Cinzia Coppola

Researcher of Neurology

Name Cinzia
Surname Coppola
Institution Università degli Studi della Campania Luigi Vanvitelli
Address Department of Medical, Surgical, Neurological, Metabolic Sciences, and Aging, 2nd Division of Neurology, Center for Rare Diseases, University of Campania "Luigi Vanvitelli", Napoli, Italy


  • Strain Analysis in the Assessment of a Mouse Model of Cardiotoxicity due to Chemotherapy: Sample for Preclinical Research.

    Publication Date: 01/05/2016 on In vivo (Athens, Greece)
    by Rea D, Coppola C, Barbieri A, Monti MG, Misso G, Palma G, Bimonte S, Zarone MR, Luciano A, Liccardo D, Maiolino P, Cittadini A, Ciliberto G, Arra C, Maurea N

    In recent years, the development of more effective anticancer drugs has provided great benefits in patients' quality of life by improving both prognosis and disease-free survival. Nevertheless, the frequency and severity of side-effects, with particular reference to cardiac toxicity, have gained particular attention. The purpose of this study was to create a precise and sensitive preclinical model, able to identify early contractile dysfunction in mice treated with chemotherapy, through use of speckle-tracking echocardiography.

  • Impact of Safety-Related Dose Reductions or Discontinuations on Sustained Virologic Response in HCV-Infected Patients: Results from the GUARD-C Cohort.

    Publication Date: 28/03/2016 on PloS one
    by Foster GR, Coppola C, Derbala M, Ferenci P, Orlandini A, Reddy KR, Tallarico L, Shiffman ML, Ahlers S, Bakalos G, Hassanein T,
    DOI: 10.1371/journal.pone.0151703

    Despite the introduction of direct-acting antiviral agents for chronic hepatitis C virus (HCV) infection, peginterferon alfa/ribavirin remains relevant in many resource-constrained settings. The non-randomized GUARD-C cohort investigated baseline predictors of safety-related dose reductions or discontinuations (sr-RD) and their impact on sustained virologic response (SVR) in patients receiving peginterferon alfa/ribavirin in routine practice.

  • WITHDRAWN:A Practical Approach for Management of QT Prolongation Induced by Anticancer Drugs.

    Publication Date: 14/03/2016 on The oncologist
    by Maurea N, Coppola C, Piscopo G, Galletta F, Riccio G, De Lorenzo C
    DOI: 10.1634/theoncologist.2015-0313

    Ahead of Print article withdrawn by publisher.

  • Impact of Telaprevir in HCV Patients with Cirrhosis and RVR: Real-Life Data from Boceprevir or Telaprevir based "Triple Therapy" Experience in Southern Italy.

    Publication Date: 01/01/2016 on Reviews on recent clinical trials
    by Morisco F, Masarone M, Rosato V, Camera S, Granata R, Tartaglione MT, Coppola C, Coppola N, Salomone-Megna A, Gentile I, De Luna A, Federico A, Precone D, Claar E, Abenavoli L, Persico M

    Background and Rationale of Study: The real-life data of triple therapy-based treatment in patients with chronic hepatitis C were investigated in this survey of 12 clinical centers of southern Italy. This retrospective study analyzed data from 176 consecutive patients.

  • A case of progressive frontal lobe syndrome in a sporadic form of Cerebral Amyloid Angiopathy: A singular overlap with fronto-temporal dementia?

    Publication Date: 15/12/2015 on Journal of the neurological sciences
    by Coppola C, Saracino D, Califano F, Barbarulo AM, Di Fede G, Piccoli E, Tagliavini F, Di Iorio G, Rossi G
    DOI: 10.1016/j.jns.2015.08.1533
  • Hepatocellular carcinoma invading portal venous system in cirrhosis: long-term results of percutaneous radiofrequency ablation of both the nodule and portal vein tumor thrombus. A case control study.

    Publication Date: 01/11/2014 on Anticancer research
    by Giorgio A, Calisti G, Montesarchio L, Scognamiglio U, Matteucci P, Coppola C, Scarano F, Amendola F, Giorgio V

    Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death. Portal vein tumor thrombus (PVTT) is one of the most dreadful complications of HCC and is associated with a median survival time of 2.7-4.0 months. The optimal treatment for HCC with PVTT has not yet been established. The aim of the present study was to report long-term results of percutaneous radiofrequency (RF) ablation of both HCC single nodule (up to 5 cm in diameter) and neoplastic main portal vein thrombus, compared to no-treatment.

  • Metabolic syndrome-breast cancer link varies by intrinsic molecular subtype.

    Publication Date: 26/09/2014 on Diabetology & metabolic syndrome
    by Capasso I, Esposito E, de Laurentiis M, Maurea N, Cavalcanti E, Botti G, Petrillo A, Montella M, D'Aiuto M, Coppola C, Crispo A, Grimaldi M, Frasci G, Fucito A, Ciliberto G, D'Aiuto G
    DOI: 10.1186/1758-5996-6-105

    Metabolic syndrome (MS) has been shown to increase the risk of breast cancer. Existing data suggest that the strength of metabolic syndrome-breast cancer link varies by intrinsic molecular subtype, but results from worldwide literature are controversial. Primary endpoint of the study was to assess whether MS is a predictor of specific breast cancer (BC) subtype. Secondary endpoint was to determine whether components of MS can individually increase the risk of specific breast cancer subtype.

  • Ranolazine protects from doxorubicin-induced oxidative stress and cardiac dysfunction.

    Publication Date: 01/04/2014 on European journal of heart failure
    by Tocchetti CG, Carpi A, Coppola C, Quintavalle C, Rea D, Campesan M, Arcari A, Piscopo G, Cipresso C, Monti MG, De Lorenzo C, Arra C, Condorelli G, Di Lisa F, Maurea N
    DOI: 10.1002/ejhf.50

    Doxorubicin is widely used against cancer; however, it can produce heart failure (HF). Among other hallmarks, oxidative stress is a major contributor to HF pathophysiology. The late INa inhibitor ranolazine has proven effective in treating experimental HF. Since elevated [Na+]i is present in failing myocytes, and has been recently linked with reactive oxygen species (ROS) production, our aim was to assess whether ranolazine prevents doxorubicin-induced cardiotoxicity, and whether blunted oxidative stress is a mechanism accounting for such protection.

  • Effects of a second-generation human anti-ErbB2 ImmunoRNase on trastuzumab-resistant tumors and cardiac cells.

    Publication Date: 01/03/2014 on Protein engineering, design & selection : PEDS
    by D'Avino C, Paciello R, Riccio G, Coppola C, Laccetti P, Maurea N, Raines RT, De Lorenzo C
    DOI: 10.1093/protein/gzt065

    The inhibition of ErbB2 by the use of human antibodies can be a valuable strategy for the treatment of breast and gastric cancer. Trastuzumab, a humanized anti-ErbB2 antibody in clinical use, is effective but can engender resistance as well as cardiotoxicity. ImmunoRNases, made up of a human anti-ErbB2 scFv and human pancreatic ribonucleases (HP-RNases), have been engineered to overcome the limits of other immunotoxins, such as immunogenicity and nonspecific toxicity. Here, we report that a novel anti-ErbB2 immunoRNase, called Erb-HPDDADD-RNase, obtained by fusing Erbicin, a human ErbB2-directed scFv, with an HP-RNase variant that resists the cytosolic inhibitor protein, binds with high affinity to a panel of ErbB2-positive gastric tumor cells and inhibits their growth more than does the parental immunoRNase, which is not resistant to the inhibitor. Moreover, Erb-HP-DDADD-RNase is endowed with antiproliferative activity for trastuzumab-resistant cancer cells both in vitro and in vivo that is more potent than that of the parental immunoRNase. Importantly, Erb-HP-DDADD-RNase does not show cardiotoxic effects in vitro on human cardiomyocytes and does not impair cardiac function in a mouse model. Thus, Erb-HP-DDADD-RNase could fulfil the therapeutic need of cancer patients ineligible for trastuzumab treatment due to primary or acquired trastuzumab resistance or to cardiac dysfunction.

  • Inhibition of cardiomyocytes late INa with ranolazine to prevent anthracyclines cardiotoxicity in experimental models in vitro and in vivo.

    Publication Date: 10/09/2013 on Journal of clinical oncology : official journal of the American Society of Clinical Oncology
    by Coppola C, Piscopo G, Cipresso C, Rea D, Tocchetti CG, De Laurentiis M, Arra C, Iaffaioli RV
    DOI: 10.1200/jco.2013.31.26_suppl.170

    170 Background: Anthracyclines are first line drugs against cancer, but produce a well-known cardiomyopathy through multiple mechanisms, which also include Ca2+ overload due to reduced SERCA2a activity and inappropriate opening of the RyR2, and impaired myocardial energetics. Anthracyclines generate Reactive Oxigen and Nitrogen Species, posing the heart at increased demand for oxygen, thus setting the stage for a metabolic ischemia that also activates late INa, the target of ranolazine (RAN). Here, we aim at assessing whether RAN, diminishing intracellular Ca2+ through its inhibition of late INa, and enhancing myocardial glucose utilization (and/or reverting impairment of glucose utilization caused by chemotherapy) blunts anthracyclines cardiotoxicity.