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Assessment of Overall Survival, Quality of Life, And
Supplementary Online Content Salas-Vega S, Iliopoulos O, Mossialos E. Assesment of overall survival, quality of life, and safety benefits associated with new cancer medicines [published online December 29, 2016]. JAMA Oncol. doi:10.1001/jamaoncol.2016.4166 eTable 1. Therapeutic profile of all cancer medicines approved by the FDA between 2003- 2013 eTable 2. Regulatory evidence in support of classification of drug clinical benefits eFigure 1. Number of cancer drugs that were evaluated by all three HTA agencies, sorted by magnitude of clinical benefits eTable 3. Interagency agreement–Krippendorff’s alpha coefficients eMethods This supplementary material has been provided by the authors to give readers additional information about their work. Online-Only Supplement © 2016 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/25/2021 Clinical value of cancer medicines Contents eExhibits ......................................................................................................................................................... 3 eTable 1. Therapeutic profile of all cancer medicines approved by the FDA between 2003- 2013 (Summary of eTable 2) ................................................................................................................... 3 eTable 2. Regulatory evidence in support of classification of drug clinical benefits ....................... 6 eFigure 1. Number of cancer drugs that were evaluated by all three HTA agencies, sorted by magnitude of clinical benefits -
In the United States Court of Appeals for the Federal Circuit
Case: 18-1959 Document: 16 Page: 1 Filed: 08/20/2018 No. 18-1959 In the United States Court of Appeals for the Federal Circuit GENENTECH, INC., APPELLANT v. HOSPIRA, INC., APPELLEE ON APPEAL FROM THE UNITED STATES PATENT AND TRADEMARK OFFICE PATENT TRIAL AND APPEAL BOARD IN NO. IPR2016-01771 BRIEF OF APPELLANT GENENTECH, INC. PAUL B. GAFFNEY ADAM L. PERLMAN THOMAS S. FLETCHER WILLIAMS & CONNOLLY LLP 725 Twelfth Street, N.W. Washington, DC 20005 (202) 434-5000 Case: 18-1959 Document: 16 Page: 2 Filed: 08/20/2018 CERTIFICATE OF INTEREST Pursuant to Federal Circuit Rule 47.4, undersigned counsel for appellant certifies the following: 1. The full name of the party represented by me is Genentech, Inc. 2. The name of the real party in interest represented by me is the same. 3. Genentech, Inc. is a wholly-owned subsidiary of Roche Holdings Inc. Roche Holdings Inc.’s ultimate parent, Roche Holdings Ltd, is a publicly held Swiss corporation traded on the Swiss Stock Exchange. Upon information and belief, more than 10% of Roche Holdings Ltd’s voting shares are held either directly or indirectly by Novartis AG, a publicly held Swiss corporation. 4. The following attorneys appeared for Genentech, Inc. in proceedings below or are expected to appear in this Court and are not already listed on the docket for the current case: Teagan J. Gregory and Christopher A. Suarez of Williams & Connolly LLP, 725 Twelfth Street, N.W., Washington, D.C. 20005. 5. The title and number of any case known to counsel to be pending in this or any other court or agency that will directly affect or be directly affected by this court’s decision in this pending appeal are Genentech, Inc. -
Or Irinotecan-Based Chemotherapy After Curative Resection of Synchronous Liver Metastases from Colorectal Cancer
ANTICANCER RESEARCH 33: 3317-3326 (2013) Efficacy of Postoperative Oxaliplatin- or Irinotecan-based Chemotherapy After Curative Resection of Synchronous Liver Metastases from Colorectal Cancer HUNG-CHIH HSU1,2, WEN-CHI CHOU1,2, WEN-CHI SHEN1,2, CHIAO-EN WU1,2, JEN-SHI CHEN1,2, CHI-TING LIAU1,2, YUNG-CHANG LIN1,2 and TSAI-SHENG YANG1,2 1Division of Hematology-Oncology, Chang Gung Memorial Hospital at Linkou, Kwei-Shan, Tao-Yuan, Taiwan, R.O.C.; 2College of Medicine, Chang Gung University, Kwei-Shan, Tao-Yuan, Taiwan, R.O.C. Abstract. Background: Postoperative 5-fluorouracil (5-FU)- to more favorable RFS than 5-FU/LV following curative based chemotherapy improves survival after resection of resection of synchronous CRLM. synchronous liver metastases from colorectal cancer (CRLM). We retrospectively assessed the efficacy of postoperative Colorectal cancer (CRC) is one of the leading causes of cancer- chemotherapy with a modern regimen containing of related mortality, accounting for more than 600,000 deaths oxaliplatin or irinotecan after curative resection of annually worldwide (1-3). In Taiwan, it is the second most synchronous CRLM. Patients and Methods: Seventy-two common type of cancer in men and women, after hepatocellular patients who received postoperative chemotherapy following carcinoma and breast cancer, respectively (4). The liver is the curative resection of synchronous CRLM were analyzed. most common site of metastasis in CRC (50-60% of cases). Patients were categorized into fluorouracil plus leucovorin (5- One-third of patients have liver metastases at the time of FU/LV, n=25), irinotecan-based regimen (FOLFIRI/IFL, diagnosis (synchronous) and two-thirds develop metastases n=21) and oxaliplatin-based regimen (FOLFOX, n=26) during the disease course (metachronous) (5). -
Impact and Relevance of the Unfolded Protein Response in HNSCC
International Journal of Molecular Sciences Review Impact and Relevance of the Unfolded Protein Response in HNSCC Olivier Pluquet 1,* and Antoine Galmiche 2,3,* 1 Institut Pasteur de Lille, Université de Lille, CNRS, UMR8161–M3T–Mechanisms of Tumorigenesis and Targeted Therapies, F-59000 Lille, France 2 Service de Biochimie, Centre de Biologie Humaine (CBH), CHU Sud, 80054 Amiens, France 3 EA7516, Université de Picardie Jules Verne (UPJV), 80054 Amiens, France * Correspondence: [email protected] (O.P.); [email protected] (A.G.) Received: 30 April 2019; Accepted: 27 May 2019; Published: 30 May 2019 Abstract: Head and neck squamous cell carcinomas (HNSCC) encompass a heterogeneous group of solid tumors that arise from the upper aerodigestive tract. The tumor cells face multiple challenges including an acute demand of protein synthesis often driven by oncogene activation, limited nutrient and oxygen supply and exposure to chemo/radiotherapy, which forces them to develop adaptive mechanisms such as the Unfolded Protein Response (UPR). It is now well documented that the UPR, a homeostatic mechanism, is induced at different stages of cancer progression in response to intrinsic (oncogenic activation) or extrinsic (microenvironment) perturbations. This review will discuss the role of the UPR in HNSCC as well as in the key processes that characterize the physiology of HNSCC. The role of the UPR in the clinical context of HNSCC will also be addressed. Keywords: Head and Neck Squamous Cell Carcinoma (HNSCC); Unfolded Protein Response (UPR); therapy; biomarkers; prognosis 1. Introduction Head and Neck Squamous Cell Carcinomas (HNSCCs) are a group of tumors that arise from the mucosal epithelia of the head and neck. -
For Health Professionals Who Care for Cancer Patients February 2007 Website Access At
Volume 10, Number 2 for health professionals who care for cancer patients February 2007 Website access at http://www.bccancer.bc.ca/HPI/ChemotherapyProtocols/stupdate.htm I NSIDE THIS ISSUE Editor’s Choice: Guidelines for the Use of GOCXRADC, GOENDCAT, GOEP, GOOVCATM, Bevacizumab in Metastatic Colorectal Cancer, GOOVCATR, GOOVCATX, UGUAJPG, GUBCG, Communities Oncology Network Contact GUBCV, GUBEP, GUBP, GUBPW, GUEP, GUKIFN, Information on Website, Highlights of Changes in GUPDOC, GUPKETO, GUPMX, GUSCARB, Protocols and Pre-Printed Orders GUSCCAVE, GUVEIP, LKCMLI, LUNAVP, Cancer Management Guidelines – Hepatitis B ULUAVERL, ULUGEF, LYABVD, ULYALEM, LYCDA, Reactivation Consult LYCHLOR, LYCHOP, LYCHOPR, LYCODOXMR, LYCSPA, LYCVP, LYCVPPABO, LYCVPR, LYCYCLO, Cancer Drug Manual: Complete Revision: LYECV, LYFLU, LYGDP, LYHDMTXP, Fludarabine Limited Revision: Alemtuzumab, LYHDMTXR, LYIT, ULYMFBEX, ULYMFECP, Bevacizumab, Imatinib, Leucovorin, Rituximab, LYPALL, ULYRICE, LYRITB, LYRITUX, LYRITZ, Chemotherapy Preparation and Stability Chart ULYRMTN, LYSNCC, UMYBORTEZ, MYMP, Nursing Resources of the Month: Webcast: Clinical UMYTHALID, SAAVGI Breakthroughs in EGFR Inhibition Website Resources Focus on: Understanding Targeted Drug Therapies Appendix: Understanding Targeted Drug Therapies List of New and Revised Protocols, Pre-Printed Orders and Patient Handouts: Revised: BRAJDTFEC, BRLAACDT, GOCXCAT, IN TOUCH phone list is provided if additional information is needed. EDITOR’S CHOICE GUIDELINES FOR THE USE OF BEVACIZUMAB (AVASTIN®) IN METASTATIC -
Fludarabine-Mediated Inhibition of Nucleotide Excision Repair Induces Apoptosis in Quiescent Human Lymphocytes1
Vol. 2, 1731-1741, October 1996 Clinical Cancer Research 1731 Fludarabine-mediated Inhibition of Nucleotide Excision Repair Induces Apoptosis in Quiescent Human Lymphocytes1 Alex Sandoval, Ugo Consoli, and 2). The deoxyadenosine analogue fludarabine is currently used William Plunkett2 alone and in combination for treating hematological malignan- cies such as chronic lymphocytic leukemia (3-5), low-grade Departments of Clinical Investigation [A. S., W. P.] and Hematology bymphoma (6, 7), acute myebogenous leukemia (8-10), and EU. C.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030 mycosis fungoides/S#{233}zary syndrome (1 1). Previous studies in- dicate that the nucleoside of fludarabine, F-ara-A,3 is a potent inhibitor of cellular DNA synthesis. This inhibition is brought ABSTRACT about by actions of the triphosphate F-ara-ATP. Indirect inhi- Incorporation of fludarabine, 941-D-arabinofuranosyl- bition occurs through the action of F-ara-AIP on ribonucleotide 2-fluoroadenine (F-ara-A), into replicating DNA inhibits reductase, causing a decrease in cellular deoxynucleotide further chain elongation and is the critical event in F-ara- triphosphate pools required for DNA synthesis (12). Reducing A-mediated cytotoxicity. We have used the normal cellular deoxynucleotide triphosphate bevels facilitates the use of F-ara- process of nucleotide excision repair to create an opportu- ATP by DNA polymerases for incorporation of F-ara-A-AMP nity for F-ara-A incorporation into the DNA of noncycling into DNA, which is the critical event in F-ara-A-mediated cells. Irradiation of quiescent lymphocytes with UV light cytotoxicity (13, 14). F-ara-ATP is also known to be a potent (254 nm, 0.5-30 J/m2) in the presence of [3H]F-ara-A pro- inhibitor of DNA primase activity (15). -
The Influences of Cytotoxic Drugs and L1210 Suspension Culture Density on De Novo Purine Synthesis Joyce Ann O'shaughnessy Yale University
Yale University EliScholar – A Digital Platform for Scholarly Publishing at Yale Yale Medicine Thesis Digital Library School of Medicine 1982 The influences of cytotoxic drugs and L1210 suspension culture density on de novo purine synthesis Joyce Ann O'Shaughnessy Yale University Follow this and additional works at: http://elischolar.library.yale.edu/ymtdl Recommended Citation O'Shaughnessy, Joyce Ann, "The influences of cytotoxic drugs and L1210 suspension culture density on de novo purine synthesis" (1982). Yale Medicine Thesis Digital Library. 2999. http://elischolar.library.yale.edu/ymtdl/2999 This Open Access Thesis is brought to you for free and open access by the School of Medicine at EliScholar – A Digital Platform for Scholarly Publishing at Yale. It has been accepted for inclusion in Yale Medicine Thesis Digital Library by an authorized administrator of EliScholar – A Digital Platform for Scholarly Publishing at Yale. For more information, please contact [email protected]. 5079 (Title of thesis) for the purpose of individual scholarly consultation or refer¬ ence is hereby granted by the author. This permission is not to be interpreted as affecting publication of this work or otherwise placing It in the public domain, and the author re¬ serves all rights of ownership guaranteed under common law protection of unpublished manuscripts. 3/H Uj- Date p J .i'' :irJ VF W'i-i Digitized by the Internet Archive in 2017 with funding from The National Endowment for the Humanities and the Arcadia Fund https://archive.org/details/influencesofcytoOOosha The Influences of Cytotoxic Drugs and L1210 Suspension Culture Density on de novo Purine Synthesis A thesis Submitted to the Yale University School of Medicine in Partial Fulfillment of the Requirements for the degree of Doctor of Medicine to be awarded in May, 1982. -
Marrakesh Agreement Establishing the World Trade Organization
No. 31874 Multilateral Marrakesh Agreement establishing the World Trade Organ ization (with final act, annexes and protocol). Concluded at Marrakesh on 15 April 1994 Authentic texts: English, French and Spanish. Registered by the Director-General of the World Trade Organization, acting on behalf of the Parties, on 1 June 1995. Multilat ral Accord de Marrakech instituant l©Organisation mondiale du commerce (avec acte final, annexes et protocole). Conclu Marrakech le 15 avril 1994 Textes authentiques : anglais, français et espagnol. Enregistré par le Directeur général de l'Organisation mondiale du com merce, agissant au nom des Parties, le 1er juin 1995. Vol. 1867, 1-31874 4_________United Nations — Treaty Series • Nations Unies — Recueil des Traités 1995 Table of contents Table des matières Indice [Volume 1867] FINAL ACT EMBODYING THE RESULTS OF THE URUGUAY ROUND OF MULTILATERAL TRADE NEGOTIATIONS ACTE FINAL REPRENANT LES RESULTATS DES NEGOCIATIONS COMMERCIALES MULTILATERALES DU CYCLE D©URUGUAY ACTA FINAL EN QUE SE INCORPOR N LOS RESULTADOS DE LA RONDA URUGUAY DE NEGOCIACIONES COMERCIALES MULTILATERALES SIGNATURES - SIGNATURES - FIRMAS MINISTERIAL DECISIONS, DECLARATIONS AND UNDERSTANDING DECISIONS, DECLARATIONS ET MEMORANDUM D©ACCORD MINISTERIELS DECISIONES, DECLARACIONES Y ENTEND MIENTO MINISTERIALES MARRAKESH AGREEMENT ESTABLISHING THE WORLD TRADE ORGANIZATION ACCORD DE MARRAKECH INSTITUANT L©ORGANISATION MONDIALE DU COMMERCE ACUERDO DE MARRAKECH POR EL QUE SE ESTABLECE LA ORGANIZACI N MUND1AL DEL COMERCIO ANNEX 1 ANNEXE 1 ANEXO 1 ANNEX -
MVASI Safely and Effectively
HIGHLIGHTS OF PRESCRIBING INFORMATION Metastatic colorectal cancer (2.2) • 5 mg/kg IV every 2 weeks with bolus-IFL These highlights do not include all the information needed to use • 10 mg/kg IV every 2 weeks with FOLFOX4 MVASI safely and effectively. See full prescribing information for • 5 mg/kg IV every 2 weeks or 7.5 mg/kg IV every 3 weeks with MVASI. fluoropyrimidine-irinotecan or fluoropyrimidine-oxaliplatin based chemotherapy after progression on a first-line bevacizumab product MVASI (bevacizumab-awwb) Solution for intravenous infusion containing regimen Initial U.S. Approval: 2017 Non-squamous non-small cell lung cancer (2.2) ® MVASI (bevacizumab-awwb) is biosimilar* to AVASTIN • 15 mg/kg IV every 3 weeks with carboplatin/paclitaxel (bevacizumab) Glioblastoma (2.2) • 10 mg/kg IV every 2 weeks Metastatic renal cell carcinoma (mRCC) (2.2) WARNING: GASTROINTESTINAL PERFORATIONS, SURGERY AND WOUND HEALING COMPLICATIONS, and HEMORRHAGE • 10 mg/kg IV every 2 weeks with interferon alfa Persistent, recurrent, or metastatic carcinoma of the cervix (2.2) See full prescribing information for complete boxed warning. Gastrointestinal Perforation: Occurs in up to 3.2%of • 15 mg/kg IV every 3 weeks with paclitaxel/cisplatin or paclitaxel/topotecan bevacizumab product-treated patients. Discontinue MVASI for gastrointestinal perforation. (5.1) --------------------DOSAGE FORMS AND STRENGTHS--------------- • Injection: 100 mg/4 mL (25 mg/ mL) in single dose vial (3) Surgery and Wound Healing Complications: Discontinue in • Injection: 400 mg/16 mL (25 mg/mL) in single dose vial (3) patients with wound dehiscence. Discontinue at least 28 days prior to elective surgery. -
An Investigation of Novel Flourescent Antimetabolites As Potential Molecular Probes in Neoplastic Cells Jeffrey Samuel Barkin Yale University
Yale University EliScholar – A Digital Platform for Scholarly Publishing at Yale Yale Medicine Thesis Digital Library School of Medicine 1987 An investigation of novel flourescent antimetabolites as potential molecular probes in neoplastic cells Jeffrey Samuel Barkin Yale University Follow this and additional works at: http://elischolar.library.yale.edu/ymtdl Recommended Citation Barkin, Jeffrey Samuel, "An investigation of novel flourescent antimetabolites as potential molecular probes in neoplastic cells" (1987). Yale Medicine Thesis Digital Library. 2378. http://elischolar.library.yale.edu/ymtdl/2378 This Open Access Thesis is brought to you for free and open access by the School of Medicine at EliScholar – A Digital Platform for Scholarly Publishing at Yale. It has been accepted for inclusion in Yale Medicine Thesis Digital Library by an authorized administrator of EliScholar – A Digital Platform for Scholarly Publishing at Yale. For more information, please contact [email protected]. TiI3 YALE MEDICAL LIBRARY +YI2 08627 8745 5404 YALE mmmll ll D* 0* , MEDICAL LIBRARV Permission for photocopying or microfilming of " /fn r ^y j f 0^ -_" for the purpose of individual scholarly consultation or reference is hereby granted by the author. This permission is not to be interpreted as affecting publication of this work, or otherwise placing it in the public domain, and the author reserves all rights of ownership guaranteed under ccanmon law protection of unpublished manuscripts. Signature of author) (Printed name) A (1^ (Date) Digitized by the Internet Archive in 2017 with funding from The National Endowment for the Humanities and the Arcadia Fund https://archive.org/details/investigationofnOObark L. i-'i . -
Phase II Clinical Trial Results Involvingtreatment with Low-Dose Daily Oral Cyclophosphamide, Weekly Vinblastine, and Rofecoxib
Cancer Therapy: Clinical Phase II Clinical Trial Results InvolvingTreatment with Low-Dose Daily Oral Cyclophosphamide, Weekly Vinblastine, and RofecoxibinPatientswithAdvancedSolidTumors Scott D. Young, Mark Whissell, Jonathan C.S. Noble, Pablo O. Cano, Pedro G. Lopez, and Colin J. Germond Abstract Purpose: Preclinical studies indicate that conventional chemotherapeutic agents given continu- ously at low doses (metronomic chemotherapy) may provide an improved therapeutic index. Cyclophosphamide and vinblastine have been best studied in experimental models, where tumor growth inhibition is achieved, at least in part, through antiangiogenic mechanisms. Experimental Design: Fifty patients with advanced solid tumors were enrolled in this phase II trial, 43 of whom had received at least one prior chemotherapy regimen. Patients were required to have Eastern Cooperative Oncology Group performance status of V2, a life expectancy of >3 months, and at least one measurable lesion. All patients received oral cyclophosphamide (50 mg) and rofecoxib (25 mg) daily in addition to weekly injections of vinblastine (3 mg/m2). Half of the patients also received minocycline (100 mg) orally twice daily with the intent of further inhibiting tumor angiogenesis. The primary end point of the study was clinical benefit, defined as the percentage of patients experiencing an objective response or exhibiting stable disease for at least 6 months. Results: For the 47 eligible patients, there were two (4%) complete responses and four (9%) partial responses, for an overall objective response rate of 13%. An additional eight patients achieved disease stabilization (stable disease z6 months) (17%).The primary end point of clinical benefit was therefore 30%, (95% confidence interval, 16-44%). The median progression-free survival for all patients was 103 days and 289 days for patients experiencing clinical benefit. -
Study Protocol and Statistical Analysis Plan
ALLIANCE FOR CLINICAL TRIALS IN ONCOLOGY CALGB/SWOG C80702 A PHASE III TRIAL OF 6 VERSUS 12 TREATMENTS OF ADJUVANT FOLFOX PLUS CELECOXIB OR PLACEBO FOR PATIENTS WITH RESECTED STAGE III COLON CANCER Investigational agent: Celecoxib/placebo, NSC #719627 (Alliance IND #107051), will be supplied by Pfizer, Inc., and distributed by CTEP, DCTD, NCI Participation limited to U.S. and Canadian sites. ClinicalTrials.gov Identifier: NCT01150045 Alliance Study Chair, Alliance GI Committee Co-Chair SWOG Study Co-Chair Jeffrey A. Meyerhardt, MD, MPH Anthony F. Shields, MD, PhD Alliance GI Committee Co-Chair SWOG GI Committee Chair Alliance Corr. Sci. Co-Chair SWOG Corr. Sci. Co-Chair PPP Co-Chair Alliance Primary Statistician SWOG Primary Statistician Secondary Statistician Data Manager Protocol Coordinator CCTG Champion NRG Oncology Champion Participating Organizations ALLIANCE / Alliance for Clinical Trials in Oncology, SWOG / SWOG, ECOG-ACRIN / ECOG-ACRIN Cancer Research Group, NRG / NRG Oncology, CCTG / Canadian Cancer Trials Group 1 Version Date: 02/24/2021 Update #13 CALGB/SWOG C80702 Study Resources Alliance Protocol Operations Program Office Alliance Statistics and Data Center Medidata RAVE® iMedidata Portal Adverse Event Reporting Alliance Patient Registration Alliance Biorepository at Ohio State University CALGB/SWOG C80702 Pharmacy Contact CALGB/SWOG C80702 Nursing Contact Drug Distribution Contact Protocol-related questions may be directed as follows: Questions Contact (via email) Questions regarding patient eligibility, treatment, Study