Leucovorin in Metastatic Colorectal Cancer
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
A Phase I and Pharmacokinetic Study of Irinotecan Given As a 7-Day
Vol. 10, 1657–1663, March 1, 2004 Clinical Cancer Research 1657 A Phase I and Pharmacokinetic Study of Irinotecan Given as a 7-Day Continuous Infusion in Metastatic Colorectal Cancer Patients Pretreated with 5-Fluorouracil or Raltitrexed Gianluca Masi,1 Alfredo Falcone,1 for activity, and we observed 3 (25%) partial responses, 2 Antonello Di Paolo,2 Giacomo Allegrini,1 (17%) minor responses, and 4 (33%) disease stabilizations. Romano Danesi,2 Cecilia Barbara,2 Conclusions: The administration of irinotecan as a 1 2 7-day continuous infusion every 21 days is feasible with Samanta Cupini, and Mario Del Tacca diarrhea being the dose-limiting toxicity; recommended 1Division of Medical Oncology, Department of Oncology, Civil 2 2 dose for Phase II studies is 20.0 mg/m /day. The comparison Hospital, Livorno, and Division of Pharmacology and of the present data with those obtained after a standard Chemotherapy, Department of Oncology, Transplants, and Advanced Technologies in Medicine, University of Pisa, Pisa, Italy 30–90 min. i.v. infusion of irinotecan demonstrates that continuous infusion improves the transformation of irinote- can to SN-38 and also results in increased glucuronidation of ABSTRACT the active metabolite. Antitumor activity in pretreated met- Purpose: The purpose is to determine the plasma phar- astatic colorectal cancer patients is encouraging. macokinetics, the maximum-tolerable dose and to prelimi- nary evaluate the antitumor activity of irinotecan admin- INTRODUCTION istered as a 7-day continuous infusion every 21 days in Irinotecan (CPT-11), a semisynthetic derivative of the nat- metastatic colorectal cancer patients pretreated with 5- ural alkaloid camptothecin, is a selective inhibitor of topoi- fluorouracil or raltitrexed. -
The Temperature-Dependent Effectiveness of Platinum-Based
cells Article The Temperature-Dependent Effectiveness of Platinum-Based Drugs Mitomycin-C and 5-FU during Hyperthermic Intraperitoneal Chemotherapy (HIPEC) in Colorectal Cancer Cell Lines Roxan F.C.P.A. Helderman 1,2 , Daan R. Löke 2, Jan Verhoeff 3 , Hans M. Rodermond 1, Gregor G.W. van Bochove 1, Menno Boon 1, Sanne van Kesteren 1, Juan J. Garcia Vallejo 3, H. Petra Kok 2, Pieter J. Tanis 4 , Nicolaas A.P. Franken 1,2 , Johannes Crezee 2 and Arlene L. Oei 1,2,* 1 Laboratory for Experimental Oncology and Radiobiology (LEXOR), Center for Experimental and Molecular Medicine (CEMM), Amsterdam University Medical Centers (UMC), University of Amsterdam, Cancer Center Amsterdam, P.O. Box 22700, 1100 DE Amsterdam, The Netherlands; [email protected] (R.F.C.P.A.H.); [email protected] (H.M.R.); [email protected] (G.G.W.v.B.); [email protected] (M.B.); [email protected] (S.v.K.); [email protected] (N.A.P.F.) 2 Department of Radiation Oncology, Amsterdam UMC, University of Amsterdam, P.O. Box 22700, 1100 DE Amsterdam, The Netherlands; [email protected] (D.R.L.); [email protected] (H.P.K.); [email protected] (J.C.) 3 Department of Molecular Cell Biology & Immunology, Amsterdam Infection & Immunity Institute and Cancer Center Amsterdam, Amsterdam UMC, P.O. Box 7057, 1007 MB Amsterdam, The Netherlands; j.verhoeff@amsterdamumc.nl (J.V.); [email protected] (J.J.G.V.) 4 Department for Surgery, Amsterdam UMC, University of Amsterdam, Cancer Center Amsterdam, P.O. -
Testicular Cancer Treatment Regimens
Testicular Cancer Treatment Regimens Clinical Trials: The NCCN recommends cancer patient participation in clinical trials as the gold standard for treatment. Cancer therapy selection, dosing, administration, and the management of related adverse events can be a complex process that should be handled by an experienced healthcare team. Clinicians must choose and verify treatment options based on the individual patient; drug dose modifications and supportive care interventions should be administered accordingly. The cancer treatment regimens below may include both U.S. Food and Drug Administration-approved and unapproved indications/regimens. These regimens are only provided to supplement the latest treatment strategies. These Guidelines are a work in progress that may be refined as often as new significant data becomes available. The National Comprehensive Cancer Network Guidelines® are a consensus statement of its authors regarding their views of currently accepted approaches to treatment. Any clinician seeking to apply or consult any NCCN Guidelines® is expected to use independent medical judgment in the context of individual clinical circumstances to determine any patient’s care or treatment. The NCCN makes no warranties of any kind whatsoever regarding their content, use, or application and disclaims any responsibility for their application or use in any way. Note: All recommendations are category 2A unless otherwise indicated. uPrimary Chemotherapy for Germ Cell Tumors1 REGIMEN DOSING Preferred Regimens BEP (Bleomycin + Etoposide + Days 1-5: Cisplatin 20mg/m2 IV over 60 minutes dailya Cisplatin)2,a,b Days 1-5: Etoposide 100mg/m2 IV over 60 minutes daily Days 1,8,15 OR Days 2,9,16: Bleomycin 30 units IV over 10 minutes daily. -
The Role of ABCG2 in Modulating Responses to Anti-Cancer Photodynamic Therapy
This is a repository copy of The role of ABCG2 in modulating responses to anti-cancer photodynamic therapy. White Rose Research Online URL for this paper: http://eprints.whiterose.ac.uk/152665/ Version: Accepted Version Article: Khot, MI orcid.org/0000-0002-5062-2284, Downey, CL, Armstrong, G et al. (4 more authors) (2020) The role of ABCG2 in modulating responses to anti-cancer photodynamic therapy. Photodiagnosis and Photodynamic Therapy, 29. 101579. ISSN 1572-1000 https://doi.org/10.1016/j.pdpdt.2019.10.014 © 2019 Elsevier B.V. All rights reserved. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/. Reuse This article is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs (CC BY-NC-ND) licence. This licence only allows you to download this work and share it with others as long as you credit the authors, but you can’t change the article in any way or use it commercially. More information and the full terms of the licence here: https://creativecommons.org/licenses/ Takedown If you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing [email protected] including the URL of the record and the reason for the withdrawal request. [email protected] https://eprints.whiterose.ac.uk/ The role of ABCG2 in modulating responses to anti-cancer photodynamic therapy List of Authors: M. Ibrahim Khot, Candice L. Downey, Gemma Armstrong, Hafdis S. Svavarsdottir, Fazain Jarral, Helen Andrew and David G. -
Fluorouracil-Methotrexate (CMF PO)
Chemotherapy Protocol BREAST CANCER CYCLOPHOSPHAMIDE (PO)-FLUOROURACIL-METHOTREXATE (CMF-PO) Regimen • Breast Cancer – Cyclophosphamide (PO)-Fluorouracil-Methotrexate (CMF PO) Indication • Adjuvant treatment of early breast cancer • WHO Performance status 0, 1, 2 Toxicity Drug Adverse Effect Cyclophosphamide Dysuria, haemorrhagic cystitis, taste disturbances Fluorouracil Diarrhoea, stomatitis Methotrexate Stomatitis, conjunctivitis, renal toxicity The presence of a third fluid compartment e.g. ascities or renal failure may delay methotrexate clearance hence increase toxicity. The adverse effects listed are not exhaustive. Please refer to the relevant Summary of Product Characteristics for full details. Monitoring Regimen • FBC, U&E’s and LFT’s prior to each cycle. • Patients with complete or partial dihydropyrimidine dehydrogenase (DPD) deficiency are at increased risk of severe and fatal toxicity during treatment with fluorouracil. All patients should be tested for DPD deficiency before initiation (cycle 1) to minimise the risk of these reactions Dose Modifications The dose modifications listed are for haematological, liver and renal function only. Dose adjustments may be necessary for other toxicities as well. In principle all dose reductions due to adverse drug reactions should not be re- escalated in subsequent cycles without consultant approval. It is also a general rule for chemotherapy that if a third dose reduction is necessary treatment should be stopped. Version 1.2 (November 2020) Page 1 of 6 Breast – Cyclophosphamide (PO)-Fluorouracil-Methotrexate (CMF-PO) Please discuss all dose reductions / delays with the relevant consultant before prescribing, if appropriate. The approach may be different depending on the clinical circumstances. The following is a general guide only. Haematological Prior to prescribing the following treatment criteria must be met on day 1 of treatment. -
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 -
5-Fluorouracil + Adriamycin + Cyclophosphamide) Combination in Differentiated H9c2 Cells
Article Doxorubicin Is Key for the Cardiotoxicity of FAC (5-Fluorouracil + Adriamycin + Cyclophosphamide) Combination in Differentiated H9c2 Cells Maria Pereira-Oliveira, Ana Reis-Mendes, Félix Carvalho, Fernando Remião, Maria de Lourdes Bastos and Vera Marisa Costa * UCIBIO, REQUIMTE, Laboratory of Toxicology, Faculty of Pharmacy, University of Porto, Rua de Jorge Viterbo Ferreira, 228, 4050-313 Porto, Portugal; [email protected] (M.P.-O.); [email protected] (A.R.-M.); [email protected] (F.C.); [email protected] (F.R.); [email protected] (M.L.B.) * Correspondence: [email protected] Received: 4 October 2018; Accepted: 3 January 2019; Published: 10 January 2019 Abstract: Currently, a common therapeutic approach in cancer treatment encompasses a drug combination to attain an overall better efficacy. Unfortunately, it leads to a higher incidence of severe side effects, namely cardiotoxicity. This work aimed to assess the cytotoxicity of doxorubicin (DOX, also known as Adriamycin), 5-fluorouracil (5-FU), cyclophosphamide (CYA), and their combination (5-Fluorouracil + Adriamycin + Cyclophosphamide, FAC) in H9c2 cardiac cells, for a better understanding of the contribution of each drug to FAC-induced cardiotoxicity. Differentiated H9c2 cells were exposed to pharmacological relevant concentrations of DOX (0.13–5 μM), 5-FU (0.13–5 μM), CYA (0.13–5 μM) for 24 or 48 h. Cells were also exposed to FAC mixtures (0.2, 1 or 5 μM of each drug and 50 μM 5-FU + 1 μM DOX + 50 μM CYA). DOX was the most cytotoxic drug, followed by 5-FU and lastly CYA in both cytotoxicity assays (reduction of 3-(4,5-dimethylthiazol-2- yl)-2,5-diphenyl tetrazolium bromide (MTT) and neutral red (NR) uptake). -
Arsenic Trioxide Targets MTHFD1 and SUMO-Dependent Nuclear De Novo Thymidylate Biosynthesis
Arsenic trioxide targets MTHFD1 and SUMO-dependent PNAS PLUS nuclear de novo thymidylate biosynthesis Elena Kamyninaa, Erica R. Lachenauera,b, Aislyn C. DiRisioa, Rebecca P. Liebenthala, Martha S. Fielda, and Patrick J. Stovera,b,c,1 aDivision of Nutritional Sciences, Cornell University, Ithaca, NY 14853; bGraduate Field of Biology and Biomedical Sciences, Cornell University, Ithaca, NY 14853; and cGraduate Field of Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, NY 14853 Contributed by Patrick J. Stover, February 12, 2017 (sent for review December 1, 2016; reviewed by I. David Goldman and Anne Parle-McDermott) Arsenic exposure increases risk for cancers and is teratogenic in levels. Decreased rates of de novo dTMP synthesis can be caused animal models. Here we demonstrate that small ubiquitin-like by the action of chemotherapeutic drugs (19), through inborn modifier (SUMO)- and folate-dependent nuclear de novo thymidylate errors of folate transport and metabolism (15, 18, 20, 21), by (dTMP) biosynthesis is a sensitive target of arsenic trioxide (As2O3), inhibiting translocation of the dTMP synthesis pathway enzymes leading to uracil misincorporation into DNA and genome instability. into the nucleus (2) and by dietary folate deficiency (22, 23). Im- Methylenetetrahydrofolate dehydrogenase 1 (MTHFD1) and serine paired dTMP synthesis leads to genome instability through well- hydroxymethyltransferase (SHMT) generate 5,10-methylenetetrahy- characterized mechanisms associated with uracil misincorporation drofolate for de novo dTMP biosynthesis and translocate to the nu- into nuclear DNA and subsequent futile cycles of DNA repair (24, cleus during S-phase, where they form a multienzyme complex with 25). Nuclear DNA is surveyed for the presence of uracil by a thymidylate synthase (TYMS) and dihydrofolate reductase (DHFR), as family of uracil glycosylases including: uracil N-glycolase (UNG), well as the components of the DNA replication machinery. -
Arsenic Trioxide As a Radiation Sensitizer for 131I-Metaiodobenzylguanidine Therapy: Results of a Phase II Study
Arsenic Trioxide as a Radiation Sensitizer for 131I-Metaiodobenzylguanidine Therapy: Results of a Phase II Study Shakeel Modak1, Pat Zanzonico2, Jorge A. Carrasquillo3, Brian H. Kushner1, Kim Kramer1, Nai-Kong V. Cheung1, Steven M. Larson3, and Neeta Pandit-Taskar3 1Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, New York; 2Department of Medical Physics, Memorial Sloan Kettering Cancer Center, New York, New York; and 3Molecular Imaging and Therapy Service, Department of Radiology, Memorial Sloan Kettering Cancer Center, New York, New York sponse rates when compared with historical data with 131I-MIBG Arsenic trioxide has in vitro and in vivo radiosensitizing properties. alone. We hypothesized that arsenic trioxide would enhance the efficacy of Key Words: radiosensitization; neuroblastoma; malignant the targeted radiotherapeutic agent 131I-metaiodobenzylguanidine pheochromocytoma/paraganglioma; MIBG therapy 131 ( I-MIBG) and tested the combination in a phase II clinical trial. J Nucl Med 2016; 57:231–237 Methods: Patients with recurrent or refractory stage 4 neuroblas- DOI: 10.2967/jnumed.115.161752 toma or metastatic paraganglioma/pheochromocytoma (MP) were treated using an institutional review board–approved protocol (Clinicaltrials.gov identifier NCT00107289). The planned treatment was 131I-MIBG (444 or 666 MBq/kg) intravenously on day 1 plus arsenic trioxide (0.15 or 0.25 mg/m2) intravenously on days 6–10 and 13–17. Toxicity was evaluated using National Cancer Institute Common Metaiodobenzylguanidine (MIBG) is a guanethidine analog Toxicity Criteria, version 3.0. Response was assessed by Interna- that is taken up via the noradrenaline transporter by neuroendo- tional Neuroblastoma Response Criteria or (for MP) by changes in crine malignancies arising from sympathetic neuronal precursors 123I-MIBG or PET scans. -
Stability of Carboplatin and Oxaliplatin in Their Infusion Solutions Is Due to Self-Association
Syracuse University SURFACE Chemistry - Faculty Scholarship College of Arts and Sciences 2011 Stability of Carboplatin and Oxaliplatin in their Infusion Solutions is Due to Self-Association Anthony J. Di Pasqua Syracuse University Deborah J. Kerwood Syracuse University Yi Shi Syracuse University Jerry Goodisman Syracuse University James C. Dabrowiak Syracuse University Follow this and additional works at: https://surface.syr.edu/che Part of the Chemistry Commons Recommended Citation Di Pasqua, Anthony J.; Kerwood, Deborah J.; Shi, Yi; Goodisman, Jerry; and Dabrowiak, James C., "Stability of Carboplatin and Oxaliplatin in their Infusion Solutions is Due to Self-Association" (2011). Chemistry - Faculty Scholarship. 29. https://surface.syr.edu/che/29 This Article is brought to you for free and open access by the College of Arts and Sciences at SURFACE. It has been accepted for inclusion in Chemistry - Faculty Scholarship by an authorized administrator of SURFACE. For more information, please contact [email protected]. View Article Online / Journal Homepage / Table of Contents for this issue Dalton Dynamic Article Links Transactions Cite this: Dalton Trans., 2011, 40, 4821 www.rsc.org/dalton COMMUNICATION Stability of carboplatin and oxaliplatin in their infusion solutions is due to self-association Anthony J. Di Pasqua,† Deborah J. Kerwood, Yi Shi, Jerry Goodisman and James C. Dabrowiak* Received 13th December 2010, Accepted 23rd March 2011 DOI: 10.1039/c0dt01758b Carboplatin and oxaliplatin are commonly used platinum anticancer agents that are sold as ready-to-use aqueous infusion solutions with shelf lives of 2 and 3 years, respectively. The observed rate constants for the hydrolysis of these drugs, however, are too large to account for their long shelf lives. -
Docetaxel Combined with Irinotecan Or 5-Fluorouracil in Patients with Advanced Oesophago-Gastric Cancer: a Randomised Phase II Study
British Journal of Cancer (2012) 107, 435–441 & 2012 Cancer Research UK All rights reserved 0007 – 0920/12 www.bjcancer.com Docetaxel combined with irinotecan or 5-fluorouracil in patients with advanced oesophago-gastric cancer: a randomised phase II study 1 *,1 2 3 4 5 5 6 A Roy , D Cunningham , R Hawkins ,HSo¨rbye , A Adenis , J-R Barcelo , G Lopez-Vivanco , G Adler , 7 8 9 10 11 12 13 14 J-L Canon , F Lofts , C Castanon , E Fonseca , O Rixe , J Aparicio , J Cassinello , M Nicolson , 15 16 17 17 18 19 20 M Mousseau , A Schalhorn , L D’Hondt , J Kerger , DK Hossfeld , C Garcia Giron , R Rodriguez , 21 22 P Schoffski and J-L Misset 1Department of Medicine, Royal Marsden Hospital, Sutton, London, SM25PT, UK; 2Department of Medical Oncology, University of Manchester, 3 4 Clinical Studies Manchester, M20 4BX UK; Department of Medical Oncology, Haukeland University Hospital, Bergen, Norway; Department of Gastrointestinal 5 6 Oncology, Centre Oscar Lambret, Lille, France; Department of Oncology, Hospital de Cruces Osakidetza, Basque Country, Spain; Department of 7 Medicine, University of Ulm, Robert-Koch-Strasse 8 D-89081, Ulm, Germany; Oncologie Me´dicale, Grand Hopital de Charleroi, 3, Grand’Rue Charleroi, 8 9 6000, Belgium; Department of Oncology, St George’s Hospital NHS Trust, London, UK; Department of Medical Oncology, Hospital Clinico de 10 11 Salamanca, Salamanca, Spain; Department of Medical Oncology, Hospital Universitario Paseo de San Vicente, Salamanca, Spain; Department of ˆ 12 13 Medical Oncology, Salpetrie`re Hospital, Paris, France; Department of Medical Oncology, Hospital Universitario La Fe, Valencia, Spain; Department of Medical Oncology, Hospital General Universitario de Guadalajara, Guadalajara, Spain; 14Department of Oncology, Aberdeen Royal Infirmary, Aberdeen, UK; 15Department of Oncology and Haematology, University Hospital, CHU de Grenoble, Grenoble, France; 16Klinikum der Universita¨t Mu¨nchen 17 18 Grosshadern, Munich, Germany; Chu Mont Godinne, Avenue Docteur G. -
Paclitaxel, Vinorelbine and 5-Fluorouracil in Breast Cancer Patients Pretreated with Adjuvant Anthracyclines
British Journal of Cancer (2005) 92, 634 – 638 & 2005 Cancer Research UK All rights reserved 0007 – 0920/05 $30.00 www.bjcancer.com Paclitaxel, vinorelbine and 5-fluorouracil in breast cancer patients pretreated with adjuvant anthracyclines Clinical Studies 1 1 1 2 2 2 3 3 A Berruti , R Bitossi , G Gorzegno , A Bottini , D Generali , M Milani , D Katsaros , IA Rigault de la Longrais , 3 4 4 4 5 6 6 7 R Bellino , M Donadio , M Ardine , O Bertetto , S Danese , MG Sarobba , A Farris , V Lorusso and ,1 L Dogliotti* 1Oncologia Medica, Azienda Ospedaliera San Luigi, Regione Gonzole 10, 10043 Orbassano (TO), Italy; 2Breast Unit, Azienda Ospedaliera Istituti Ospitalieri, largo Priori, 26100 Cremona, Italy; 3Ginecologia Oncologica, Azienda Ospedaliera OIRM Sant’Anna, via Ventimiglia 3, 10126 Torino, Italy; 4 Oncologia Medica, Centro Oncologico Ematologico Subalpino, Azienda Ospedaliera San Giovanni Battista Molinette, corso Bramante 88, 10126 Torino, 5 6 Italy; Ginecologia Divisione A, Azienda Ospedaliera OIRM Sant’Anna, corso Spezia 60, 10126 Torino, Italy; Oncologia Medica, Istituto Clinica Medica 7 Universitaria, via San Pietro 8, 07100 Sassari, Italy; Oncologia Medica, Istituto Oncologico, via Amendola 209, 70126 Bari, Italy We investigated the activity and toxicity of a combination of vinorelbine (VNB), paclitaxel (PTX) and 5-fluorouracil (5-FU) continuous infusion administered as first-line chemotherapy in metastatic breast cancer patients pretreated with adjuvant À2 À2 anthracyclines. A total of 61 patients received a regimen consisting of VNB 25 mg m on days 1 and 15, PTX 60 mg m on days 1, 8 À2 and 15 and continuous infusion of 5-FU at 200 mg m every day.