LCA Oral SACT Counselling Handbook
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
LYSODREN Safely and Effectively
HIGHLIGHTS OF PRESCRIBING INFORMATION -----------------------WARNINGS AND PRECAUTIONS------------------------ These highlights do not include all the information needed to use • Central Nervous System (CNS) Toxicity: Plasma concentrations LYSODREN safely and effectively. See full prescribing information for exceeding 20 mcg/mL are associated with a greater incidence of toxicity. LYSODREN. (5.2) • Adrenal Insufficiency: Institute steroid replacement as clinically LYSODREN® (mitotane) tablets, for oral use indicated. Measure free cortisol and corticotropin (ACTH) levels to Initial U.S. Approval: 1970 achieve optimal steroid replacement. (5.3) • Embryo-Fetal Toxicity: Can cause fetal harm. Advise women of WARNING: ADRENAL CRISIS IN THE SETTING OF SHOCK OR reproductive potential of the potential risk to a fetus and use of effective SEVERE TRAUMA contraception. (5.4, 8.1, 8.3) See full prescribing information for complete boxed warning. • Ovarian Macrocysts in Premenopausal Women: Advise women to seek medical advice if they experience gynecological symptoms such as In patients taking LYSODREN, adrenal crisis occurs in the setting of vaginal bleeding and/or pelvic pain. (5.5) shock or severe trauma and response to shock is impaired. Administer hydrocortisone, monitor for escalating signs of shock and discontinue -------------------------------ADVERSE REACTIONS------------------------------ LYSODREN until recovery. (2.2, 5.1) Common adverse reactions (≥15%) include: anorexia, nausea, vomiting and diarrhea; depression, dizziness or vertigo; and rash. (6) ---------------------------INDICATIONS AND USAGE---------------------------- LYSODREN is an adrenal cytotoxic agent indicated for the treatment of To report SUSPECTED ADVERSE REACTIONS, contact Bristol-Myers inoperable, functional or nonfunctional, adrenal cortical carcinoma. (1) Squibb at 1-800-721-5072 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch. -
EDP & Mitotane Protocol
THE CLATTERBRIDGE CANCER CENTRE NHS FOUNDATION TRUST Systemic Anti Cancer Treatment Protocol EDP + mitotane PROCEDURE REF: MPHA HANEDP (Version No: 1.0) Approved for use in: Symptomatic treatment for advanced (unresectable, metastatic or relapsed) adrenocortical carcinoma ECOG performance status of 0 - 2 All possible tumour tissues should be surgically removed from large metastatic masses before mitotane administration is instituted. This is necessary to minimise the possibility of infarction and haemorrhage in the tumour due to a rapid cytotoxic effect of mitotane Exclusion criteria: Previous complete cumulative doses of anthracyclines Decompensated heart failure (ejection fraction <50%) Unstable angina, uncontrolled cardiac arrhythmias, MI or revascularisation procedure within last 6 months Dosage: Drug Dosage Route Frequency Etoposide 100mg/m2 IV Daily on days 2, 3 and 4 of each cycle Doxorubicin 40mg/m2 IV Once only on day 1 of each cycle Cisplatin 40mg/m2 IV Daily on days 3 and 4 of each cycle Variable, max Continuous, started a week prior to IV Mitotane PO 6g daily chemotherapy if not already taking With cycles repeated at 28 day intervals until disease progression Supportive treatments: Domperidone 10mg oral tablets maximum 3 times a day or as required Issue Date: May 2017 Page 1 of 8 Protocol reference: MPHAHANEDP 1 Authorised by: Drugs & Therapeutics Author: Helen Flint Committee & Dr D Husband Version No: 1.0 THE CLATTERBRIDGE CANCER CENTRE NHS FOUNDATION TRUST Extravasation risk: Doxorubicin is a vesicant and must be observed during administration. Follow the procedure for anthracycline extravasation. Erythematous streaking (a histamine release phenomenon) along the vein proximal to the site of injection has been reported, and must be differentiated from an extravasation event. -
A Phase II Study of Paclitaxel and Capecitabine As a First-Line Combination Chemotherapy for Advanced Gastric Cancer
British Journal of Cancer (2008) 98, 316 – 322 & 2008 Cancer Research UK All rights reserved 0007 – 0920/08 $30.00 www.bjcancer.com A phase II study of paclitaxel and capecitabine as a first-line combination chemotherapy for advanced gastric cancer Clinical Studies HJ Kang1, HM Chang1, TW Kim1, M-H Ryu1, H-J Sohn1, JH Yook2,STOh2, BS Kim2, J-S Lee1 and Y-K Kang*,1 1 2 Division of Oncology, Department of Medicine, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea; Department of Surgery, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea Paclitaxel and capecitabine, which have distinct mechanisms of action and toxicity profiles, have each shown high activity as single agents in gastric cancer. Synergistic interaction between these two drugs was suggested by taxane-induced upregulation of thymidine phosphorylase. We, therefore, evaluated the antitumour activity and toxicities of paclitaxel and capecitabine as first-line therapy in patients with advanced gastric cancer (AGC). Patients with histologically confirmed unresectable or metastatic AGC were treated À2 À2 with capecitabine 825 mg m p.o. twice daily on days 1–14 and paclitaxel 175 mg m i.v. on day 1 every 3 weeks until disease progression or unacceptable toxicities. Between June 2002 and May 2004, 45 patients, of median age 57 years (range ¼ 38–73 years), were treated with the combination of capecitabine and paclitaxel. After a median 6 cycles (range ¼ 1–9 cycles) of chemotherapy, 43 were evaluable for toxicity and response. A total of 2 patients showed complete response and 20 showed partial response making the overall response rate 48.9% (95% CI ¼ 30.3–63.5%). -
A Phase II Study of Capecitabine and Docetaxel Combination Chemotherapy in Patients with Advanced Gastric Cancer
British Journal of Cancer (2004) 90, 1329 – 1333 & 2004 Cancer Research UK All rights reserved 0007 – 0920/04 $25.00 www.bjcancer.com A phase II study of capecitabine and docetaxel combination chemotherapy in patients with advanced gastric cancer YH Park*,1, B-Y Ryoo1, S-J Choi1and H-T Kim1 1 Division of Haematology and Oncology, Department of Internal Medicine, Korea Institute of Radiological and Medical Science, Seoul, Korea Clinical Capecitabine and docetaxel have considerable single-agent activity in gastric cancer with distinct mechanisms of action and no overlap of key toxicities. A synergistic interaction between these two drugs is mediated by taxane-induced upregulation of thymidine phosphorylase. We investigated the activity and the feasibility of capecitabine and docetaxel combination chemotherapy in patients with previously untreated advanced gastric cancer (AGC). From September 2001 to March 2003, 42 patients with AGC received À2 À2 21-day cycles of oral capecitabine (1250 mg m twice daily on days 1–14) and docetaxel (75 mg m i.v. on day 1). The patients received a total of 164 cycles of chemotherapy. The median age was 53.5 years (range 33–73 years). The overall response rate in the 38 efficacy-evaluable patients was 60% (95% confidence interval, 45–74%). The median progression-free survival was 5.2 months (range, 1.0–15.5 þ months) and the median overall survival was 10.5 months (range, 2.9–23.7 þ months). The most common grade 3/4 adverse events were hand–foot syndrome (HFS: G3 50%), neutropenia (15%) and leucopenia (12%). Further studies of this combination are clearly warranted, albeit with lower doses of both agents (1000 mg mÀ2 twice daily and 60 mg mÀ2) to reduce the rate of HFS and onycholysis. -
Targeting Fibrosis in the Duchenne Muscular Dystrophy Mice Model: an Uphill Battle
bioRxiv preprint doi: https://doi.org/10.1101/2021.01.20.427485; this version posted January 21, 2021. 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. 1 Title: Targeting fibrosis in the Duchenne Muscular Dystrophy mice model: an uphill battle 2 Marine Theret1#, Marcela Low1#, Lucas Rempel1, Fang Fang Li1, Lin Wei Tung1, Osvaldo 3 Contreras3,4, Chih-Kai Chang1, Andrew Wu1, Hesham Soliman1,2, Fabio M.V. Rossi1 4 1School of Biomedical Engineering and the Biomedical Research Centre, Department of Medical 5 Genetics, 2222 Health Sciences Mall, Vancouver, BC, V6T 1Z3, Canada 6 2Department of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, Minia 7 University, Minia, Egypt 8 3Developmental and Stem Cell Biology Division, Victor Chang Cardiac Research Institute, 9 Darlinghurst, NSW, 2010, Australia 10 4Departamento de Biología Celular y Molecular and Center for Aging and Regeneration (CARE- 11 ChileUC), Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331150 12 Santiago, Chile 13 # Denotes Co-first authorship 14 15 Keywords: drug screening, fibro/adipogenic progenitors, fibrosis, repair, skeletal muscle. 16 Correspondence to: 17 Marine Theret 18 School of Biomedical Engineering and the Biomedical Research Centre 19 University of British Columbia 20 2222 Health Sciences Mall, Vancouver, British Columbia 21 Tel: +1(604) 822 0441 fax: +1(604) 822 7815 22 Email: [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.01.20.427485; this version posted January 21, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. -
Novartis R&D and Investor Update
Novartis AG Investor Relations Novartis R&D and investor update November 5, 2018 Disclaimer This presentation contains forward-looking statements within the meaning of the United States Private Securities Litigation Reform Act of 1995, that can generally be identified by words such as “potential,” “expected,” “will,” “planned,” “pipeline,” “outlook,” “agreement to acquire,” or similar expressions, or by express or implied discussions regarding potential marketing approvals, new indications or labeling for the investigational or approved products described in this presentation, or regarding potential future revenues from such products, or regarding the proposed acquisition of Endocyte, Inc. (Endocyte) by Novartis including the potential outcome and expected timing for completion of the proposed acquisition, and the potential impact on Novartis of the proposed acquisition, including express or implied discussions regarding potential future sales or earnings of Novartis, and any potential strategic benefits, synergies or opportunities expected as a result of the proposed acquisition. You should not place undue reliance on these statements. Such forward-looking statements are based on our current beliefs and expectations regarding future events, and are subject to significant known and unknown risks and uncertainties. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those set forth in the forward-looking statements. There can be no guarantee that the investigational or approved products described in this presentation will be submitted or approved for sale or for any additional indications or labeling in any market, or at any particular time. Nor can there be any guarantee that such products will be commercially successful in the future. -
Targeting the Mitochondrial Metabolic Network: a Promising Strategy in Cancer Treatment
International Journal of Molecular Sciences Review Targeting the Mitochondrial Metabolic Network: A Promising Strategy in Cancer Treatment Luca Frattaruolo y , Matteo Brindisi y , Rosita Curcio, Federica Marra, Vincenza Dolce and Anna Rita Cappello * Department of Pharmacy, Health and Nutritional Sciences, University of Calabria, Via P. Bucci, 87036 Rende (CS), Italy; [email protected] (L.F.); [email protected] (M.B.); [email protected] (R.C.); [email protected] (F.M.); [email protected] (V.D.) * Correspondence: [email protected] These authors contributed equally and should be considered co-first authors. y Received: 31 July 2020; Accepted: 19 August 2020; Published: 21 August 2020 Abstract: Metabolic reprogramming is a hallmark of cancer, which implements a profound metabolic rewiring in order to support a high proliferation rate and to ensure cell survival in its complex microenvironment. Although initial studies considered glycolysis as a crucial metabolic pathway in tumor metabolism reprogramming (i.e., the Warburg effect), recently, the critical role of mitochondria in oncogenesis, tumor progression, and neoplastic dissemination has emerged. In this report, we examined the main mitochondrial metabolic pathways that are altered in cancer, which play key roles in the different stages of tumor progression. Furthermore, we reviewed the function of important molecules inhibiting the main mitochondrial metabolic processes, which have been proven to be promising anticancer candidates in recent years. In particular, inhibitors of oxidative phosphorylation (OXPHOS), heme flux, the tricarboxylic acid cycle (TCA), glutaminolysis, mitochondrial dynamics, and biogenesis are discussed. The examined mitochondrial metabolic network inhibitors have produced interesting results in both preclinical and clinical studies, advancing cancer research and emphasizing that mitochondrial targeting may represent an effective anticancer strategy. -
Chapter 1.Pdf
CHAPTER 1 INTRODUCTION AND OUTLINE OF THIS THESIS INTRODUCTION Inflammatory bowel diseases (IBD), comprising Crohn’s disease, ulcerative colitis and IBD- 1 unclassified, are chronic recurrent inflammatory disorders of the (large) intestine with a heterogeneous, but often disabling disease presentation. The prevalence of IBD is increasing worldwide and medical therapies are introduced earlier to improve health-related quality of life and postpone surgical interventions1,2. This has led to the more extensive use of immunosuppressive therapies including biologicals and thiopurines. While the use of tioguanine was soon abandoned due to toxicity concerns3, over the years efficacy data on the use of azathioprine and mercaptopurine for the treatment of IBD has grown4,5. However, due to side effects and ineffectiveness, related to unprofitable metabolism, thiopurine therapy often fails; up to 50% of patients discontinues treatment within 2 years6. Increasing the knowledge on thiopurine metabolism may provide opportunities to further explore the therapeutic usefulness of thiopurines, which both from a patient’s perspective and a pharmacoeconomic perspective is essential. THIOPURINES In the 1950’s Gertrude Elion (1918-1999) worked as an assistant to George Hitchings (1905- 1998), both employees of Burroughs-Wellcome, focussing on the advent of drugs that inhibited cell growth without doing harm to the host cells. They discovered that purine bases are essential components of nucleic acids and vital for cell growth7. Subsequently, they designed the purine antagonists diaminopurine and tioguanine that blocked the synthesis of original nucleic acids and inhibited cell growth8. For the first time a successful treatment of leukaemia became available. Some years later Elion and colleagues also developed mercaptopurine, azathioprine, allopurinol, trimethoprim and acyclovir. -
Nurse-Led Drug Monitoring Clinic Protocol for the Use of Systemic Therapies in Dermatology for Patients
Group arrangements: Salford Royal NHS Foundation Trust (SRFT) Pennine Acute Hospitals NHS Trust (PAT) Nurse-led drug monitoring clinic protocol for the use of systemic therapies in dermatology for patients with inflammatory dermatoses Lead Author: Dawn Lavery Dermatology Advanced Nurse Practitioner Additional author(s) N/A Division/ Department:: Dermatology, Clinical Support and Tertiary Medicine Applies to: (Please delete) Salford Royal Care Organisation Approving Committee Dermatology clinical governance committee Salford Royal Date approved: 13 February 2019 Expiry date: February 2022 Contents Contents Section Page Document summary sheet 1 Overview 2 2 Scope & Associated Documents 2 3 Background 3 4 What is new in this version? 3 5 Policy 4 Drugs monitored by nurses 4 Acitretin 7 Alitretinoin Toctino 11 Apremilast 22 Azathioprine 26 Ciclosporin 29 Dapsone 34 Fumaric Acid Esters – Fumaderm and Skilarence 36 Hydroxycarbamide 39 Hydroxychloroquine 43 Methotrexate 50 Mycophenolate moefetil 57 Nurse-led drug monitoring clinic protocol for the use of systemic therapies in dermatology for patients with inflammatory dermatoses Reference Number GSCDerm01(13) Version 3 Issue Date: 11/06/2019 Page 1 of 77 It is your responsibility to check on the intranet that this printed copy is the latest version Standards 67 6 Roles and responsibilities 67 7 Monitoring document effectiveness 67 8 Abbreviations and definitions 68 9 References 68 10 Appendices N/A 11 Document Control Information 71 12 Equality Impact Assessment (EqIA) screening tool 73 Group arrangements: Salford Royal NHS Foundation Trust (SRFT) Pennine Acute Hospitals NHS Trust (PAT) 1. Overview (What is this policy about?) The dermatology directorate specialist nurses are responsible for ensuring prescribing and monitoring for patients under their care, is in accordance with this protocol. -
BC Cancer Benefit Drug List September 2021
Page 1 of 65 BC Cancer Benefit Drug List September 2021 DEFINITIONS Class I Reimbursed for active cancer or approved treatment or approved indication only. Reimbursed for approved indications only. Completion of the BC Cancer Compassionate Access Program Application (formerly Undesignated Indication Form) is necessary to Restricted Funding (R) provide the appropriate clinical information for each patient. NOTES 1. BC Cancer will reimburse, to the Communities Oncology Network hospital pharmacy, the actual acquisition cost of a Benefit Drug, up to the maximum price as determined by BC Cancer, based on the current brand and contract price. Please contact the OSCAR Hotline at 1-888-355-0355 if more information is required. 2. Not Otherwise Specified (NOS) code only applicable to Class I drugs where indicated. 3. Intrahepatic use of chemotherapy drugs is not reimbursable unless specified. 4. For queries regarding other indications not specified, please contact the BC Cancer Compassionate Access Program Office at 604.877.6000 x 6277 or [email protected] DOSAGE TUMOUR PROTOCOL DRUG APPROVED INDICATIONS CLASS NOTES FORM SITE CODES Therapy for Metastatic Castration-Sensitive Prostate Cancer using abiraterone tablet Genitourinary UGUMCSPABI* R Abiraterone and Prednisone Palliative Therapy for Metastatic Castration Resistant Prostate Cancer abiraterone tablet Genitourinary UGUPABI R Using Abiraterone and prednisone acitretin capsule Lymphoma reversal of early dysplastic and neoplastic stem changes LYNOS I first-line treatment of epidermal -
COMPARISON of the WHO ATC CLASSIFICATION & Ephmra/Intellus Worldwide ANATOMICAL CLASSIFICATION
COMPARISON OF THE WHO ATC CLASSIFICATION & EphMRA/Intellus Worldwide ANATOMICAL CLASSIFICATION: VERSION June 2019 2 Comparison of the WHO ATC Classification and EphMRA / Intellus Worldwide Anatomical Classification The following booklet is designed to improve the understanding of the two classification systems. The development of the two systems had previously taken place separately. EphMRA and WHO are now working together to ensure that there is a convergence of the 2 systems rather than a divergence. In order to better understand the two classification systems, we should pay attention to the way in which substances/products are classified. WHO mainly classifies substances according to the therapeutic or pharmaceutical aspects and in one class only (particular formulations or strengths can be given separate codes, e.g. clonidine in C02A as antihypertensive agent, N02C as anti-migraine product and S01E as ophthalmic product). EphMRA classifies products, mainly according to their indications and use. Therefore, it is possible to find the same compound in several classes, depending on the product, e.g., NAPROXEN tablets can be classified in M1A (antirheumatic), N2B (analgesic) and G2C if indicated for gynaecological conditions only. The purposes of classification are also different: The main purpose of the WHO classification is for international drug utilisation research and for adverse drug reaction monitoring. This classification is recommended by the WHO for use in international drug utilisation research. The EphMRA/Intellus Worldwide classification has a primary objective to satisfy the marketing needs of the pharmaceutical companies. Therefore, a direct comparison is sometimes difficult due to the different nature and purpose of the two systems. -
Australian Pi – Pomalyst (Pomalidomide) Capsules
AUSTRALIAN PI – POMALYST (POMALIDOMIDE) CAPSULES Teratogenic effects: Pomalyst (pomalidomide) is a thalidomide analogue. Thalidomide is a known human teratogen that causes severe life-threatening human birth defects. If pomalidomide is taken during pregnancy, it may cause birth defects or death to an unborn baby. Women should be advised to avoid pregnancy whilst taking Pomalyst (pomalidomide), during dose interruptions, and for 4 weeks after stopping the medicine. 1 NAME OF THE MEDICINE Australian Approved Name: pomalidomide 2 QUALITATIVE AND QUANTITATIVE COMPOSITION Each 1 mg capsule contains 1 mg pomalidomide. Each 2 mg capsule contains 2 mg pomalidomide. Each 3 mg capsule contains 3 mg pomalidomide. Each 4 mg capsule contains 4 mg pomalidomide. For the full list of excipients, see Section 6.1. Description Pomalidomide is a yellow solid powder. It is practically insoluble in water over the pH range 1.2-6.8 and is slightly soluble (eg. acetone, methylene chloride) to practically insoluble (eg. heptanes, ethanol) in organic solvents. Pomalidomide has a chiral carbon atom and exists as a racemic mixture of the R(+) and S(-) enantiomers. 3 PHARMACEUTICAL FORM Pomalyst (pomalidomide) 1 mg capsules: dark blue/yellow size 4 gelatin capsules marked “POML” in white ink and “1 mg” in black ink. Each 1 mg capsule contains 1 mg of pomalidomide. Pomalyst (pomalidomide) 2 mg capsules: dark blue/orange size 2 gelatin capsules marked “POML 2 mg” in white ink. Each 2 mg capsule contains 2 mg of pomalidomide. Pomalyst (pomalidomide) 3 mg capsules: dark blue/green size 2 gelatin capsules marked “POML 3 mg” in white ink.