DOCSLIB.ORG

ADH-1 in the Treatment of Metastatic Adrenocortical Carcinoma - Case Report

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
ADH-1 in the Treatment of Metastatic Adrenocortical Carcinoma - Case Report ANTICANCER RESEARCH 31: 3921-3926 (2011) ADH-1 in the Treatment of Metastatic Adrenocortical Carcinoma - Case Report NIRIT YAROM1, DAVID STEWART3, LEONARD AVRUCH1, RAJESH MALIK2, JULIE WELLS1 and DEREK J. JONKER1 1The Ottawa Hospital Cancer Centre, Ottawa, ON, Canada; 2Agennix Incorporated, Houston, TX, U.S.A.; 3MD Anderson Cancer Centre, Houston, TX, U.S.A. Abstract. Adrenocortical Carcinoma (ACC) is rare with an AdrenoCortical Carcinoma (ACC) is a rare disease, with a annual incidence of 0.5-2 cases per million worldwide. Some worldwide annual incidence of 0.5-2 cases per million. It ACC tumors over express N-cadherin, which correlates with accounts for 0.04-0.2% of all cancer deaths(1). For advanced metastatic potential. ADH-1 (Exherin™) is a competitive unresectable disease, treatment improvements have been inhibitor of N-cadherin, resulting in rapid onset of tumor limited, and prognosis remains poor. In an attempt to vascular angiolysis and apoptosis in preclinical models. establish a treatment standard, there is currently an ongoing Targeting N-cadherin may cause direct anti-tumor and anti- international randomized phase III trial (FIRM-ACT) vascular effects. We report a case of ACC with benefit from comparing etoposide, doxorubicin, cisplatin plus mitotane vs. ADH-1 therapy. A 24 year old woman with an N-cadherin streptozotocin plus mitotane (2). In addition, recently expressing metastatic ACC was treated on a phase I trial and published case reports have described beneficial effects of treated with ADH-1 subsequently received additional doses biological agents in individuals with this disease (3). through a special access program. The patient presented with In view of the poor response to conventional chemotherapy cushingoid features from cortisol over-secretion and was there is a need for novel therapeutic agents. Cadherins diagnosed with metastatic ACC in January 2003. Tumor represent a novel target in cancer therapy. Many carcinomas progression followed treatment with a combination of overexpress N-cadherin, with concomitant down-regulation of doxorubicin, cisplatin and mitotane. In October 2003, as a E-cadherin (the cadherin switch). This phenomenon correlates part of a phase I clinical trial she was treated with as a single with a phenotypic change termed the epithelial mesanchymal dose of ADH-1 at 150 mg/m2. This resulted in transient transition (EMT) and with acquired tumor invasiveness and normalization of cortisol, tumor necrosis on CT imaging, and metastatic potential. The cadherin switch has been observed reduction in tumor perfusion on DCE-MRI. Following in various types of cancers, including adrenal tumors (4, 5). It progression on several additional lines of chemotherapy, she is also thought that N-cadherin prevents ligand-induced was again treated with ADH-1 under a Special Access receptor internalization and down-regulation, resulting in Program (SAP). After 33 weekly doses (22 with 150 mg/m2 sustained (MAPK) signaling, thus promoting proliferation (6). and 11 with 300 mg/m2) radiographic tumor progression was With both tumor overexpression and association with tumor demonstrated and treatment discontinued. She survived 40 aggressiveness, cadherins represent an attractive novel target months with metastatic disease, dying 12 months after her for cancer therapy. last dose of ADH-1. This observation merits consideration for ADH-1 is a cyclic pentapeptide which contains the prospectively evaluating the efficacy of ADH-1 in patients cadherin cell adhesion recognition sequence His-Ala-Val and with cortisol secreting ACC that over express N-cadherin. competitively inhibits N-cadherin function, resulting in rapid onset of tumor vascular angiolysis and apoptosis in preclinical models. Targeting N-cadherin may cause direct anti-tumor and anti-vascular effects. Correspondence to: Nirit Yarom, 60 Ha’amakim, Ganey-Tikva, Previous reports showed that peptides containing this Israel 55900. Tel: +973 545619418, Fax: +972 89779714, e-mail: sequence disrupt cell adhesion, induce apoptosis, and alter [email protected]; [email protected] the intracellular distribution of h-catenin and actin in Key Words: Adrenocortical carcinoma, ADH-1, Dynamic contrast endothelial cells (6). enhancing magnetic resonance imaging (DCE-MRI), phase-I, N- Injection of ADH-1 into tumor-bearing mice has been cadherin. shown to induce angiolysis. ADH-1 damages tumor blood 0250-7005/2011 $2.00+.40 3921 ANTICANCER RESEARCH 31: 3921-3926 (2011) vessels, but not normal, mature blood vessels, and herewith Table I. Mean Ktrans (1/min) in the region of interest. Post treatment inhibits growth of breast, ovarian, colon and lung carcinomas there is an increase in the mean ktrans, suggesting increased vascular (7). ADH-1 results in a tumor specific local increase in blood permeability due to vascular disruption. vessel permeability that leads to highly synergistic effects Pre-treatment Post-treatment with conventional cytotoxic drugs such as melphalan (5). Even at very high doses, ADH-1 does not affect mature Right tumor 0.211 0.376 blood vessels, as shown in a preclinical rat toxicity model. Left tumor 0.273 0.356 ADH-1 is being studied in phase II trials in a variety of cancers, including esophageal, non-small cell lung, renal cell, and hepatocellular carcinomas (5). In murine melanoma xenografts, ADH-1 in combination measuring 12.5×10.0 cm with extensive necrosis, 8 mitoses with melphalan significantly reduced tumor growth up to 30- per 10 high power fields, invasion of the inferior vena cava fold over melphalan alone. ADH-1 enhancement of response (IVC), negative nodes, and a positive microscopic margin at to melphalan was associated with increased formation of the IVC. By the McFarlane system, disease was stage 3 (13). DNA adducts, increased apoptosis, and intracellular No adjuvant therapy was prescribed, and she was well signaling changes (8). until February 2003 when she experienced two weeks of dry In sixteen human patients with metastatic melanoma, cough without fever and mild left flank pain. CT scan including six patients who had not responded to melphalan confirmed recurrence in the abdomen and metastases in both alone, treatment with ADH-1 plus melphalan was associated lungs. Her cortisol levels were within normal limits. with promising activity. Within three months of treatment, She received 4 months treatment with combination eight patients had complete responses, two had partial epirubicin, cisplatin, mitotane, and ketoconazole with responses, two had stable disease, and four had progressive radiological clinical progression associated with increased disease (9). cushingoid features. The patient consented to a phase I clinical Results from two Phase I studies with ADH-1 have been trial with ADH-1, and her tumor was found to be positive for reported (10, 11). In both, ADH-1 was generally well N-cadherin expression. She received intravenous ADH-1 at a tolerated and the maximal tolerated dose (MTD) was not dose of 150 mg/m2. She developed transient normalization of reached. The most common adverse events at the doses used steroid hormones (Figure 1), increased disruption of blood were nausea, fatigue, dysgeusia and hot flashes. Some vessels seen by increased permeability (k trans) on dynamic cardiovascular effects were seen but were thought to be contrast enhanced – magnetic resonance imaging (DCE-MRI) related, at least in part, to prior cardiac history and injection 90 min post ADH-1 (Table I and Figures 2 and 3) and rate. No responses or changes in blood flow were reported evidence of tumor necrosis on her six-week MRI scan. in patients with N-cadherin-negative tumors. Four patients However, according to the protocol she was withdrawned from with N-cadherin-positive tumors showed some evidence of the trial, since only patients responding by the World Health antitumor activity, including a PR in esophageal cancer. In Organiztion criteria were permitted to receive additional addition, phase I studies where ADH-1 is being evaluated in therapy. For the next year she was treated with various three separate combinations with docetaxel, carboplatin or chemotherapies (temozolomide, gemcitabine, docetaxel, 5- capecitabine are ongoing (12). fluorouracil, cisplatin, and doxorubicin) and modifiers of We report here for the first time the results of a young steroidogenesis (ketoconazole, aminoglutethemide and patient with metastatic ACC who was treated with ADH-1 mitotane) none of which yielded a sustained reduction of both as part of a clinical trial and subsequently through an cortisol levels. unrelated special access program (SAP). She subsequently was permitted to receive ADH-1 under an approved SAP and was treated with an additional 33 Case Report weekly doses (22 with 150 mg/m2 and 11 with 300 mg/m2). She tolerated the treatment well, with reported grade 1 In January 2002, a 22-year-old woman previously healthy nausea and diarrhea. In addition, an episode of facial flashing presented with increasing abdominal pressure and occurred immediately after infusion of ADH-1. The patient discomfort. An ultrasound identified a mass in the left was hemodynamically stable and there were no associated adrenal gland measuring 10 cm which was displacing the symptoms. On another occasion she experienced chest spleen, pancreas and left kidney. There were no metastases discomfort occurring a few days after administration of seen. This was confirmed by MRI. A CT scan of her thorax ADH-1, thought to be possibly related. This was not and head showed
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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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
    [Show full text]
  • Case Report: Exceptional Response to Second Line Temozolomide Therapy in a Patient with Metastatic Adrenocortical Carcinoma
    CASE REPORT published: 22 April 2021 doi: 10.3389/fendo.2021.674039 Case Report: Exceptional Response to Second Line Temozolomide Therapy in a Patient With Metastatic Adrenocortical Carcinoma † † Deborah Cosentini 1 , Antonella Turla 1 , Ornella Carminati 2, Salvatore Grisanti 1, Vittorio Domenico Ferrari 1, Marta Laganà 1, Giovanni Rosti 3, Sandra Sigala 4 and Alfredo Berruti 1* 1 Medical Oncology Unit, Azienda Socio Sanitaria Territoriale (ASST) Spedali Civili, Department of Medical and Surgical Specialties, Radiological Sciences, and Public Health, University of Brescia, Brescia, Italy, 2 Medical Oncology, Department of Edited by: Oncology and Hematology, Azienda Unità Sanitaria Locale (AUSL), Romagna, Ravenna, Italy, 3 Medical Oncology, Barbara Altieri, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy, 4 Section of Pharmacology, Department of Molecular and Translational University Hospital of Wuerzburg, Medicine, University of Brescia, Brescia, Italy Germany Reviewed by: Background: In a recently published retrospective case series, Temozolomide was found Peter Igaz, Semmelweis University, Hungary active as second line approach in advanced ACC patients. The disease control rate obtained, Jaydira Del Rivero, however, was short-lived. We report here an ACC patient with extensive metastatic disease National Cancer Institute (NIH), who obtained a remarkable long lasting response with this alkylating agent. United States *Correspondence: Case Presentation: a 22-year-old female patient with ACC presented at our Medical Alfredo Berruti Oncology Department in poor general condition due the presence of extensive metastatic [email protected] pulmonary involvement. The disease had progressed to etoposide, doxorubicin and † These authors have contributed cisplatin plus mitotane therapy. Second line temozolomide therapy was prescribed equally to this work and share first authorship leading to a progressive improvement of patient general conditions.
    [Show full text]
  • For Health Professionals Who Care for Cancer Patients
    November 2014 Volume 17, Number 11 For Health Professionals Who Care For Cancer Patients Inside This Issue: . Editor’s Choice – New Programs: nab-Paclitaxel and . Provincial Systemic Therapy Program – Reformat of Gemcitabine for Pancreatic Cancer, Neoadjuvant Paclitaxel BCCA Policy on Prevention and Management of and AC for Breast Cancer, Chlorambucil plus Rituximab for Extravasation of Chemotherapy Lymphomas, Chemotherapy plus Mitotane for . Drug Update – Enzalutamide Patient Assistance Adrenocortical Cancer Program . Cancer Drug Manual – Revised: Filgrastim, Gemcitabine, . List of New and Revised Protocols, Provincial Pre- Oxaliplatin, Paclitaxel, nab-Paclitaxel, Dexamethasone Printed Orders and Patient Handouts – New: . Medication Safety – Improving Website Clarity for Protocol BRLATACG, BRLATWAC, UGIPGEMABR, GUEDPM, Selection LYCHLRR Revised: BRAVEVEX, UCNBEV, GICIRB, . Benefit Drug List – New: BRLATACG, BRLATWAC, GIFFIRB, UGIFFOXB, UGIFIRINOX, GOCXCRT, GOENDH, UGIPGEMABR, GUEDPM, LYCHLRR Revised: ULYRMTN GUPLHRH, GUSCPE, HNAVP, LYIVACR, HNLAPRT, Deleted: BRLAACTW ULKATOATRA, ULKATOP, ULKATOR, ULUAVAFAT, LYABVD, LYCHOP, LYCHOPR, LYCHOPRMTX, LYRMTN . Continuing Professional Development – Workshop on Deleted: BRLAACTW Education in Palliative and End of Life Care for Oncology . Website Resources and Contact Information EDITOR’S CHOICE NEW PROGRAMS The Provincial Systemic Therapy Program has approved the following programs effective 1 November 2014: nab-Paclitaxel (ABRAXANE®) and Gemcitabine for Locally Advanced and Metastatic Pancreatic
    [Show full text]
  • 2015 Antiemesis.Pdf
    NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) Antiemesis Version 2.2015 NCCN.org Continue Version 2.2015, 09/22/15 © National Comprehensive Cancer Network, Inc. 2015, All rights reserved. The NCCN Guidelines® and this illustration may not be reproduced in any form without the express written permission of NCCN®. Printed by Alexandre Ferreira on 10/25/2015 6:12:07 AM. For personal use only. Not approved for distribution. Copyright © 2015 National Comprehensive Cancer Network, Inc., All Rights Reserved. NCCN Guidelines Version 2.2015 Panel Members NCCN Guidelines Index Antiemesis Table of Contents Antiemesis Discussion David S. Ettinger, MD/Chair † Steve Kirkegaard, PharmD Σ Eric Roeland, MD The Sidney Kimmel Comprehensive Huntsman Cancer Institute UC San Diego Moores Cancer Cancer Center at Johns Hopkins at the University of Utah Center Michael J. Berger, PharmD/Vice Chair, BCOP Σ Dwight D. Kloth, PharmD, BCOP Σ Hope S. Rugo, MD † ‡ The Ohio State University Comprehensive Fox Chase Cancer Center UCSF Helen Diller Family Cancer Center - James Cancer Hospital Comprehensive Cancer Center and Solove Research Institute Ruth Lagman, MD £ Mayo Clinic Cancer Center Bridget Scullion, PharmD, BCOP Jonathan Aston, PharmD, BCOP, BCPS Σ Dana-Farber/Brigham and Women’s Vanderbilt-Ingram Cancer Center Dean Lim, MD † Cancer Center | Massachusetts City of Hope Comprehensive Cancer Center General Hospital Cancer Center Sally Barbour, PharmD, BCOP, CCP Σ Duke Cancer Institute Cynthia Ma, MD, PhD † John Timoney, PharmD, BCOP † Siteman Cancer Center at Barnes-Jewish Memorial Sloan Kettering Cancer Philip J. Bierman, MD † ‡ Hospital and Washington University School Center Fred & Pamela Buffet Cancer Center of Medicine Barbara Todaro, PharmD Σ Debra Brandt, DO Belinda Mandrell, PhD, RN † Roswell Park Cancer Institute Yale Cancer Center/Smilow Cancer Hospital St.
    [Show full text]
  • Avelumab in Patients with Previously Treated Metastatic Adrenocortical
    Le Tourneau et al. Journal for ImmunoTherapy of Cancer (2018) 6:111 https://doi.org/10.1186/s40425-018-0424-9 RESEARCH ARTICLE Open Access Avelumab in patients with previously treated metastatic adrenocortical carcinoma: phase 1b results from the JAVELIN solid tumor trial Christophe Le Tourneau1,2,3*†, Christopher Hoimes4†, Corrine Zarwan5, Deborah J. Wong6, Sebastian Bauer7,8, Rainer Claus9,10, Martin Wermke11, Subramanian Hariharan12, Anja von Heydebreck13, Vijay Kasturi14, Vikram Chand15 and James L. Gulley16 Abstract Background: We assessed the efficacy and safety of avelumab, an anti-programmed death ligand 1 (PD-L1) antibody, in patients with previously treated metastatic adrenocortical carcinoma (mACC). Methods: In this phase 1b expansion cohort, patients with mACC and prior platinum-based therapy received avelumab at 10 mg/kg intravenously every 2 weeks. Continuation of mitotane was permitted; however, mitotane levels during the study were not recorded. Tumor response was assessed by Response Evaluation Criteria In Solid Tumors v1.1. Results: Fifty patients received avelumab and were followed for a median of 16.5 months. Prior treatment included ≥2 lines in 74.0%; mitotane was continued in 50.0%. The objective response rate (ORR) was 6.0% (95% CI, 1.3% to 16.5%; partial response in 3 patients). Twenty-one patients (42.0%) had stable disease as best response (disease control rate, 48.0%). Median progression-free survival was 2.6 months (95% CI, 1.4 to 4.0), median overall survival (OS) was 10.6 months (95% CI, 7.4 to 15.0), and the 1-year OS rate was 43.4% (95% CI, 27.9% to 57.9%).
    [Show full text]
  • Mitomycin/Mitotane
    Mitomycin/Mitotane 753 Mitomycin is used, with other antineoplastic agents, in Thiotepa has been applied postoperatively as 0.05% eye drops lenticular opacities, and retinopathy. Other adverse ef- the treatment of many solid tumours including those of for several weeks, but pterygium may still recur2 and adverse ef- fects include hypersensitivity reactions, haematuria, al- fects include conjunctival injection, granuloma, hypertrophic the bladder, breast, cervix, eye, liver, lung, stomach, conjunctiva, and black deposits in the conjunctival fornix.1 Depig- buminuria, skin rashes, fever, myalgia, haemorrhagic and prostate as indicated by the cross-references given mentation of the eyelids may also be a problem, so patients cystitis, flushing, hypertension, and orthostatic hypo- below. Mitomycin has been tried in other neoplasms should avoid direct sunlight during thiotepa use.1 tension. including those of the gastrointestinal tract, head and Mitomycin has been applied topically to the surgical site, or giv- neck, pancreas, in melanoma, sarcomas, and in leukae- en as eye drops postoperatively.1 The optimal intra-operative ex- Precautions mias. posure time and concentration are uncertain: concentrations of 0.02 or 0.04% have been applied for up to 5 minutes,1,3 and low- Mitotane inhibits the adrenal cortex and adrenocortical Dosage regimens include an initial dose of 10 to dose treatment with mitomycin 0.02% for 30 seconds has been insufficiency may develop during treatment; cortico- 20 mg/m2 intravenously; subsequent doses are repeat- reported to be effective with few complications.4 Postoperative steroid therapy is often required. In trauma, infection, ed at intervals of 6 to 8 weeks if blood counts permit, treatment has generally been given as 0.02, 0.04, or 0.1% eye or shock the drug should be temporarily withdrawn drops for up to 2 weeks, but the higher concentrations and longer and corticosteroids should be given systemically.
    [Show full text]
  • Standard Oncology Criteria C16154-A
    Prior Authorization Criteria Standard Oncology Criteria Policy Number: C16154-A CRITERIA EFFECTIVE DATES: ORIGINAL EFFECTIVE DATE LAST REVIEWED DATE NEXT REVIEW DATE DUE BEFORE 03/2016 12/2/2020 1/26/2022 HCPCS CODING TYPE OF CRITERIA LAST P&T APPROVAL/VERSION N/A RxPA Q1 2021 20210127C16154-A PRODUCTS AFFECTED: See dosage forms DRUG CLASS: Antineoplastic ROUTE OF ADMINISTRATION: Variable per drug PLACE OF SERVICE: Retail Pharmacy, Specialty Pharmacy, Buy and Bill- please refer to specialty pharmacy list by drug AVAILABLE DOSAGE FORMS: Abraxane (paclitaxel protein-bound) Cabometyx (cabozantinib) Erwinaze (asparaginase) Actimmune (interferon gamma-1b) Calquence (acalbrutinib) Erwinia (chrysantemi) Adriamycin (doxorubicin) Campath (alemtuzumab) Ethyol (amifostine) Adrucil (fluorouracil) Camptosar (irinotecan) Etopophos (etoposide phosphate) Afinitor (everolimus) Caprelsa (vandetanib) Evomela (melphalan) Alecensa (alectinib) Casodex (bicalutamide) Fareston (toremifene) Alimta (pemetrexed disodium) Cerubidine (danorubicin) Farydak (panbinostat) Aliqopa (copanlisib) Clolar (clofarabine) Faslodex (fulvestrant) Alkeran (melphalan) Cometriq (cabozantinib) Femara (letrozole) Alunbrig (brigatinib) Copiktra (duvelisib) Firmagon (degarelix) Arimidex (anastrozole) Cosmegen (dactinomycin) Floxuridine Aromasin (exemestane) Cotellic (cobimetinib) Fludara (fludarbine) Arranon (nelarabine) Cyramza (ramucirumab) Folotyn (pralatrexate) Arzerra (ofatumumab) Cytosar-U (cytarabine) Fusilev (levoleucovorin) Asparlas (calaspargase pegol-mknl Cytoxan (cyclophosphamide)
    [Show full text]
  • Treating Adrenal Cancer If You've Been Diagnosed with Adrenal Cancer, Your Care Team Will Discuss Treatment with You
    cancer.org | 1.800.227.2345 Treating Adrenal Cancer If you've been diagnosed with adrenal cancer, your care team will discuss treatment with you. It's important to take time and think about your options. It's important to weigh the benefits of each option against the possible risks and side effects, and an experienced care team can help. How is adrenal cancer treated? The main types of treatment for adrenal cancer are: ● Surgery for Adrenal Cancer ● Radiation Therapy for Adrenal Cancer ● Chemotherapy for Adrenal Cancer ● Other Drugs Used to Treat Adrenal Cancer Common treatment approaches Depending on the type and stage of your cancer, you might need more than one type of treatment. ● Treatment Choices by Stage of Adrenal Cancer Who treats adrenal cancer? Doctors on your cancer treatment team might include: ● A surgical oncologist: a doctor who uses surgery to treat cancer ● An endocrinologist: a doctor who treats diseases in glands that secrete hormones ● A radiation oncologist: a doctor who uses radiation to treat cancer 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 ● A medical oncologist: a doctor who uses chemotherapy and other medicines to treat cancer You might have many other specialists on your treatment team as well, including physician assistants (PAs), nurse practitioners (NPs), nurses, psychologists, social workers, rehabilitation specialists, and other health professionals. ● Health Professionals Associated With Cancer Care Making treatment decisions It’s important to discuss all treatment options, including their goals and possible side effects, with your doctors to help make the decision that best fits your needs. You may feel that you need to make a decision quickly, but it’s important to give yourself time to absorb the information you have learned.
    [Show full text]
  • CYTOTOXIC and NON-CYTOTOXIC HAZARDOUS MEDICATIONS
    CYTOTOXIC and NON-CYTOTOXIC HAZARDOUS MEDICATIONS1 CYTOTOXIC HAZARDOUS MEDICATIONS NON-CYTOTOXIC HAZARDOUS MEDICATIONS Altretamine IDArubicin Acitretin Iloprost Amsacrine Ifosfamide Aldesleukin Imatinib 3 Arsenic Irinotecan Alitretinoin Interferons Asparaginase Lenalidomide Anastrazole 3 ISOtretinoin azaCITIDine Lomustine Ambrisentan Leflunomide 3 azaTHIOprine 3 Mechlorethamine Bacillus Calmette Guerin 2 Letrozole 3 Bleomycin Melphalan (bladder instillation only) Leuprolide Bortezomib Mercaptopurine Bexarotene Megestrol 3 Busulfan 3 Methotrexate Bicalutamide 3 Methacholine Capecitabine 3 MitoMYcin Bosentan MethylTESTOSTERone CARBOplatin MitoXANtrone Buserelin Mifepristone Carmustine Nelarabine Cetrorelix Misoprostol Chlorambucil Oxaliplatin Choriogonadotropin alfa Mitotane CISplatin PACLitaxel Cidofovir Mycophenolate mofetil Cladribine Pegasparaginase ClomiPHENE Nafarelin Clofarabine PEMEtrexed Colchicine 3 Nilutamide 3 Cyclophosphamide Pentostatin cycloSPORINE Oxandrolone 3 Cytarabine Procarbazine3 Cyproterone Pentamidine (Aerosol only) Dacarbazine Raltitrexed Dienestrol Podofilox DACTINomycin SORAfenib Dinoprostone 3 Podophyllum resin DAUNOrubicin Streptozocin Dutasteride Raloxifene 3 Dexrazoxane SUNItinib Erlotinib 3 Ribavirin DOCEtaxel Temozolomide Everolimus Sirolimus DOXOrubicin Temsirolimus Exemestane 3 Tacrolimus Epirubicin Teniposide Finasteride 3 Tamoxifen 3 Estramustine Thalidomide Fluoxymesterone 3 Testosterone Etoposide Thioguanine Flutamide 3 Tretinoin Floxuridine Thiotepa Foscarnet Trifluridine Flucytosine Topotecan Fulvestrant
    [Show full text]