Chemotherapy Carboplatin, Etoposide, and Thorax: First Published As 10.1136/Thx.47.5.369 on 1 May 1992

Total Page:16

File Type:pdf, Size:1020Kb

Chemotherapy Carboplatin, Etoposide, and Thorax: First Published As 10.1136/Thx.47.5.369 on 1 May 1992 Thorax 1992;47:369-371 369 Treatment of relapse of small cell lung cancer in selected patients with the initial combination chemotherapy carboplatin, etoposide, and Thorax: first published as 10.1136/thx.47.5.369 on 1 May 1992. Downloaded from epirubicin Ph Collard, P Weynants, Ch Francis, D 0 Rodenstein Abstract Case reports Background Relapse of small cell lung From January 1987 to December 1990 small cancer is not usually treated with further cell lung cancer was diagnosed in 78 patients, chemotherapy as results are considered 36 with limited disease and 42 with extensive to be disappointing. disease. All were treated with intravenous Methods and results Six patients with carboplatin 330 mg/M2 and epirubicin 60 relapse of small cell lung cancer after a mg/m2 on day 1 and intravenous etoposide complete initial response and remission 120 mg/m2 on days 1, 3, and 5; courses were of more than one year responded to separated by three week intervals. The effect of repeat treatment with the initial the carboplatin-etoposide-epirubicin regimen chemotherapy comprising carboplatin, was not assessed in 15 patients as they etoposide, and epirubicin. The second received less than two courses of chemo- remission ranged from six months to therapy. Of the remaining 63 patients, six more than 15 months. were non-responders, 33 partial responders, Conclusion In patients with a relapse of and 24 complete responders (18 of whom had small cell lung cancer after a complete limited disease at initial staging); in most of initial response and prolonged remission the complete responders chemotherapy was retreatment with the initial combination followed by radiotherapy to the primary chemotherapy cannot be dismissed and tumour mass (60 Gy) and the mediastinum requires further study. (50 Gy), and they also received prophylactic cranial irradiation (30 Gy). Of the 24 com- plete responders, 12 relapsed early (less than 12 months after stopping treatment) and Small cell lung cancer has an aggressive seven had a late relapse (all had had limited http://thorax.bmj.com/ course and is usually widespread at presenta- disease initially); five patients have not yet tion. Surgery has been advocated in truly relapsed. The patients with a late relapse were Pulmonary Division, limited disease, but this is rare.' The best treated with further courses of carboplatin- Cliniques therapeutic approach for the time being is etoposide-epirubicin and are described in this Universitaires Saint- chemotherapy. Several combination regimens paper. Luc, avenue Hippocrate 10, B-1200 administered over three to six months have The clinical characteristics and the response Brussels, Belgium improved median survival and there is at to treatment of six of the patients are summar- Ph Collard present no clear advantage for any particular ised in the table. Clinical tolerance to on October 2, 2021 by guest. Protected copyright. Ch Francis regimen.2 Unfortunately, the disease usually chemotherapy was excellent in all cases and no D 0 Rodenstein relapses a few months after discontinuation of febrile episodes occurred; patient 2 required Pulmonary Division, Cliniques chemotherapy and the benefit of further treat- an occasional blood transfusion during Universitaires de ment at this stage is less clear. chemotherapy. The six patients experienced Mont-Godinne, B-5530 We report six patients with disease relapse considerable improvement in symptoms and Yvoir, Belgium P Weynants who showed a good response to a repeat gained weight after repeat treatment with car- course of chemotherapy with the initial drug boplatin-etoposide-epirubicin; patients 1 and Reprint requests to: Dr D 0 Rodenstein regimen of carboplatin, etoposide, and 3 returned to sedentary work for several Accepted 19 December 1991 epirubicin.3 months while in their second remission. Data on the patients Patient No: 1 2 3 4 5 6 Sex, age (y) M, 57 F, 59 M, 62 F, 62 M, 60 F, 71 Initial extension Limited Limited Limited Limited Limited Limited Initial treatment 4 Cx, LI, CI 6 Cx, CI 6 Cx, LI, CI 4 Cx, LI, CI 6 Cx, LI, CI 6 Cx, CI First response Complete Complete Complete Complete Complete Complete Remission (months) 19 17 22 31 21 29 Relapse site Local and brain Local Local Local Local Local and liver Relapse treatment 6 Cx 6 Cx 4 Cx 4 Cx 4 Cx 4 Cx Second response Complete Complete Partial Partial Partial Partial Remission (months) 10 11 6 12 Final relapse site Brain Brain Brain Local and liver Survival (months) 32 28 28 51 > 36 > 36 Cx-polychemotherapy course with carboplatin, etoposide, and epirubicin; LI-local irradiation; CI-cranial irradiation. 370 Collard, Weynants, Francis, Rodenstein Figure 1 Patient 1: Thoracic computed tomogram at the level of the heart at the initial presentation, showing a right lower lobe mass Thorax: first published as 10.1136/thx.47.5.369 on 1 May 1992. Downloaded from extending to the mediastinum (left) and complete response after three carboplatin- etoposide-epirubicin polychemotherapy induction courses (right). Figure 2 Patient 1: Thoracic computed tomogram at the same level at relapse, showing recurrence of the right lower lobe tumour (left) and resolution after three carboplatin-etoposide- epirubicin polychemotherapy reinduction courses (right). Figure 3 Patient 1: Cerebral computed http://thorax.bmj.com/ tomogram at relapse, showing the parietal metastasis (arrow, left) and its disappearance after three carboplatin- etoposide-epirubicin polychemotherapy reinduction courses (right). on October 2, 2021 by guest. Protected copyright. The seventh patient, with a late relapse of treatment, with evidence of aeration of the small cell lung cancer, developed left lung left lung; he survived for 23 months after atelectasis from an occluded main bronchus diagnosis. 15 months after achieving a complete response from carboplatin-etoposide-epirubicin induc- tion treatment. He was treated again with Discussion carboplatin-etoposide-epirubicin but died A four to eight course induction chemo- after a single course from an infected perineal therapy regimen is regarded as standard initial haematoma (presumably facilitated by the treatment for small cell lung cancer. Most chemotherapy induced pancytopenia). There studies have shown that maintenance or late was already an objective response to the repeat intensification treatment does not provide Treatment of relapse ofsmall cell lung cancer in selected patients with the initial combination chemotherapy carboplatin, etoposide, and epirubicin 371 appreciable survival advantage and may in etoposide-epirubicin chemotherapy regimen fact be deleterious in terms of quality of for relapse in small cell lung cancer may be an life.246 With modern induction treatment a effective (albeit palliative) treatment provided complete response is achieved in a growing that the initial response was complete and the number of patients, who subsequently enjoy first remission was prolonged. Thorax: first published as 10.1136/thx.47.5.369 on 1 May 1992. Downloaded from several months of good quality remission. Although the response to chemotherapy at Treatment policy on relapse is controversial relapse is disappointing for most patients with and many patients and physicians are reluc- small cell lung cancer, identifying patients tant to consider further chemotherapy.7 A likely to derive benefit from repeated chemo- recent editorial states that further chemo- therapy is important, in terms both of survival therapy after the induction phase is not useful and of quality of life. The subgroup we have and that survival is not improved.8 It is also defined represents about 10% of patients with widely believed that if further treatment is small cell lung cancer. If our findings are prescribed it should be based on drugs other confirmed in a larger number of patients, with than those used in the induction regimen. similar characteristics, the current policy of no When a patient has shown a complete res- further treatment after relapse will need to be ponse to induction treatment we have elected revised so that patients will not be denied a to use the same treatment for relapse. As these potentially useful and well tolerated retreat- cases show, we have had encouraging results ment. with minimal toxicity. So far we have ob- served a response to relapse treatment with We thank Dr Y Humblet for his useful comments on the carboplatin-etoposide-epirubicin in every manuscript. patient meeting the conditions of a complete initial response and a prolonged first remission 1 Crompton G. Small cell lung cancer [editorial]. BMJ 1990; 300:209-10. of at least 12 months after finishing induction 2 Feld R, Ginsber RJ, Payne DG. Treatment ofsmall cell lung treatment. cancer. In: Roth JA, Ruckdeschel JC, Weisenburger TH, A further course of induction treatment has eds. Thoracic oncology. Philadelphia: Saunders, 1989: 229-62. proved effective in other malignancies, such as 3 Humblet Y, Weynants P, Bosly A, et al. Carboplatin in breast cancer,910 ovarian cancer," multiple association with etoposide and either Adriamycin or epirubicin for untreated small cell lung cancer: a dose myeloma,"2 and Hodgkin's disease.'3 A few escalation study of carboplatin. Med Oncol Tumor studies have indicated that further treatment Pharmacother 1989;6:207-12. with the initial chemotherapeutic regimen 4 Medical Research Council Lung Cancer Working Party. Controlled trial of twelve versus six courses of chemo- may be effective in patients with small cell therapy in the treatment of small cell lung cancer. Br J lung cancer who relapse after a short induc- Cancer 1989;59:584-90. 5 Leonard RCF. Small cell lung cancer [editorial]. Br J Cancer tion course.""'6 The response to initial treat- 1989;59:487-90. ment, the length of remission, and perform- 6 Byrne MJ, van Hazel G, Trotter J, et al. Maintenance http://thorax.bmj.com/ ance status may have prognostic significance in chemotherapy in limited small cell lung cancer: a ran- domised controlled clinical trial. Br J Cancer 1989; this context. As in our cases, the complete 60:413-8.
Recommended publications
  • Chemotherapy Protocol
    Chemotherapy Protocol BREAST CANCER CYCLOPHOSPHAMIDE-EPIRUBICIN-PACLITAXEL (7 day) Regimen • Breast Cancer – Cyclophosphamide-Epirubicin-Paclitaxel (7 day) Indication • Neoadjuvant / adjuvant therapy of early breast cancer • WHO Performance status 0, 1 Toxicity Drug Adverse Effect Cyclophosphamide Dysuria, haemorrhagic cystitis, taste disturbances Epirubicin Cardio-toxicity, urinary discolouration (red) Hypersensitivity, hypotension, bradycardia, peripheral Paclitaxel neuropathy, myalgia and back pain on administration The adverse effects listed are not exhaustive. Please refer to the relevant Summary of Product Characteristics for full details. Monitoring Regimen • FBC, U&Es and LFTs prior to each cycle. • Ensure adequate cardiac function before starting treatment with epirubicin. Baseline LVEF should be measured, particularly in patients with a history of cardiac problems or in the elderly. 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. 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. Version 1.2 (November 2020) Page 1 of 7 Breast – Cyclophosphamide-Epirubicin-Paclitaxel (7 day) Haematological Prior to prescribing the following treatment criteria must be met on day one of treatment. Criteria Eligible Level Neutrophils equal to or more than 1x10 9/L Platelets equal to or more than 100x10 9/L Consider blood transfusion if patient symptomatic of anaemia or has a haemoglobin of less than 8g/dL If counts on day one are below these criteria for neutrophils and platelets then delay treatment for seven days.
    [Show full text]
  • BC Cancer Protocol Summary for Neoadjuvant Or Adjuvant Therapy for Breast Cancer Using Fluorouracil, Epirubicin, Cyclophosphamide and Docetaxel
    BC Cancer Protocol Summary for Neoadjuvant or Adjuvant Therapy for Breast Cancer Using Fluorouracil, Epirubicin, Cyclophosphamide and DOCEtaxel Protocol Code BRAJFECD Tumour Group Breast Contact Physician Dr. Stephen Chia ELIGIBILITY: . Node positive (any T, N1-3) or high risk, node negative early stage breast cancer . Less than or equal to 65 years of age or fit patients greater than 65 years deemed appropriate by supervising physician . ECOG 0-1 . HER-2 negative . Adequate renal and hepatic function . Adequate cardiac function EXCLUSIONS: . ECOG 2-4 . Significant hepatic dysfunction . Congestive heart failure (LVEF less than 45%) or other significant heart disease . Greater than or equal to grade 2 sensory or motor neuropathy . Pregnancy or lactation . Unsuitable for aggressive adjuvant chemotherapy TESTS: . Baseline: CBC & diff, platelets, creatinine, bilirubin, ALT, Alk Phos, LDH, GGT . Before each treatment (Day 1): CBC & diff, platelets. Prior to Cycle #4: CBC & diff, platelets, bilirubin, ALT, Alk Phos (see Precaution #5 for guidelines regarding hepatic dysfunction and DOCEtaxel). If clinically indicated: bilirubin, ALT, Alk Phos, creatinine, protein level, albumin, GGT, LDH, urea, MUGA scan or echocardiogram PREMEDICATIONS: . For the 3 cycles of epirubicin, fluorouracil and cyclophosphamide, antiemetic protocol for highly emetogenic chemotherapy (see protocol SCNAUSEA) . For the 3 cycles of DOCEtaxel: Dexamethasone 8 mg PO bid for 3 days, starting one day prior to each DOCEtaxel administration. Patient must receive minimum of 3 doses pre-treatment. Additional antiemetics not usually required. DOCEtaxel-induced onycholysis and cutaneous toxicity of the hands may be prevented by wearing frozen gloves starting 15 minutes before DOCEtaxel infusion until 15 minutes after end of DOCEtaxel infusion; gloves should be changed after 45 minutes of wearing to ensure they remain cold during the entire DOCEtaxel infusion.
    [Show full text]
  • In Advanced Upper Tract Urothelial Carcinoma
    ANTICANCER RESEARCH 37 : 1875-1883 (2017) doi:10.21873/anticanres.11525 Comparison of Efficacy of Adjuvant MEC (Methotrexate, Epirubicin and Cisplatin) and GC (Gemcitabine and Cisplatin) in Advanced Upper Tract Urothelial Carcinoma SHENG-CHUN HUNG 1, SHIAN-SHIANG WANG 1,2,3 , CHUN-KUANG YANG 1, JIAN-RI LI 1, CHEN-LI CHENG 1, YEN-CHUAN OU 1, HAO-CHUNG HO 1, KUN-YUAN CHIU 1 and CHUAN-SHU CHEN 1 1Division of Urology, Department of Surgery, Taichung Veterans General Hospital, Taichung, Taiwan, R.O.C.; 2School of Medicine, Chung Shan Medical University, Taichung, Taiwan, R.O.C.; 3Department of Applied Chemistry, National Chi Nan University, Puli, Taiwan, R.O.C. Abstract. Aim: To evaluate the efficacy of methotrexate, (3). Its behavior appears multi-focal and in 17% of cases, epirubicin and cisplatin (MEC) or gemcitabine and cisplatin concurrent bladder cancer is present (4). Furthermore, an (GC) as adjuvant chemotherapy in advanced upper tract estimated 22-47% of patients with UTUC may suffer from urothelium carcinoma (UTUC). Patients and Methods: From bladder recurrence (5) and 2-6% of patients suffer from 2002 January to 2008 December, a total of 70 patients with contralateral recurrence (6). advanced UTUC received radical nephroureterctomy at our A radical nephroureterectomy and bladder cuff excision is Institute with MEC and GC as adjuvant chemotherapy. Disease- standard treatment for UTUC, while offering the benefits of free survival (DFS), cancer-specific survival (CSS) and overall preventing tumor spreading and an entire urinary tract resection survival (OS) among the two groups were evaluated. Results: (7). However, after definite and en bloc surgical removal of the The MEC (n=30) and GC group (n=40) were compared and kidney, it still appears to be a poor prognosis for advanced showed no significant differences in DFS (p=0.859), CSS disease, with a <50% 5-year cancer-specific survival rate in (p=0.722) and OS (p=0.691).
    [Show full text]
  • Natural Products. a History of Success and Continuing Promise for Drug Discovery and Development
    Natural Products. A History of Success and Continuing Promise for Drug Discovery and Development Gordon M. Cragg NIH Special Volunteer [email protected] David J. Newman Natural Products Branch Developmental Therapeutics Program National Cancer Institute EARLY DOCUMENTATION OF USE OF MEDICINAL PLANTS http://www.nlm.nih.gov/hmd/collections/archives/index.html • Mesopotamian ~2,600 B. C. E. • Egyptian ~ 1,800 B. C. E. • Chinese – ~1,100 B. C. E. and continuing • Indian ~ 1,000 B. C. E. and continuing • Greek ~ 500 B. C. E. Greco-Roman expertise preserved and coordinated with other traditions by Islamic cultures during the Dark Ages ~ 400-1,100 CE Avicenna. Persian pharmacist, physician, poet, philosopher author: canon medicinae – “final codification of Greco-Roman medicine” Great Moments in Pharmacy Collection APhA Traditional Medicine and Drug Discovery • 80% of the world population resides in developing countries • 80% of people in developing countries utilize plants to meet their primary health care needs • Global pop. ca. 7 billion ca. 4.5 billion people utilize plants to meet their primary health care needs Farnsworth NR, et al. Medicinal Plants in Therapy. Bull. W.H.O. 63:965-981 (1985) Fabricant and Farnsworth, EnViron. Health Perspect. 109, 69-75 (2001) Cordell and Clovard, J. Nat. Prod., 75, 514-525 (2012) Norman Farnsworth 1800s. Discovery of some active principles of major herbal preparations Newman and Cragg. Natural Product Chemistry for Drug Discovery, eds. Buss and Butler, M. S., Royal Soc. Chem., Cambridge, 2010, pp. 3-27 European chemists (apothecaries) revolutionized drug discovery and development. 1817. Sertϋrner reports isolation of morphine from Papaver somniferum.
    [Show full text]
  • Breast Pathway Group – FEC75 (Fluorouracil / Epirubicin / Cyclophosphamide) in Advanced Breast Cancer
    Breast Pathway Group – FEC75 (Fluorouracil / Epirubicin / Cyclophosphamide) in Advanced Breast Cancer Indication: First line palliative therapy in selected patients with advanced breast cancer Regimen details: Fluorouracil 600mg/m2 IV Day 1 Epirubicin *75mg/m2 IV Day 1 Cyclophosphamide 600mg/m2 IV Day 1 * Consider using FEC60 regimen in patients > 60 years Administration: Epirubicin IV bolus injection via a fast-running Sodium Chloride 0.9% infusion Fluorouracil IV bolus injection via a fast-running Sodium Chloride 0.9% infusion Cyclophosphamide may be administered as IV bolus injection via a fast-running Sodium Chloride 0.9% infusion or as a short infusion e.g. in 100-250ml Sodium Chloride 0.9% over 30 minutes Frequency: Day 1, every 21 days, for 6 cycles Pre-medication: Not routinely required Anti- emetics: Highly Emetogenic Follow local anti-emetic policy. Supportive medication: Mouthcare as per local policy. Extravasation: Fluorouracil: Irritant Epirubicin: Vesicant Cyclophosphamide: Non-vesicant Epirubicin should be administered with appropriate precautions to prevent extravasation. If there is any possibility that extravasation Version: 1.0 Supersedes: all other versions Approved by LCA Breast Pathway Chemotherapy Lead: Mark Harries November 2014 Reason for Update: LCA Protocol Approved by LCA Joint Delivery Subgroup Co-Chairs: Pauline McCalla & Rebecca Johl Development Prepared by: Anabel Rodriguez Marina Approved by LCA Medicines & Chemotherapy Steering Group Chair: Jamie Ferguson Second check by: Lisa Yuen Date prepared: November 2014 Review Date: November 2016 Disclaimer: The Joint Delivery Chemotherapy Nurse/Oncology Pharmacist Group is a sub-group of the Medicines & Chemotherapy Steering Group (MCSG) working within the London Cancer Alliance Integrated Cancer System (LCA).
    [Show full text]
  • Epirubicin Ebewe Solution for Injection 2 Mg/Ml 2
    NEW ZEALAND DATA SHEET EPIRUBICIN EBEWE (EPIRUBICIN HYDROCHLORIDE) 1. PRODUCT NAME Epirubicin Ebewe solution for injection 2 mg/mL 2. QUALITATIVE AND QUANTITATIVE COMPOSITION Active: Epirubicin hydrochloride Each vial contains 2 mg/mL of epirubicin hydrochloride Epirubicin hydrochloride is a red-orange, almost odourless, hygroscopic powder, sparingly soluble in water and dilute alcohol. List of excipients with known effect: Sodium chloride For the full list of excipients, see Section 6.1 List of excipients. 3. PHARMACEUTICAL FORM Solution for injection (clear red solution, vials). 4. CLINICAL PARTICULARS 4.1. THERAPEUTIC INDICATIONS Epirubicin hydrochloride has produced responses in a wide spectrum of neoplastic diseases, and is indicated for the treatment of breast cancer, gastric cancer, ovarian cancer, small cell lung cancer, lymphoma (non-Hodgkin's lymphoma), advanced/ metastatic soft tissue sarcoma, and superficial bladder cancer (Tis, Ta). In bladder cancer, epirubicin hydrochloride is also indicated in the prophylaxis of recurrence after transurethral resection of stage T1 papillary cancers and stage Ta multifocal papillary cancers (grade 2 and 3). 4.2. DOSE AND METHOD OF ADMINISTRATION Dosage The safety and efficacy of epirubicin in children has not been established. Care in the intravenous administration of epirubicin hydrochloride will reduce the chance of perivenous infiltration. It may also decrease the chance of local reactions, such as urticaria and erythematous streaking (see Section 4.4 Special warnings and precautions for use). Note. The recommended lifetime cumulative dose limit of epirubicin is 900 mg/m2 body surface area. Under conditions of normal recovery from drug induced toxicity (particularly bone marrow depression and stomatitis), the recommended dosage schedule in adults, as described below, is as a single intravenous injection administered at 21 day intervals.
    [Show full text]
  • PATIENT INFORMATION LEAFLET Epirubicin Hydrochloride 2 Mg/Ml Solution for Injection Or Infusion Epirubicin Hydrochloride
    PATIENT INFORMATION LEAFLET Epirubicin Hydrochloride 2 mg/ml solution for injection or infusion Epirubicin Hydrochloride Read all of this leaflet carefully before you are given this medicine. Keep this leaflet. You may need to read it again. If you have further questions, please ask your doctor or pharmacist. This medicine has been prescribed for you do not pass it on to others. It may harm them, even if their symptoms are the same as yours. If any of the side effects gets serious, or if you notice any side effects not listed in this leaflet, please tell your doctor or pharmacist. In this leaflet: 1. What Epirubicin Hydrochloride Injection is and what it is used for 2. Before you are given Epirubicin Hydrochloride Injection 3. How Epirubicin Hydrochloride Injection is given to you 4. Possible side effects 5. How to store Epirubicin Hydrochloride Injection 6. Further information 1. What Epirubicin Hydrochloride Injection is and what it is used for The name of your medicine is ‘Epirubicin Hydrochloride 2 mg/ml solution for injection or infusion’ but in the rest of the leaflet it will be called ‘Epirubicin Hydrochloride Injection’. What Epirubicin Hydrochloride Injection is Epirubicin Hydrochloride Injection is an anti-cancer medicine. Treatment with an anti-cancer medicine is sometimes called cancer chemotherapy. Epirubicin Hydrochloride Injection is part of a group of medicines called anthracyclines. These act upon cells that are actively growing, to slow or stop their growth and increase the chance that the cells die. What Epirubicin Hydrochloride Injection is used for Epirubicin Hydrochloride Injection is used to treat a variety of cancers, either alone or in combination with other drugs.
    [Show full text]
  • Screening of Conditionally Reprogrammed Patient-Derived Carcinoma Cells Identifies
    Author Manuscript Published OnlineFirst on July 6, 2016; DOI: 10.1158/1078-0432.CCR-16-0149 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Screening of conditionally reprogrammed patient-derived carcinoma cells identifies ERCC3-MYC interactions as a target in pancreatic cancer. Natalya Beglyarova1, Eugenia Banina1, Yan Zhou2, Ramilia Mukhamadeeva3, Grigorii Andrianov3, Egor Bobrov1, Elena Lysenko1, Natalya Skobeleva1, Linara Gabitova1, Diana Restifo1, Max Pressman1, Ilya G. Serebriiskii1, John P. Hoffman1, Keren Paz4, Diana Behrens5, Vladimir Khazak6, Sandra A. Jablonski7, Erica A. Golemis1, Louis M. Weiner7, and Igor Astsaturov1† 1Program in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, PA, USA. 2Biostatistics and Bioinformatics Facility, Fox Chase Cancer Center, Philadelphia, PA, USA. 3Department of Biochemistry, Kazan Federal University, Kazan, Russian Federation. 4Champions Oncology, Baltimore, MD. 5EPO Experimental Pharmacology and Oncology GmbH, Berlin, Germany. 6Nexus Pharma, Langhorne, PA. 7Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA. †To whom correspondence should be addressed: Igor Astsaturov, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111. Phone (215) 728-3135, (443) 465-5212; Fax (215) 728-3616. E-mail: [email protected]. The authors disclose no potential conflicts of interest. Author contributions: S.J., I.G.S., V.K., E.A.G., L.M.W. and I.A. designed research; N.B., Eu.B., Eg.B., N.S., L.G., D.R., Y.Z., E.L., M.P., D.B. and S.J. performed research; J.P.H., N.I.A., R.M., G. A. and I.G.S. contributed new reagents/analytical tools; Y.Z., I.S., R.M., G.A., I.G.S., N.I.A., V.K.
    [Show full text]
  • Cardio-Oncology: Basics and Knowing When You Need an Echo
    1/10/2018 Cardio-oncology: Basics and Knowing When You Need an Echo Vera H. Rigolin, MD, FASE, FACC, FAHA Professor of Medicine Northwestern University Feinberg School of Medicine Medical Director, Echocardiography Laboratory Northwestern Memorial Hospital Chicago, Illinois President, American Society of Echocardiography No Disclosures • Acknowledgement: Nausheen Akhter, MD, Director of the cardio-oncology program at Northwestern 1 1/10/2018 Introduction • The number of cancer therapies have significantly increased • Cancer survival has improved • A number of cancer therapies have cardiotoxic effects Cardiotoxic Syndromes Associated with Chemo Agents associated with LV Agents associated with dysfunction hypertension • Bevacizumab (Avastin) • Anthracylines • Cisplatin • Mitoxanthrone • IL-2 • Cyclophosphamide • Trastuzumab Agents associated with Other toxic effects • Ifosfamide • Tamponade or endomyocardial • All-trans retinoic acid fibrosis (Busulfan) • Hemorrhagic Myocarditis Agents associated with (Cyclophosphamide) ischemia • Bradycardia (Taxol, Thalidomide) • 5-FU • Raynaud’s (Vinblastine) • Cisplatin • Autonomic neurop (Vincristine) • Capecitabine (Xeloda) • Long QT (Arsenic trioxide) • Pulm fibrosis (Bleo) • IL-2 Yeh et al. Circulation 2004 2 1/10/2018 Angiogenesis Inhibitors • Angiogenesis is a key factor for tumor growth and survival. • Angiogenesis inhibitors have shown to improve outcomes in various malignancies • Tumor growth suppression achieved by: – Direct inhibition of VEGF ligand’s ability to target receptor (bevacizumab, ramucirumab, aflibercept) – Small molecules that inhibit tyrosine kinases (sunitinib, sorafenib, pazopanid, vandetanib, vatalanib, cobazantinib, axitinib, regorafenib) Mechanisms of Action of Angiogenic Inhibitors Maurea N et. J Cardiovasc Med 2016;17(suppl):e-19-e26 3 1/10/2018 Odds ratio for adverse cardiac events due to angiogenesis inhibitors Abdel-Qadir H et al. Cancer Treatment Reviews 20178;53:120-127. J Am Soc Echocardiogr2014;27:911-39.
    [Show full text]
  • INTRAVESICAL CHEMOTHERAPY; Your Treatment Guide to Mitomycin C Or Epirubicin Instillation
    Patient and Carer Information INTRAVESICAL CHEMOTHERAPY; Your treatment guide to Mitomycin C or Epirubicin Instillation What is Intravesical Chemotherapy? Non- invasive bladder cancers are an early form of cancer but without treatment, many will recur after initial removal. Intravesical chemotherapy is given to people who have had several non-invasive bladder cancers. It is given by filling the bladder with medication to fight the cancer cells. The aim of intravesical chemotherapy is to reduce the likelihood of a further tumour growing or to lengthen the time until recurrence. There are two commonly used drugs given into the bladder, namely Mitomycin C and Epirubicin. This leaflet will tell you briefly what you can expect to happen when you attend for your treatment. Where is treatment given? All chemotherapy is given in a private area on the Sir Robert Ogden Macmillan Centre. You can expect to be here no longer than 2 hours. Treatment is given weekly for 5-6 weeks. What does it involve? You will be asked to remove your lower garments and lie on a couch. A small catheter will be passed into your bladder with the help of some anaesthetic gel. The Mitomycin C or Epirubicin is then introduced into your bladder through the catheter. The catheter will then be removed and you will be asked to hold the drug in your bladder for 1 hour. After 1 hour you can empty your bladder. You are advised to wash your hands and genital area immediately afterwards. Are there any side effects? There are some side effects which vary from person to person.
    [Show full text]
  • Cancer Drug Costs for a Month of Treatment at Initial Food
    Cancer drug costs for a month of treatment at initial Food and Drug Administration approval Year of FDA Monthly Cost Monthly cost (2013 Generic name Brand name(s) approval (actual $'s) $'s) Vinblastine Velban 1965 $78 $575 Thioguanine, 6-TG Thioguanine Tabloid 1966 $17 $122 Hydroxyurea Hydrea 1967 $14 $97 Cytarabine Cytosar-U, Tarabine PFS 1969 $13 $82 Procarbazine Matulane 1969 $2 $13 Testolactone Teslac 1969 $179 $1,136 Mitotane Lysodren 1970 $134 $801 Plicamycin Mithracin 1970 $50 $299 Mitomycin C Mutamycin 1974 $5 $22 Dacarbazine DTIC-Dome 1975 $29 $125 Lomustine CeeNU 1976 $10 $41 Carmustine BiCNU, BCNU 1977 $33 $127 Tamoxifen citrate Nolvadex 1977 $44 $167 Cisplatin Platinol 1978 $125 $445 Estramustine Emcyt 1981 $420 $1,074 Streptozocin Zanosar 1982 $61 $147 Etoposide, VP-16 Vepesid 1983 $181 $422 Interferon alfa 2a Roferon A 1986 $742 $1,573 Daunorubicin, Daunomycin Cerubidine 1987 $533 $1,090 Doxorubicin Adriamycin 1987 $521 $1,066 Mitoxantrone Novantrone 1987 $477 $976 Ifosfamide IFEX 1988 $1,667 $3,274 Flutamide Eulexin 1989 $213 $399 Altretamine Hexalen 1990 $341 $606 Idarubicin Idamycin 1990 $227 $404 Levamisole Ergamisol 1990 $105 $187 Carboplatin Paraplatin 1991 $860 $1,467 Fludarabine phosphate Fludara 1991 $662 $1,129 Pamidronate Aredia 1991 $507 $865 Pentostatin Nipent 1991 $1,767 $3,015 Aldesleukin Proleukin 1992 $13,503 $22,364 Melphalan Alkeran 1992 $35 $58 Cladribine Leustatin, 2-CdA 1993 $764 $1,229 Asparaginase Elspar 1994 $694 $1,088 Paclitaxel Taxol 1994 $2,614 $4,099 Pegaspargase Oncaspar 1994 $3,006 $4,713
    [Show full text]
  • Original Article Arsenic Trioxide Inhibits Cell Growth and Elevates T Cell Subgroup of Bladder Cancer in Vitro and in Vivo
    Int J Clin Exp Pathol 2016;9(1):244-249 www.ijcep.com /ISSN:1936-2625/IJCEP0013287 Original Article Arsenic trioxide inhibits cell growth and elevates T cell subgroup of bladder cancer in vitro and in vivo Liang Shi1, Lu Wang2, Ping Wang1, Wei Wang2, Wei Zhang2 1Department of Urologic Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang 110032, Liaoning Province, China; 2Department of Endocrinology, The Fourth Affiliated Hospital of China Medical University, Shenyang 110032, Liaoning Province, China Received July 23, 2015; Accepted October 28, 2015; Epub January 1, 2016; Published January 15, 2016 Abstract: Purpose: This study aimed to explore the effects of arsenic trioxide (As2O3) on the growth and apoptosis of MBT-2 bladder cancer (BC) cells, and on T cell subgroup and natural killer (NK) cell cytoactivity of bladder tumor- bearing mice. Methods: After MBT-2 cells were treated with As2O3 at the concentration of 0.5 μmol/l, 1.0 μmol/l, 2.0 μmol/l and 5.0 μmol/l for 24 h, 48 h and 72 h, the growth and apoptosis rates of MBT-2 cells were respectively determined by MTT assay and terminal transferase labeling in situ. The expression of B-cell lymphoma-2 (bcl-2) in MBT-2 cells was detected by immunohistochemistry. Then BC mice models were constructed. T cell subgroup and NK cell cytoactivity of bladder tumor-bearing mice after treated with As2O3 were respectively detected by flow cy- tometry and lactate dehydrogenase release assay. Results: The growth inhibition rate and apoptotic rate increased significantly with the increase of As2O3 concentration (P < 0.05) and treatment time (P < 0.01).
    [Show full text]