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.
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,
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.
on The oncologist
by Maurea N, Coppola C, Piscopo G, Galletta F, Riccio G, De Lorenzo C
Ahead of Print article withdrawn by publisher.
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.
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
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.
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
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.
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
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.
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
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.
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
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.