 aLaboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA 92037; and bHubrecht Institute, Utrecht, The Netherlands Contributed by Inder M. Verma, October 12, 2015 (sent for review July 28, 2015; reviewed by Anton Berns, Tyler Jacks, and Frank McCormick) Lung adenocarcinoma, a major form of non-small cell lung cancer, injections in embryonic skin cells identified several potential tu- is the leading cause of cancer deaths. The Cancer Genome Atlas morigenic factors (14–16). None of the reported studies have analysis of lung adenocarcinoma has identified a large number of performed direct shRNA-mediated high-throughput approaches previously unknown copy number alterations and mutations, re- in adult mice recapitulating the mode of tumorigenesis in humans. quiring experimental validation before use in therapeutics. Here, we Activating mutations at positions 12, 13, and 61 amino acids in describe an shRNA-mediated high-throughput approach to test a set Kirsten rat sarcoma viral oncogene homolog (KRas) contributes of genes for their ability to function as tumor suppressors in the to tumorigenesis in 32% of lung adenocarcinoma patients (2) by background of mutant KRas and WT Tp53. We identified several activating downstream signaling cascades. Mice with the KRasG12D candidate genes from tumors originated from lentiviral delivery of allele develop benign adenomatous lesions with long latency to shRNAs along with Cre recombinase into lungs of Loxp-stop-Loxp- develop adenocarcinoma (17, 18). -
A Study on a Large Cohort of Renal Transplant Patients This Information Is Current As of September 24, 2021
Generation of Catalytic Antibodies Is an Intrinsic Property of an Individual's Immune System: A Study on a Large Cohort of Renal Transplant Patients This information is current as of September 24, 2021. Ankit Mahendra, Ivan Peyron, Olivier Thaunat, Cécile Dollinger, Laurent Gilardin, Meenu Sharma, Bharath Wootla, Desirazu N. Rao, Séverine Padiolleau-Lefevre, Didier Boquet, Abhijit More, Navin Varadarajan, Srini V. Kaveri, Christophe Legendre and Sébastien Lacroix-Desmazes Downloaded from J Immunol 2016; 196:4075-4081; Prepublished online 11 April 2016; doi: 10.4049/jimmunol.1403005 http://www.jimmunol.org/content/196/10/4075 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2016/04/09/jimmunol.140300 Material 5.DCSupplemental References This article cites 20 articles, 12 of which you can access for free at: http://www.jimmunol.org/content/196/10/4075.full#ref-list-1 by guest on September 24, 2021 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 *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 © 2016 by The American Association of Immunologists, Inc. -
The Effects of Oncogenic G12d Mutation on K-Ras Structure, Conformation and Dynamics
bioRxiv preprint doi: https://doi.org/10.1101/178483; this version posted August 19, 2017. 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. THE EFFECTS OF ONCOGENIC G12D MUTATION ON K-RAS STRUCTURE, CONFORMATION AND DYNAMICS Sezen Vatansever1, 2, 3, Zeynep H. Gümüş2, 3*, Burak Erman1* 1Department of Chemical and Biological Engineering, College of Engineering, Koç University, Rumelifeneri Yolu, 34450, Sarıyer, Istanbul, Turkey 2Department of Genetics and Genomics, 3Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029 *Correspondence: [email protected] (B.E.) and [email protected] (Z.H.G.) ABSTRACT K-Ras is the most frequently mutated protein in human tumors. Activating K-Ras mutations drive cancer initiation, progression and drug resistance, directly leading to nearly a million deaths per year. To understand the mechanisms by which mutations alter K-Ras function, we need to understand their effects on protein dynamics. However, despite decades of research, how oncogenic mutations in K-Ras alter its conformation and dynamics remain to be understood. Here, we present how the most recurrent K-Ras oncogenic mutation, G12D, leads to structural, conformational and dynamical changes that lead to constitutively active K- Ras. We have developed a new integrated MD simulation data analysis approach to quantify such changes in a protein and applied it to K-Ras. Our results show that G12D mutation induces strong negative correlations between the fluctuations of SII and those of the P-loop, Switch I (SI) and α3 regions in K-RasG12D. -
Differential Serum Interferon-Β Levels in Autoimmune Thyroid Diseases
Clinical research Differential serum interferon-β levels in autoimmune thyroid diseases Chao-Wen Cheng1,2,3, Kam-Tsun Tang4, Wen-Fang Fang5, Ting-I Lee6,7, Jiunn-Diann Lin7,8 1Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Corresponding author: Taipei 11031, Taiwan Jiunn-Diann Lin MD 2Traditional Herb Medicine Research Center, Taipei Medical University Hospital, Division of Endocrinology Taipei Medical University, Taipei 11031, Taiwan Department of Internal 3Cell Physiology and Molecular Image Research Center, Wan Fang Hospital, Taipei Medical Medicine University, Taipei 11696, Taiwan Shuang Ho Hospital 4Division of Endocrinology and Metabolism, Department of Internal Medicine, Taipei Taipei Medical University Veterans General Hospital, Taipei 11217, Taiwan 291 Jhongzheng Rd. 5Department of Family Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei Jhonghe District City 23561, Taiwan New Taipei City 23561, 6Division of Endocrinology and Metabolism, Department of Internal Medicine, Wan Fang Taiwan Hospital, Taipei Medical University, Taipei 11696, Taiwan Phone: +886-2-22490088 7Division of Endocrinology and Metabolism, Department of Internal Medicine, School Fax: +886-2-22490088 of Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan E-mail: 8Division of Endocrinology, Department of Internal Medicine, Shuang Ho Hospital, [email protected] Taipei Medical University, New Taipei City 23561, Taiwan Submitted: 18 December 2018 Accepted: 21 June 2019 Arch Med Sci DOI: https://doi.org/10.5114/aoms/110164 Copyright © 2021 Termedia & Banach Abstract Introduction: Interferon (IFN)-β is known as an environmental trigger for the occurrence of autoimmune thyroid disease (AITD). However, the association of another type-1 IFN, IFN-β, with AITD is unknown.