DOCSLIB.ORG

Dctd Programs and Initiatives (2013-2017) Biometric Research Program 46

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

DIVISION OF CANCER TREATMENT AND DIAGNOSIS PROGRAMS AND INITIATIVES (2013-2017) U.S. Department of Health & Human Services | National Institutes of Health NATIONAL CANCER INSTITUTE DIVISION OF CANCER TREATMENT AND DIAGNOSIS PROGRAMS AND INITIATIVES (2013-2017) U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES NATIONAL INSTITUTES OF HEALTH TABLE OF CONTENTS ACRONYMS VIII LIST OF TABLES XIII LIST OF FIGURES XIV PREFACE XVI OVERVIEW 1 MAJOR INITIATIVES SUPPORTING THE CANCER COMMUNITY 4 Current Research Emphasis 5 Future Research Emphasis 5 Mechanisms of Cancer Drug Resistance and Sensitivity 5 Development of Improved Patient-Derived Models to Enhance Early Phase Clinical Trials 5 Development of Cancer Immunotherapy Biomarkers 5 New Cancer Immunotherapy Model Systems 5 Understanding the Microenvironment of Pancreatic Cancer to Enhance Immunotherapeutic Options 5 Current Programs and Initiatives 6 NCI’s Precision Medicine Trials 6 Precision Medicine Initiative (PMI) – Oncology Supplements 11 NCI National Clinical Trials Network (NCTN) 12 NCI Experimental Therapeutics Clinical Trials Network (ETCTN) 18 Specialized Programs of Research Excellence (SPORE) 23 NCI Experimental Therapeutics (NExT) Program 24 NCI Patient-Derived Models Repository (PDMR) Program 31 Pharmacodynamic Assay Development and Implementation Section (PADIS) 32 The Cancer Imaging Archive (TCIA) 35 Innovative Molecular Analysis Technologies (IMAT) 37 The Cancer Immunotherapy Trials Network (CITN) 38 Childhood Cancer Survivor Study (CCSS) 38 NCI Developmental Therapeutics Clinic (DTC) 39 NCI Program for Natural Products Discovery (NPNPD) 41 NCI Formulary 42 Exploring the Horizon 42 NCI Exceptional Responders Initiative 43 Provocative Question Initiative 44 Recalcitrant Cancer Research Act of 2012 44 NCI R21 Program: Translational and Clinical Exploratory Research 45 II DCTD PROGRAMS AND INITIATIVES (2013-2017) BIOMETRIC RESEARCH PROGRAM 46 Overview 47 Structure and Function 47 Biostatistics Branch 47 Computational and Systems Biology Branch 50 Future Directions 51 CANCER DIAGNOSIS PROGRAM 52 Overview 53 Structure and Function 56 Biorepositories and Biospecimen Research Branch 57 Diagnostic Biomarkers and Technology Branch 58 Diagnostics Evaluation Branch 58 The Pathology Investigation and Resources Branch 59 CDP Grants Overview 60 Assistance to the Cancer Community 61 Molecular Characterization Laboratory (MoCha) 61 Program for the Assessment of Clinical Cancer Tests (PACCT) 61 Strategic Partnerships to Evaluate Cancer Signatures (SPECS) 62 Biomarker Evaluation in NCI Cancer Therapy Trials 63 REMARK and the EORTC-NCI Cancer Molecular Markers Collaborations 63 Clinical Assay Standardization 64 Biospecimen Access for the Cancer Research Community 65 NIH Genotype Tissue Expression (GTEx) Program 66 Biospecimen Research Network (BRN) 67 Tools and Guidance for Biobanking 67 Pathology Evaluation of Tissue Specimens for Research 68 Future Directions 69 Biomarker Support for Immunotherapy 69 Preclinical and Clinical Molecular Characterization for Developmental Therapeutics 69 Circulating Tumor Nucleic Acids 70 Bioethics and Science in Biobanking 70 DIVISION OF CANCER TREATMENT AND DIAGNOSIS III CANCER IMAGING PROGRAM 72 Overview 73 Structure and Function 76 Molecular Imaging Branch 77 Clinical Trials Branch 77 Image-Guided Intervention Branch 77 Imaging Technology Development Branch 78 Nanodelivery Systems and Devices Branch 78 CIP Grants Overview 78 Assistance to the Cancer Community 79 Specialized Initiatives 79 Imaging Informatics 81 In Vivo Cellular and Molecular Imaging Centers 81 Molecular Imaging Clinic 82 Synthesis of Agents 83 Molecular Imaging Radiopharmaceutical Resources 84 Clinical Trials 84 Quantitative Imaging Network (QIN) for the Measurement of Therapy Response 91 Ongoing Strategies in Imaging – National Strategic Plans, Initiatives, & Roadmaps 94 Specialized Workshops 96 Future Directions 97 CANCER THERAPY EVALUATION PROGRAM 98 Overview 99 Structure and Function 99 Investigational Drug Branch 100 Clinical Investigations Branch 101 Clinical Grants and Contracts Branch 101 Regulatory Affairs Branch 102 Pharmaceutical Management Branch 103 Clinical Trials Monitoring Branch 103 Clinical Trials Operations and Informatics Branch 104 CTEP Grants Overview 104 IV DCTD PROGRAMS AND INITIATIVES (2013-2017) Assistance to the Cancer Community 104 CTEP-Sponsored Phase 2 Trials Leading to Pivotal Trials 104 Fostering Career Development of Junior Clinical Investigators 105 Clinical Trials Program 105 Future Directions 124 DEVELOPMENTAL THERAPEUTICS PROGRAM 126 Overview 127 Structure and Function 127 Office of the Associate Director 127 Preclinical Therapeutics Grants Branch 128 Molecular Pharmacology Branch 128 Biological Testing Branch 129 Drug Synthesis and Chemistry Branch 131 Natural Products Branch 131 Biological Resources Branch 131 Toxicology and Pharmacology Branch 132 Pharmaceutical Resources Branch 132 Information Technology Branch 132 DTP Grants Overview 132 Assistance to the Cancer Research Community 134 NCI-60 Cell Line Screen 134 In vivo Model Development and Testing 134 Tumors, Cells, Cell Lines, and Mice 134 Collection and Distribution of Synthetic Compounds 134 Acquisition of Small-Molecule Oncology Agents 135 Laboratory of Synthetic Chemistry 136 Natural Products Repository 136 cGMP Manufacturing and Formulation 138 Investigative Toxicology Laboratory 139 The Biopharmaceutical Development Program 140 BRB Preclinical Repository 143 IT Enhancements Facilitating Interactions with the Research Community 144 Future Directions 145 DIVISION OF CANCER TREATMENT AND DIAGNOSIS V RADIATION RESEARCH PROGRAM 146 Overview 147 Structure and Function 147 Radiotherapy Development Branch 149 Clinical Radiation Oncology Branch 149 Molecular Radiation Therapeutics 150 RRP Grants Overview 151 Assistance to the Cancer Research Community 152 Imaging and Radiation Oncology Core (IROC) 152 Radiobiology Bioterrorism Research and Training Group 153 Workshop on Utilizing the Biological Consequences of Radiation Therapy in the Development of New Treatment Approaches 153 Future Directions 154 TRANSLATIONAL RESEARCH PROGRAM 156 Overview 157 TRP Mission 157 TRP Grants Overview 158 Organized SPORE Workshops 159 Brain SPORE Workshops (2013-2017) 159 Gastrointestinal (GI) and Pancreas workshops (2013-2017) 159 Skin SPORE Workshops (2013-2017) 160 Lung Cancer SPORE Workshops (2013-2017) 160 Prostate and Genitourinary (GU) SPORE Workshops (2103-2014) 161 Leukemia Inter-SPORE Meeting (2014) 162 Head and Neck Cancer SPORE Workshop (2014) 162 Hematologic Malignancies SPORE Workshop (2015) 162 Translational Research in Ovarian and Gynecologic Cancers Workshop (2016) 162 Translational Science in Prostate Cancer Workshop (2016) 162 Head and Neck/Thyroid Cancer SPORE Workshop (2017) 163 Future Directions 163 VI DCTD PROGRAMS AND INITIATIVES (2013-2017) OFFICE OF CANCER COMPLEMENTARY AND ALTERNATIVE MEDICINE 164 Overview 165 Mission 165 OCCAM Grants Overview 166 Assistance to the Scientific Community 167 Herbal Mixture Program Project Grant 167 NCI Best Case Series Program 167 Patient Education Resource 167 Conferences 168 Training 170 Research Resources 170 Collaborations 170 Future Directions 172 2017 DCTD STAFF ROSTER 174 Office of the Division Director 175 Biometric Research Program 177 Cancer Diagnosis Program 178 Cancer Imaging Program 179 Cancer Therapy Evaluation Program 181 Developmental Therapeutics Program 184 Radiation Research Program 187 Translational Research Program 188 Office of Cancer Complementary and Alternative Medicine 189 DCTD STAFF PUBLICATIONS 190 2013 191 2014 196 2015 203 2016 210 2017 216 DIVISION OF CANCER TREATMENT AND DIAGNOSIS VII ACRONYMS AACR – American Association for Cancer Research BRD – Biospecimen Research Database AAPM – American Association for Physicists in Medicine BRISQ – Biospecimen Reporting for Improved ABTC – Adult Brain Tumor Consortium Study Quality ACG – Agreement Coordination Group BRMs – biological response modifiers ACR – American College of Radiology BRN – Biospecimen Research Network ACRIN – American College of Radiology BRP – Biometric Research Program Imaging Network BTB – Biological Testing Branch ACT – NCTN Accrual Core Team ADCC – antibody directed cellular cytotoxicity caAERS – cancer adverse event reporting system ADME – absorption, distribution, metabolism, CADP – Clinical Assay Development Program and excretion caDSR – NCI Cancer Data Standards Registry and ADTTP – Advanced Development Therapeutics Repository Training Program caHUB – NCI Cancer Human Biobank AERS – Adverse Event Reporting System CALGB – Cancer and Leukemia Group B AFRRI – The Department of Defense Armed Forces CAM – complementary and alternative medicine Radiobiology and Research Institute CAP – Corrective Action Plan AHRQ – Agency for Healthcare Research and Quality CBC – Chemical Biology Consortium ALCHEMIST – Adjuvant Lung Cancer Enrichment CBCTR – NCI Cooperative Breast Cancer Tissue Resource Marker Identification and Sequencing Trial CBIIT – NCI Center for Biomedical Informatics and ALL – acute lymphoblastic leukemia Information Technology allo HCT – allogenic hematopoietic cell transplantation CCCT – NCI Director’s Coordinating Center for AML – acute myeloid leukemia Clinical Trials APEC – Asia Pacific Economical Collaboration CCOP – Community Clinical Oncology Program ARRA – American Recovery and Reinvestment Act CCR – Center for Cancer Research of 2009 CCSS – Childhood Cancer Survivor Study ASCO – American Society of Clinical Oncology CCTG – Canadian Cancer
Recommended publications
  • The Hypotensive Effect of Activated Apelin Receptor Is Correlated with Β

    The Hypotensive Effect of Activated Apelin Receptor Is Correlated with Β

    This is the accepted (postprint) version of the following article: Besserer-Offroy É, et al. (2018), Pharmacol Res. doi: 10.1016/j.phrs.2018.02.032, which has been accepted and published in its final form at https://www.sciencedirect.com/science/article/pii/S1043661817313804 The hypotensive effect of activated apelin receptor is correlated with β-arrestin recruitment Élie Besserer-Offroya,c,ORCID ID, Patrick Bérubéa,c, Jérôme Côtéa,c, Alexandre Murzaa,c, Jean-Michel Longpréa,c, Robert Dumainea, Olivier Lesurb,c, Mannix Auger-Messierb,ORCID ID, Richard Leduca,c,ORCID ID, Éric Marsaulta,c,*,ORCID ID, Philippe Sarreta,c* Affiliations a Department of Pharmacology-Physiology, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Québec, CANADA J1H 5N4 b Department of Medicine, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, Québec, CANADA J1H 5N4 c Institut de pharmacologie de Sherbrooke, Université de Sherbrooke, Sherbrooke, Québec, CANADA J1H 5N4 e-mail addresses [email protected] (ÉBO); [email protected] (PB); [email protected] (JC); [email protected] (AM); Jean- [email protected] (JML); [email protected] (RD); [email protected] (OL); [email protected] (MAM); [email protected] (RL); [email protected] (EM); [email protected] (PS) © 2018. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ This is the accepted (postprint) version of the following article: Besserer-Offroy É, et al. (2018), Pharmacol Res. doi: 10.1016/j.phrs.2018.02.032, which has been accepted and published in its final form at https://www.sciencedirect.com/science/article/pii/S1043661817313804 Corresponding Authors *To whom correspondence should be addressed: Philippe Sarret, Ph.D.; [email protected]; Tel.
  • Oncolytic Viruses PANVAC and Pelareorep As Treatment for Metastatic Breast Cancer

    Oncolytic Viruses PANVAC and Pelareorep As Treatment for Metastatic Breast Cancer

    Oncolytic Viruses PANVAC and Pelareorep as Treatment for Metastatic Breast Cancer Willie Mieke Iwema Rijksuniversiteit Groningen S2673622 BSc Thesis Life science & Technology July 5, 2019 Department of Medical Microbiology: Molecular Virology D. Bhatt PhD candidate Prof. dr. C.A.H.H. Daemen Table of content 1. Introduction ................................................................................................................................ 4 2. PANVAC ....................................................................................................................................... 7 2.1 Vaccinia virus mechanism of action .............................................................................................. 7 2.2 Activation of the host immune system .......................................................................................... 8 2.3 PANVAC in advanced carcinomas ................................................................................................. 9 2.4 PANVAC and docetaxel in metastatic breast cancer ................................................................... 11 3. Pelareorep ................................................................................................................................. 13 3.1 Reovirus mechanism of action .................................................................................................... 13 3.2 Activation of the host immune system ........................................................................................ 14 3.3 Pelareorep
  • How I Treat Myelofibrosis

    How I Treat Myelofibrosis

    From www.bloodjournal.org by guest on October 7, 2014. For personal use only. Prepublished online September 16, 2014; doi:10.1182/blood-2014-07-575373 How I treat myelofibrosis Francisco Cervantes Information about reproducing this article in parts or in its entirety may be found online at: http://www.bloodjournal.org/site/misc/rights.xhtml#repub_requests Information about ordering reprints may be found online at: http://www.bloodjournal.org/site/misc/rights.xhtml#reprints Information about subscriptions and ASH membership may be found online at: http://www.bloodjournal.org/site/subscriptions/index.xhtml Advance online articles have been peer reviewed and accepted for publication but have not yet appeared in the paper journal (edited, typeset versions may be posted when available prior to final publication). Advance online articles are citable and establish publication priority; they are indexed by PubMed from initial publication. Citations to Advance online articles must include digital object identifier (DOIs) and date of initial publication. Blood (print ISSN 0006-4971, online ISSN 1528-0020), is published weekly by the American Society of Hematology, 2021 L St, NW, Suite 900, Washington DC 20036. Copyright 2011 by The American Society of Hematology; all rights reserved. From www.bloodjournal.org by guest on October 7, 2014. For personal use only. Blood First Edition Paper, prepublished online September 16, 2014; DOI 10.1182/blood-2014-07-575373 How I treat myelofibrosis By Francisco Cervantes, MD, PhD, Hematology Department, Hospital Clínic, IDIBAPS, University of Barcelona, Barcelona, Spain Correspondence: Francisco Cervantes, MD, Hematology Department, Hospital Clínic, Villarroel 170, 08036 Barcelona, Spain. Phone: +34 932275428.
  • PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity Both in Cancer Cells and Healthy Bone Marrow

    PARP1 Trapping by PARP Inhibitors Drives Cytotoxicity Both in Cancer Cells and Healthy Bone Marrow

    Author Manuscript Published OnlineFirst on November 14, 2018; DOI: 10.1158/1541-7786.MCR-18-0138 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. 1 Title: PARP1 trapping by PARP inhibitors drives cytotoxicity both in cancer 2 cells and healthy bone marrow 3 4 Authors: Todd A. Hopkins, William B. Ainsworth, Paul A. Ellis, Cherrie K. 5 Donawho, Enrico L. DiGiammarino, Sanjay C. Panchal, Vivek C. 6 Abraham, Mikkel A. Algire, Yan Shi, Amanda M. Olson, Eric F. Johnson, 7 Julie L. Wilsbacher, David Maag* 8 9 Author affiliations: AbbVie, Inc., North Chicago, Illinois, USA 10 Running title: PARP trapping: impact on in vivo activity of PARP inhibitors 11 Keywords: PARP, DNA damage, veliparib,talazoparib, rucaparib, A-934935 12 Financial support: This work was financially supported by AbbVie, Inc. 13 Corresponding author: *David Maag, Oncology Development, AbbVie, Inc., 1 N. Waukegan 14 Road, North Chicago, Illinois, USA 60064. Phone: 847-937-3969; E- 15 mail: [email protected]. 16 Disclosure: All authors are employees of AbbVie. The design, study conduct, and 17 financial support for this research were provided by AbbVie. AbbVie 18 participated in the interpretation of data, review, and approval of the 19 publication. 20 Word count: 5163/5000 21 Total number of figures and tables: 12 (6 plus 6 supplemental) 22 1 Downloaded from mcr.aacrjournals.org on September 26, 2021. © 2018 American Association for Cancer Research. Author Manuscript Published OnlineFirst on November 14, 2018; DOI: 10.1158/1541-7786.MCR-18-0138 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited.
  • Research in Your Backyard Developing Cures, Creating Jobs

    Research in Your Backyard Developing Cures, Creating Jobs

    Research in Your Backyard Developing Cures, Creating Jobs PHARMACEUTICAL CLINICAL TRIALS IN ILLINOIS Dots show locations of clinical trials in the state. Executive Summary This report shows that biopharmaceutical research com- Quite often, biopharmaceutical companies hire local panies continue to be vitally important to the economy research institutions to conduct the tests and in Illinois, and patient health in Illinois, despite the recession. they help to bolster local economies in communities all over the state, including Chicago, Decatur, Joliet, Peoria, At a time when the state still faces significant economic Quincy, Rock Island, Rockford and Springfield. challenges, biopharmaceutical research companies are conducting or have conducted more than 4,300 clinical For patients, the trials offer another potential therapeutic trials of new medicines in collaboration with the state’s option. Clinical tests may provide a new avenue of care for clinical research centers, university medical schools and some chronic disease sufferers who are still searching for hospitals. Of the more than 4,300 clinical trials, 2,334 the medicines that are best for them. More than 470 of the target or have targeted the nation’s six most debilitating trials underway in Illinois are still recruiting patients. chronic diseases—asthma, cancer, diabetes, heart dis- ease, mental illnesses and stroke. Participants in clinical trials can: What are Clinical Trials? • Play an active role in their health care. • Gain access to new research treatments before they In the development of new medicines, clinical trials are are widely available. conducted to prove therapeutic safety and effectiveness and compile the evidence needed for the Food and Drug • Obtain expert medical care at leading health care Administration to approve treatments.
  • Pembrolizumab in Combination with the Oncolytic Virus Pelareorep And

    Pembrolizumab in Combination with the Oncolytic Virus Pelareorep And

    Published OnlineFirst November 6, 2019; DOI: 10.1158/1078-0432.CCR-19-2078 CLINICAL CANCER RESEARCH | CLINICAL TRIALS: IMMUNOTHERAPY Pembrolizumab in Combination with the Oncolytic Virus Pelareorep and Chemotherapy in Patients with Advanced Pancreatic Adenocarcinoma: A Phase Ib Study A C Devalingam Mahalingam1,2, Grey A. Wilkinson3, Kevin H. Eng4, Paul Fields5, Patrick Raber5, Jennifer L. Moseley2, Karol Cheetham3, Matt Coffey3, Gerard Nuovo6, Pawel Kalinski4, Bin Zhang1, Sukeshi Patel Arora2, and Christos Fountzilas4 ABSTRACT ◥ Background: Pelareorep is an intravenously delivered oncolytic achieved partial response for 17.4 months. Two additional patients reovirus that can induce a T-cell–inflamed phenotype in pancreatic achieved stable disease, lasting 9 and 4 months, respectively. ductal adenocarcinoma (PDAC). Tumor tissues from patients Treatment was well tolerated, with mostly grade 1 or 2 treat- treated with pelareorep have shown reovirus replication, T-cell ment-related adverse events, including flu-like symptoms. Viral infiltration, and upregulation of PD-L1. We hypothesized that replication was observed in on-treatment tumor biopsies. T-cell pelareorep in combination with pembrolizumab and chemotherapy receptor sequencing from peripheral blood revealed the creation of in patients with PDAC would be safe and effective. new T-cell clones during treatment. High peripheral clonality and Methods: A phase Ib single-arm study enrolled patients with changes in the expression of immune genes were observed in PDAC who progressed after first-line treatment. Patients received patients with clinical benefit. pelareorep, pembrolizumab, and either 5-fluorouracil, gemcitabine, Conclusions: Pelareorep and pembrolizumab added to che- or irinotecan until disease progression or unacceptable toxicity. motherapy did not add significant toxicity and showed encour- Study objectives included safety and dose-limiting toxicities, tumor aging efficacy.
  • Targeting BCL-2 in Cancer: Advances, Challenges, and Perspectives

    Targeting BCL-2 in Cancer: Advances, Challenges, and Perspectives

    cancers Review Targeting BCL-2 in Cancer: Advances, Challenges, and Perspectives Shirin Hafezi 1 and Mohamed Rahmani 1,2,* 1 Research Institute of Medical & Health Sciences, University of Sharjah, P.O. Box 27272 Sharjah, United Arab Emirates; [email protected] 2 Department of Basic Medical Sciences, College of Medicine, University of Sharjah, P.O. Box 27272 Sharjah, United Arab Emirates * Correspondence: [email protected]; Tel.: +971-6505-7759 Simple Summary: Apoptosis, a programmed form of cell death, represents the main mechanism by which cells die. Such phenomenon is highly regulated by the BCL-2 family of proteins, which includes both pro-apoptotic and pro-survival proteins. The decision whether cells live or die is tightly controlled by a balance between these two classes of proteins. Notably, the pro-survival Bcl-2 proteins are frequently overexpressed in cancer cells dysregulating this balance in favor of survival and also rendering cells more resistant to therapeutic interventions. In this review, we outlined the most important steps in the development of targeting the BCL-2 survival proteins, which laid the ground for the discovery and the development of the selective BCL-2 inhibitor venetoclax as a therapeutic drug in hematological malignancies. The limitations and future directions are also discussed. Abstract: The major form of cell death in normal as well as malignant cells is apoptosis, which is a programmed process highly regulated by the BCL-2 family of proteins. This includes the antiapoptotic proteins (BCL-2, BCL-XL, MCL-1, BCLW, and BFL-1) and the proapoptotic proteins, which can be divided into two groups: the effectors (BAX, BAK, and BOK) and the BH3-only proteins Citation: Hafezi, S.; Rahmani, M.
  • MET Or NRAS Amplification Is an Acquired Resistance Mechanism to the Third-Generation EGFR Inhibitor Naquotinib

    MET Or NRAS Amplification Is an Acquired Resistance Mechanism to the Third-Generation EGFR Inhibitor Naquotinib

    www.nature.com/scientificreports OPEN MET or NRAS amplifcation is an acquired resistance mechanism to the third-generation EGFR inhibitor Received: 5 October 2017 Accepted: 16 January 2018 naquotinib Published: xx xx xxxx Kiichiro Ninomiya1, Kadoaki Ohashi1,2, Go Makimoto1, Shuta Tomida3, Hisao Higo1, Hiroe Kayatani1, Takashi Ninomiya1, Toshio Kubo4, Eiki Ichihara2, Katsuyuki Hotta5, Masahiro Tabata4, Yoshinobu Maeda1 & Katsuyuki Kiura2 As a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), osimeritnib is the standard treatment for patients with non-small cell lung cancer harboring the EGFR T790M mutation; however, acquired resistance inevitably develops. Therefore, a next-generation treatment strategy is warranted in the osimertinib era. We investigated the mechanism of resistance to a novel EGFR-TKI, naquotinib, with the goal of developing a novel treatment strategy. We established multiple naquotinib-resistant cell lines or osimertinib-resistant cells, two of which were derived from EGFR-TKI-naïve cells; the others were derived from geftinib- or afatinib-resistant cells harboring EGFR T790M. We comprehensively analyzed the RNA kinome sequence, but no universal gene alterations were detected in naquotinib-resistant cells. Neuroblastoma RAS viral oncogene homolog (NRAS) amplifcation was detected in naquotinib-resistant cells derived from geftinib-resistant cells. The combination therapy of MEK inhibitors and naquotinib exhibited a highly benefcial efect in resistant cells with NRAS amplifcation, but the combination of MEK inhibitors and osimertinib had limited efects on naquotinib-resistant cells. Moreover, the combination of MEK inhibitors and naquotinib inhibited the growth of osimertinib-resistant cells, while the combination of MEK inhibitors and osimertinib had little efect on osimertinib-resistant cells.
  • New Contributions in Undergraduate Research

    New Contributions in Undergraduate Research

    PSU McNair Scholars Online Journal Volume 11 Issue 1 Without Borders: Original Contributions Article 6 in Undergraduate Research 2017 Wings Outstretched: New Contributions in Undergraduate Research Follow this and additional works at: https://pdxscholar.library.pdx.edu/mcnair Let us know how access to this document benefits ou.y Recommended Citation (2017) "Wings Outstretched: New Contributions in Undergraduate Research," PSU McNair Scholars Online Journal: Vol. 11: Iss. 1, Article 6. https://doi.org/10.15760/mcnair.2017.01 This open access Full Issue is distributed under the terms of the Creative Commons Attribution-NonCommercial- ShareAlike 4.0 International License (CC BY-NC-SA 4.0). All documents in PDXScholar should meet accessibility standards. If we can make this document more accessible to you, contact our team. Portland State University McNair Research Journal 2017 Without Borders: Original Contributions in Undergraduate Research 2017 Ronald E. McNair Scholars Journal Portland State University 1 About the Program The Portland State University (PSU) Ronald E. McNair Scholars Program at Portland State University works with motivated and talented undergraduates who want to pursue PhDs. It introduces juniors and seniors who are first-generation and low income, and/or members of under-represented groups to academic research and to effective strategies for getting into and graduating from PhD programs. The McNair Scholars Program has academic-year activities and a full-time summer research internship. Scholars take academic and skills-building seminars and workshops during the year, and each scholar works closely with a faculty mentor on original research in the summer. Scholars present their research findings at the McNair Summer Symposium and at other conferences, and are encouraged to publish their papers in the McNair Journal and other scholarly publications.
  • Daiichi Sankyo Group Value Report 2019

    Daiichi Sankyo Group Value Report 2019

    External Evaluations (as of June 30,2019) ™ Daiichi Sankyo Group Value Report 2019 Value Daiichi Sankyo Group MSCI Japan Empowering Women Select Index THE INCLUSION OF DAIICHI SANKYO CO.,LTD. IN ANY MSCI INDEX, AND THE USE OF MSCI LOGOS, TRADEMARKS, SERVICE MARKS OR INDEX NAMES HEREIN, DO NOT CONSTITUTE A SPONSORSHIP, ENDORSEMENT OR PROMOTION OF DAIICHI SANKYO CO.,LTD. BY MSCI OR ANY OF ITS AFFILIATES. THE MSCI INDEXES ARE THE EXCLUSIVE PROPERTY OF MSCI. MSCI AND THE MSCI INDEX NAMES AND LOGOS ARE TRADE- MARKS OR SERVICE MARKS OF MSCI OR ITS AFFILIATES. “Eruboshi” Certification Mark “Kurumin” Certification Mark Logo given to Certified Health and Productivity Management Organization (White500) This report uses FSC® certified paper, which indicates that the paper used to print this Paper report was produced from properly managed forests. 3-5-1, Nihonbashi-honcho, Chuo-ku, Tokyo 103-8426, Japan This report was printed using 100% Inks biodegradable printing inks from vegetable Corporate Communications Department oil. Daiichi Sankyo Group Tel: +81-3-6225-1126 CSR Department The waterless printing method used for this Value Report 2019 Tel: +81-3-6225-1067 Printing report minimized the use and release of harmful liquid wastes. https://www.daiichisankyo.com/ Printed in Japan 005_7045687911909.indd 1 2019/09/27 18:22:19 Introduction Our Mission The Core Values and Commitments serve as the criteria for business activities and In addition, we have established the DAIICHI SANKYO Group Corporate Conduct Charter . decision-making used by executive officers and employees in working to fulfill Our Mission . This charter calls on us to fulfill our social responsibilities by acting with the highest ethical Our Corporate Slogan succinctly explains the spirit of Our Mission, Core Values and standards and a good social conscience appropriate for a company engaged in business Commitments.
  • Targeted Therapies in Melanoma: Knowledge, Resistance And

    Targeted Therapies in Melanoma: Knowledge, Resistance And

    ooggeenneessii iinn ss && rrcc aa MM CC uu tt ff aa Journal ofJournal of oo gg ll ee ee aa aa nn nn nn nn ee ee rr rr ss ss uu uu ii ii Colombino et al., J Carcinog Mutagen 2014, S4:S4 ss ss oo oo JJ JJ ISSN: 2157-2518 CarCarcinogenesiscinogenesis & Mutagenesis DOI: 10.4172/2157-2518.S4-004 Review Article Open Access Targeted Therapies in Melanoma: Knowledge, Resistance and Perspectives Maria Colombino1*, Maria Cristina Sini1, Amelia Lissia2, Antonio Cossu2, and Giuseppe Palmieri1 1Unit of Cancer Genetics, Institute of Biomolecular Chemistry (ICB), National Research Council (CNR), Italy 2University Hospital Health Unit - Azienda Ospedaliero Universitaria (AOU), Via Matteotti, 07100 Sassari, Italy *Corresponding author: Dr. Maria Colombino, Unit of Cancer Genetics, Institute of Biomolecular Chemistry (ICB), National Research Council (CNR), Traversa La Crucca, 3 - Baldinca Li Punti, 07100 Sassari, Italy, Tel. +39 079 2841239; Fax +39 079 2841299; E-mail: [email protected] Received date: Mar 18, 2014, Accepted date: May 25, 2014, Published date: May 31, 2014 Copyright: © 2014 Colombino M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Several molecular mechanisms appear to play a major role in melanoma genesis and progression. Current targeted therapies focus on contrasting the activation of RAS/RAF/MEK/ERK and, to a less extent, PI3K/AKT pathways. Development of inhibitors of key effectors (mainly, BRAF mutant and MEK) has significantly improved treatment of patients with advanced melanoma.
  • AIFM2 Monoclonal Antibody (M13A), Clone 2C6

    AIFM2 Monoclonal Antibody (M13A), Clone 2C6

    AIFM2 monoclonal antibody (M13A), clone 2C6 Catalog # : H00084883-M13A 規格 : [ 200 uL ] List All Specification Application Image Product Mouse monoclonal antibody raised against a partial recombinant Western Blot (Transfected lysate) Description: AIFM2. Immunogen: AIFM2 (AAH06121, 1 a.a. ~ 339 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa. Sequence: MGSQVSVESGALHVVIVGGGFGGIAAASQLQALNVPFMLVDMKDSFHHN VAALRASVETGFAKKTFISYSVTFKDNFRQGLVVGIDLKNQMVLLQGGE ALPFSHLILATGSTGPFPGKFNEVSSQQAAIQAYEDMVRQVQRSRFIVVV enlarge GGGSAGVEMAAEIKTEYPEKEVTLIHSQVALADKELLPSVRQEVKEILLRK Western Blot (Recombinant GVQLLLSERVSNLEELPLNEYREYIKVQTDKGTEVATNLVILCTGIKINSSA protein) YRKAFESRLASSGALRVNEHLQVEGHSNVYAIGDCADVRTPKMAYLAGL HANIAVANIVNSVKQRPLQAYKPGALTFLLSMGRNDGVG ELISA Host: Mouse Reactivity: Human Isotype: IgG1 Kappa Quality Control Antibody Reactive Against Recombinant Protein. Testing: Western Blot detection against Immunogen (62.92 KDa) . Storage Buffer: In ascites fluid Storage Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing. Instruction: MSDS: Download Interspecies Mouse (90); Rat (90) Antigen Sequence: Datasheet: Download Applications Western Blot (Transfected lysate) Page 1 of 3 2021/6/18 Western Blot analysis of AIFM2 expression in transfected 293T cell line by AMID monoclonal antibody (M13A), clone 2C6. Lane 1: AIFM2 transfected lysate(40.5 KDa). Lane 2: Non-transfected lysate. Protocol Download Western Blot (Recombinant protein) Protocol Download ELISA Gene Information Entrez GeneID: 84883 GeneBank BC006121 Accession#: Protein AAH06121 Accession#: Gene Name: AIFM2 Gene Alias: AMID,PRG3,RP11-367H5.2 Gene apoptosis-inducing factor, mitochondrion-associated, 2 Description: Omim ID: 605159 Gene Ontology: Hyperlink Gene Summary: The protein encoded by this gene has significant homology to NADH oxidoreductases and the apoptosis-inducing factor PDCD8/AIF. Overexpression of this gene has been shown to induce apoptosis. The expression of this gene is found to be induced by tumor suppressor protein p53 in colon caner cells.