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4. Targeting breast cancer exosomes with nucleic aptamers: Innovative tools for early diagnosis and therapy

Author

Esposito C. L., Quintavalle C., Ingenito F., Rotoli D., Roscigno G., Nuzzo S., Thomas R., Catuogno S., Minic Z., Berezovski M., de Franciscis V., Condorelli G., Esposito, C. L., Quintavalle, C., Ingenito, F., Rotoli, D., Roscigno, G., Nuzzo, S., Thomas, R., Catuogno, S., Minic, Z., Berezovski, M., de Franciscis, V., and Condorelli, G.

Subjects
Exosome, Aptamer, Oncology, Therapy, Diagnosi
Abstract

Exosomes are emerging as promising target for early diagnosis and therapy in different oncological conditions including breast cancer (BC). However, the development of tools able to easily and specifically target cancer cell-derived exosomes still represent a fundamental issue that is required to realize their clinical utility. Nucleic-acid aptamers are a promising class of structured single stranded oligonucleotides that serve as high affinity ligands of disease-associated proteins. Given their high potential in diagnosis and therapy, we addressed the development of aptamers specific for BC-derived exosomes. To this end, we developed a novel SELEX strategy by using exosomes purified from primary BC cells as positive selection target. By such a strategy we isolated nuclease resistant RNA aptamers able to specifically discriminate BC-derived exosomes from those produced by normal cells. The best sequences were optimized identifying short molecules (about 30-35 mer) that was characterized as tools for exosome detection. Further, we demonstrated that the developed aptamers inhibited exosome cellular uptake antagonizing cancer exosome-induced cell migration. By proteomic approach we identified possible targets that we are characterizing. Our results underline the great potential of isolated aptamers as tools for the development of innovative strategies for BC early diagnosis and therapy.

Published
2021

9. Evaluation on ‘real life’ prescriptions of antifungal prophylaxis in acute myeloid leukemia: Final results from a prospective survey: C12-3

Author

Caira, M., Busca, A., Candoni, A., Melillo, L., Blasi, R. Di, Cuccaro, A., Caramatti, C., Specchia, G., Fanci, R., Rossi, G., Vacca, A., Quintavalle, C., Picardi, M., Mitra, M. E., Delia, M., Landini, B., Aversa, F., Gasbarrino, C., Invernizzi, R., Salutari, P., Martino, B., Garzia, M. G., Chierichini, A., Caprio, L. Di, Vianelli, N., Nadali, G., Luppi, M., Nosari, A., and Pagano, L.

Published
2012

11. Delineation of human prostate cancer evolution identifies chromothripsis as a polyclonal event and FKBP4 as a potential driver of castration resistance

Author

Federer-Gsponer J.R., Quintavalle C., Muller D.C., Dietsche T., Perrina V., Lorber T., Juskevicius D., Lenkiewicz E., Zellweger T., Gasser T., Barrett M.T., Rentsch C.A., Bubendorf L., and Ruiz C.

Subjects
FKBP4, FKBP52, castration resistance, chromothripsis, evolution, hormone-naïve, prostate cancer, punctualism, survival
Abstract

Understanding the evolutionary mechanisms and genomic events leading to castration-resistant (CR) prostate cancer (PC) is key to improve the outcome of this otherwise deadly disease. Here, we delineated the tumour history of seven patients progressing to castration resistance by analysing matched prostate cancer tissues before and after castration. We performed genomic profiling of DNA content-based flow-sorted populations in order to define the different evolutionary patterns. In one patient, we discovered that a catastrophic genomic event, known as chromothripsis, resulted in multiple CRPC tumour populations with distinct, potentially advantageous copy number aberrations, including an amplification of FK506 binding protein 4 (FKBP4, also known as FKBP52), a protein enhancing the transcriptional activity of androgen receptor signalling. Analysis of FKBP4 protein expression in more than 500 prostate cancer samples revealed increased expression in CRPC in comparison to hormone-naïve (HN) PC. Moreover, elevated FKBP4 expression was associated with poor survival of patients with HNPC. We propose FKBP4 amplification and overexpression as a selective advantage in the process of tumour evolution and as a potential mechanism associated with the development of CRPC. Furthermore, FKBP4 interaction with androgen receptor may provide a potential therapeutic target in PC. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Published
2018

14. The discovery of RNA-aptamers that selectively bind and inhibit glioblastoma stem cells by targeting EphA2

Author

Affinito, A., primary, Quintavalle, C., additional, Esposito, C.L., additional, Roscigno, G., additional, Vilardo, C., additional, Nuzzo, S., additional, Ricci Vitiani, L., additional, De Luca, G., additional, Minic, Z., additional, Giannetti, S., additional, Pallini, R., additional, Berezovski, M.V., additional, Kichkailo, A.S., additional, Lapin, I.N., additional, De Franciscis, V., additional, and Condorelli, G., additional

Published
2019
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15. Liver damage and senescence increases in patients developing hepatocellular carcinoma

Author

Rey S., Quintavalle C., Burmeister K., Calabrese D., Schlageter M., Quagliata L., Cathomas G., Diebold J., Molinolo A., Heim M.H., Terracciano L.M., and Matter M.S.

Subjects
hepatocellular carcinoma, senescence, telomeres, neoplasms, digestive system diseases
Abstract

BACKGROUND AND AIM: Most patients with a hepatocellular carcinoma (HCC) have an underlying chronic liver inflammation, which causes a continuous damage leading to liver cirrhosis and eventually HCC. However, only a minority of cirrhotic patients develop HCC. To assess a possible differential impact of liver inflammation in patients developing HCC versus patients remaining tumor-free, we designed a longitudinal study and analysed liver tissue of the same patients (n = 33) at two points in time: once when no HCC was present and once several years later when an HCC was present. As a control group, we followed cirrhotic patients (n = 37) remaining tumor-free over a similar time frame. METHODS: We analysed cell damage and senescence of hepatocytes by measuring ?-H2AX positivity, p16INK4 and p21WAF/Cip1 expression, nuclear size, and telomere length. RESULTS: ?-H2AX positivity, p16INK4 and p21WAF/Cip1 expression, in the first liver biopsy was similar in patients developing HCC later on and cirrhotic patients remaining tumor free. In contrast, ?-H2AX positivity, p16INK4 and p21WAF/Cip1 expression, was significantly higher in the second non-tumoral liver biopsy of HCC patients than in the control patients. Consequently, the individual increase in ?-H2AX positivity, p16INK4 and p21WAF/Cip1 expression, from the first biopsy to the second biopsy was significantly higher in patients developing HCC than in patients remaining tumor free. In addition, changes in nuclear size and telomere length revealed a more pronounced cell aging in patients developing HCC than in patients remaining tumor free. CONCLUSIONS: Hepatocytes from patients developing HCC go through more pronounced cell damage and senescence in contrast to cirrhotic patients remaining tumor free.

Published
2017
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16. Genetic profiling using plasma-derived cell-free DNA in therapy-naïve hepatocellular carcinoma patients: A pilot study

Author

Di Costanzo, G.G., primary, Ng, C.K.Y., additional, Tosti, N., additional, Tortora, R., additional, Paradiso, V., additional, Coto-Llerena, M., additional, Roscigno, G., additional, Perrina, V., additional, Quintavalle, C., additional, Boldanova, T., additional, Wieland, S., additional, Marino-Marsilia, G., additional, Lanzafame, M., additional, Quagliata, L., additional, Condorelli, G., additional, Matter, M.S., additional, Heim, M.H., additional, Guarracino, M., additional, Terracciano, L.M., additional, and Piscuoglio, S., additional

Published
2018
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17. UbcH10 expression can predict prognosis and sensitivity to the antineoplastic treatment for colorectal cancer patients

Author

Cacciola NA1, Calabrese C, Malapelle U, Pellino G, De Stefano A, Sepe R, Sgariglia R, Quintavalle C, Federico A, Bianco A, Uchimura Bastos A, Milone M, Bellevicine C, Milone F, Carlomagno C, Selvaggi F, Troncone G, Fusco A, and Pallante P.

Subjects
KRAS, UbcH10, cetuximab, colorectal cancer, irinotecan, Cetuximab, Irinotecan, neoplasms, Colorectal cancer, digestive system diseases
Abstract

Colorectal cancer (CRC) is one of the most frequent and deadly malignancies worldwide. Despite the progresses made in diagnosis and treatment, the identification of tumor markers is still a strong clinical need, because current treatments are efficacious only in a subgroup of patients. UbcH10 represents a potential candidate biomarker, whose expression levels could be employed to predict response or resistance to chemotherapy or targeted agents. UbcH10 mRNA and protein expression levels have been evaluated in a large group of CRC patients and correlated with clinico-pathological characteristics, including KRAS mutations. Moreover, the endogenous levels of UbcH10 and its role on cell growth have been evaluated in CRC cells. Finally, to investigate the impact of UbcH10 protein expression on the response to irinotecan, its active metabolite SN-38 and cetuximab treatment, UbcH10 silencing experiments were carried-out on two colon carcinoma cell lines, Caco-2, and DLD1. Overexpression of UbcH10 mRNA and protein was observed in the vast majority of patients analyzed. UbcH10 suppression decreased CRC cell growth rate (at least in part through deregulation of Cyclin B and ERK1) and sensitized them to pharmacological treatments with irinotecan, SN-38 and cetuximab (at least in part through a down-regulation of AKT). Taken together, these findings indicate that UbcH10 expression regulates CRC growth and could play an important role in the personalization of the therapy of CRC patients. © 2015 Wiley Periodicals, Inc.

Published
2016

20. Late INa Inhibition with Ranolazine Blunts Doxorubicin- Induced Cardiac Dysfunction and Remodeling in Mice

Author

TOCCHETTI, CARLO GABRIELE, Coppola C, Domenica Rea, Quintavalle C, Barbieri A, Piscopo G, Palma G, Gala M, Luciano A, Giudice A, Iaffaioli RV, Scala S, Condorelli G, Arra C, Maurea N., Conference: Basic Cardiovascular Sciences Scientific Session, Tocchetti, CARLO GABRIELE, Coppola, C, Domenica, Rea, Quintavalle, C, Barbieri, A, Piscopo, G, Palma, G, Gala, M, Luciano, A, Giudice, A, Iaffaioli, Rv, Scala, S, Condorelli, G, Arra, C, and Maurea, N.

Published
2012

21. ANTHRACYCLINE INDUCED CARDIOTOXICITY IN MICE IS PREVENTED BY LATE INA INHIBITION WITH RANOLAZINE, WITH IMPROVEMENT IN HEART FUNCTION, FIBROSIS, APOPTOSIS

Author

Maurea N, Coppola C, Quintavalle C, Rea D, Barbieri A, Piscopo G, Iaffaioli RV, Condorelli G, Arra C, TOCCHETTI, CARLO GABRIELE, Conference: 37th Congress of the European-Society-for-Medical-Oncology (ESMO), Maurea, N, Coppola, C, Quintavalle, C, Rea, D, Barbieri, A, Piscopo, G, Iaffaioli, Rv, Condorelli, G, Arra, C, and Tocchetti, CARLO GABRIELE

Published
2012

25. The anticancer mTOR-inhibitor temsirolimus induces cardiac dysfunction in mice

Author

TOCCHETTI, CARLO GABRIELE, Coppola C, Quintavalle C, Barbieri A, Rea D, Palma G, Gala M, Luciano A, Giudice A, Capasso I, Arra C, Iaffaioli RV, Condorelli G, Maurea N., Tocchetti, CARLO GABRIELE, Coppola, C, Quintavalle, C, Barbieri, A, Rea, D, Palma, G, Gala, M, Luciano, A, Giudice, A, Capasso, I, Arra, C, Iaffaioli, Rv, Condorelli, G, and Maurea, N.

Published
2011

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

Author

Cg, Tocchetti, Carpi A, Coppola C, Quintavalle C, Rea D, Campesan M, Arcari A, Piscopo G, Cipresso C, Mg, Monti, De Lorenzo C, Arra C, Condorelli G, Fabio Di Lisa, Maurea N, Tocchetti, CARLO GABRIELE, Andrea, Carpi, Carmela, Coppola, Quintavalle, Cristina, Domenica, Rea, Marika, Campesan, Antonella, Arcari, Giovanna, Piscopo, Clemente, Cipresso, Monti, MARIA GAIA, DE LORENZO, Claudia, Claudio, Arra, Condorelli, Gerolama, Fabio Di, Lisa, and Nicola, Maurea

Subjects
Antibiotics, Antineoplastic, Reverse Transcriptase Polymerase Chain Reaction, Blotting, Western, Sodium, Connective Tissue Growth Factor, Real-Time Polymerase Chain Reaction, Cardiotoxicity, Piperazines, Mice, Inbred C57BL, Mice, Oxidative Stress, Ventricular Dysfunction, Left, Doxorubicin, Ranolazine, Natriuretic Peptide, Brain, Animals, Matrix Metalloproteinase 2, Acetanilides, Myocytes, Cardiac, RNA, Messenger, Enzyme Inhibitors, Poly(ADP-ribose) Polymerases, Reactive Oxygen Species, Atrial Natriuretic Factor, Ultrasonography
Abstract

AIMS: 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. METHODS AND RESULT: In C57BL6 mice, doxorubicin treatment for 7 days produced LV dilation and decreased echo-measured fractional shortening (FS). Ranolazine (305 mg/kg/day) prevented LV dilation and dysfunction when co-administered with doxorubicin. Doxorubicin-induced cardiotoxicity was accompanied instead by elevations in atrial natriuretic peptide (ANP), BNP, connective tissue growth factor (CTGF), and matrix metalloproteinase 2 (MMP2) mRNAs, which were not elevated on co-treatment with ranolazine. Alterations in extracellular matrix remodelling were confirmed by an increase in interstitial collagen, which did not rise in ranolazine-co-treated hearts. Levels of poly(ADP-ribose) polymerase (PARP) and pro-caspase-3 measured by western blotting were lowered with doxorubicin, with increased cleavage of caspase-3, indicating activation of the proapoptotic machinery. Again, ranolazine prevented this activation. Furthermore, in HL-1 cardiomyocytes transfected with HyPer to monitor H2 O2 emission, besides reducing the extent of cell death, ranolazine prevented the occurrence of oxidative stress caused by doxorubicin. Interestingly, similar protective results were obtained with the Na+ /Ca2+ exchanger (NCX) inhibitor KB-R7943. CONCLUSIONS: Ranolazine protects against experimental doxorubicin cardiotoxicity. Such protection is accompanied by a reduction in oxidative stress, suggesting that INa modulates cardiac redox balance, resulting in functional and morphological derangements.

Published
2014

27. MicroRNA signatures of TRAIL resistance in human non small cell lung cancer. Oncogene

Author

Garofalo M., Quintavalle C., Di Leva G., Zanca C., Romano G., Taccioli C., Liu C. G., Croce C. M., CONDORELLI, GEROLAMA, Garofalo, M., Quintavalle, C., Di Leva, G., Zanca, C., Romano, G., Taccioli, C., Liu, C. G., Croce, C. M., and Condorelli, Gerolama

Subjects
lung cancer, microRNA, apoptosi
Abstract

To define novel pathways that regulate susceptibility to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in non-small cell lung cancer (NSCLC), we have performed genome-wide expression profiling of microRNAs (miRs). We show that in TRAIL-resistant NSCLC cells, levels of different miRs are increased, and in particular, miR-221 and -222. We demonstrate that these miRs impair TRAIL-dependent apoptosis by inhibiting the expression of key functional proteins. Indeed, transfection with anti-miR-221 and -222 rendered CALU-1-resistant cells sensitive to TRAIL. Conversely, H460-sensitive cells treated with -221 and -222 pre-miRs become resistant to TRAIL. miR-221 and -222 target the 3'-UTR of Kit and p27(kip1) mRNAs, but interfere with TRAIL signaling mainly through p27(kip1). In conclusion, we show that high expression levels of miR-221 and -222 are needed to maintain the TRAIL-resistant phenotype, thus making these miRs as promising therapeutic targets or diagnostic tool for TRAIL resistance in NSCLC.

Published
2008

28. Akt regulates drugs induced cell death through the anti-apoptotic protein Bcl-w

Author

Garofalo M, Quintavalle C, Zanca C, de Rienzo A., Romano G, Acunzo M, Puca L, Incoronato M, Croce CM, CONDORELLI, GEROLAMA, Garofalo, M, Quintavalle, C, Zanca, C, de Rienzo, A., Romano, G, Acunzo, M, Puca, L, Incoronato, M, Croce, Cm, and Condorelli, Gerolama

Subjects
apoptosis cancer bcl-w
Abstract

Akt is a serine threonine kinase with a major role in transducing survival signals and regulating proteins involved in apoptosis. To find new interactors of Akt involved in cell survival, we performed a two-hybrid screening in yeast using human full-length Akt c-DNA as bait and a murine c-DNA library as prey. Among the 80 clones obtained, two were identified as Bcl-w. Bcl-w is a member of the Bcl-2 family that is essential for the regulation of cellular survival, and that is up-regulated in different human tumors, such as gastric and colorectal carcinomas. Direct interaction of Bcl-w with Akt was confirmed by immunoprecipitation assays. Subsequently, we addressed the function of this interaction: by interfering with the activity or amount of Akt, we have demonstrated that Akt modulates the amount of Bcl-w protein. We have found that inhibition of Akt activity may promote apoptosis through the downregulation of Bcl-w protein and the consequential reduction in interaction of Bcl-w with proapoptotic members of the Bcl-2 family. Our data provide evidence that Bcl-w is a new member of the Akt pathway and that Akt may induce anti-apoptotic signals at least in part through the regulation of the amount and activity of Bcl-w.

Published
2008

29. Electrochemical detection of miRNA-222 by use of a magnetic bead-based bioassay

Author

Bettazzi F, Hamid-Asl E, Esposito CL, Quintavalle C, Formisano N, Laschi S, Catuogno S, Iaboni M, Marrazza G, Mascini M, Cerchia L, De Franciscis V, Condorelli G, and Palchetti I.

Abstract

MicroRNAs (miRNAs, miRs) are naturally occurring small RNAs (approximately 22 nucleotides in length) that have critical functions in a variety of biological processes, including tumorigenesis. They are an important target for detection technology for future medical diagnostics. In this paper we report an electrochemical method for miRNA detection based on paramagnetic beads and enzyme amplification. In particular, miR 222 was chosen as model sequence, because of its involvement in brain, lung, and liver cancers. The proposed bioassay is based on biotinylated DNA capture probes immobilized on streptavidin-coated paramagnetic beads. Total RNA was extracted from the cell sample, enriched for small RNA, biotinylated, and then hybridized with the capture probe on the beads. The beads were then incubated with streptavidin-alkaline phosphatase and exposed to the appropriate enzymatic substrate. The product of the enzymatic reaction was electrochemically monitored. The assay was finally tested with a compact microfluidic device which enables multiplexed analysis of eight different samples with a detection limit of 7 pmol L(-1) and RSD = 15 %. RNA samples from non-small-cell lung cancer and glioblastoma cell lines were also analyzed.

Published
2013

30. Impact of a high loading dose of atorvastatin on contrast-induced acute kidney injury

Author

Quintavalle C, Fiore D, De Micco F, Visconti G, Focaccio A, Golia B, Ricciardelli B, Donnarumma E, Bianco A, Zabatta MA, Troncone G, Colombo A, Briguori C, and Condorelli G.

Abstract

The role of statins in the prevention of contrast-induced acute kidney injury (CIAKI) is controversial. METHODS AND RESULTS: First, we investigated the in vivo effects of atorvastatin on CIAKI. Patients with chronic kidney disease enrolled in the Novel Approaches for Preventing or Limiting Events (NAPLES) II trial were randomly assigned to (1) the atorvastatin group (80 mg within 24 hours before contrast media [CM] exposure; n=202) or (2) the control group (n=208). All patients received a high dose of N-acetylcysteine and sodium bicarbonate solution. Second, we investigated the in vitro effects of atorvastatin pretreatment on CM-mediated modifications of intracellular pathways leading to apoptosis or survival in renal tubular cells. CIAKI (ie, an increase >10% of serum cystatin C concentration within 24 hours after CM exposure) occurred in 9 of 202 patients in the atorvastatin group (4.5%) and in 37 of 208 patients in the control group (17.8%) (P=0.005; odds ratio=0.22; 95% confidence interval, 0.07-0.69). CIAKI rate was lower in the atorvastatin group in both diabetics and nondiabetics and in patients with moderate chronic kidney disease (estimated glomerular filtration rate, 31-60 mL/min per 1.73 m(2)). In the in vitro model, pretreatment with atorvastatin (1) prevented CM-induced renal cell apoptosis by reducing stress kinases activation and (2) restored the survival signals (mediated by Akt and ERK pathways). CONCLUSIONS: A single high loading dose of atorvastatin administered within 24 hours before CM exposure is effective in reducing the rate of CIAKI. This beneficial effect is observed only in patients at low to medium risk.

Published
2012

31. Renal insufficiency following contrast media administration trial II (REMEDIAL II): RenalGuard system in high-risk patients for contrast-induced acute kidney injury: rationale and design

Author

Briguori, C, Visconti, G, Ricciardelli, B, Condorelli, G, Airoldi, F, De Micco, F, Focaccio, A, Giannone, R, Golia, B, Quintavalle, C, Caiazzo, G, Zanca, C, Iaboni, M, Rivera, N, Tavano, D, Bertoli, S, Staine, T, Valgimigli, M, Ferrari, R, Monti, M, Sangiorgi, G, Lambertini, S, Briguori, C., Visconti, Gabriella, Ricciardelli, B., Condorelli, Gerolama, and REMEDIAL II, I. n. v. e. s. t. i. g. a. t. o. r. s.

Subjects
Time Factors, Contrast Media, Settore MED/11 - Malattie dell'Apparato Cardiovascolare, Radiography, Interventional, law.invention, chemistry.chemical_compound, Randomized controlled trial, law, Furosemide, Risk Factors, Clinical endpoint, Renal Insufficiency, Diuretics, Framingham Risk Score, Interventional, Acute kidney injury, Equipment Design, Acute Kidney Injury, Chi-Square Distribution, Humans, Research Design, Italy, Risk Assessment, Fluid Therapy, Treatment Outcome, Acetylcysteine, Kidney Diseases, Triiodobenzoic Acids, Sodium Bicarbonate, Drug Therapy, Combination, Creatinine, Glomerular Filtration Rate, Chronic Disease, Biological Markers, Combination, Cardiology and Cardiovascular Medicine, medicine.drug, medicine.medical_specialty, Urology, Renal function, Drug Therapy, medicine, business.industry, medicine.disease, Iodixanol, Surgery, Radiography, chemistry, business, Biomarkers, Kidney disease
Abstract

Aims The combined prophylactic strategy of sodium bicarbonate plus N-acetylsyteine (NAC) seems to be effective in preventing contrast induced acute kidney injury (CI-AKI) in patients at low-to-medium risk. However, in patients at high and very high risk the rate of CI-AKI is still high. In this subset of patients the anticipated advantages of the RenalGuard(tm) System should be investigated. The RenalGuard(tm) System (PLC Medical Systems, Inc., Franklin, MA, USA) is a real-time measurement and real time matched fluid replacement device designed to accommodate the RenalGuard therapy, which is based on the theory that creating and maintaining a high urine output is beneficial by allowing a quick elimination of contrast media, and, therefore, reducing its toxic effects. Methods and results The REMEDIAL II trial is a randomised, multicentre, investigator-sponsored trial addressing the hypothesis that the RenalGuard System is superior to the prophylaxis with sodium bicarbonate infusion plus NAC in preventing CI-AKI in high and very high risk patients. Consecutive patients with chronic kidney disease (CKD) and at high to very high risk for CI-AKI, referred to our institutions for coronary and/or peripheral procedures, will be randomly assigned to 1) prophylactic administration of sodium bicarbonate plus NAC (control group) and 2) RenalGuard System treatment (RenalGuard group). All enrolled patients must have an estimated glomerular filtration rate ≤ 30 ml/min/1.73 m2 and/or a contrast nephropathy risk score ≥ 11. In all cases iodixanol (an iso-osmolar, non-ionic contrast agent) will be administered. The primary endpoint is an increase of ≥ 0.3 mg/dL in the serum creatinine concentration 48 hours after the procedure. Conclusions The REMEDIAL II trial will give important answers on how to prevent CI-AKI in high and very high risk patients undergoing contrast media exposure.

Published
2011

35. Poster Session: Right ventricular systolic function

Author

Altman, M., primary, Bergerot, C., additional, Thibault, H., additional, Aussoleil, A., additional, Skuldadt Davidsen, E., additional, Barthelet, M., additional, Derumeaux, G. A., additional, Grapsa, J., additional, Zimbarra Cabrita, I., additional, Afilalo, J., additional, Paschou, S., additional, Dawson, D., additional, Durighel, G., additional, O'regan, D., additional, Howard, L., additional, Gibbs, J., additional, Nihoyannopoulos, P., additional, Morenate Navio, M., additional, Mesa Rubio, M., additional, Ortega, M. D., additional, Ruiz Ortiz, M., additional, Castillo Bernal, F., additional, Del Pino, C. L., additional, Toledano, F., additional, Alvarez-Ossorio, M. P., additional, Ojeda Pineda, S., additional, Lezo Cruz-Conde, J. S. D., additional, Jasaityte, R., additional, Claus, P., additional, Teske, A., additional, Herbots, L., additional, Verheyden, B., additional, Rademakers, F., additional, D'hooge, J., additional, Tocchetti, C. G., additional, Coppola, C., additional, Rea, D., additional, Quintavalle, C., additional, Guarino, L., additional, Castaldo, N., additional, De Lorenzo, C., additional, Condorelli, G., additional, Arra, C., additional, Maurea, N., additional, Voilliot, D., additional, Huttin, O., additional, Camara, Y., additional, Djaballah, W., additional, Carillo, S., additional, Zinzius, P., additional, Sellal, J., additional, Angioi, M., additional, Juilliere, Y., additional, Selton-Suty, C., additional, Dobrowolski, P., additional, Klisiewicz, A., additional, Florczak, E., additional, Prejbisz, A., additional, Szwench, E., additional, Rybicka, J., additional, Januszewicz, A., additional, Hoffman, P., additional, Jurado Roman, A., additional, De Dios Perez, S., additional, De Nicolas, J. M. M., additional, Diaz Anton, B., additional, Rubio Alonso, B., additional, Martin Asenjo, R., additional, Mayordomo Gomez, S., additional, Villagraz Tecedor, L., additional, Blazquez, L., additional, De Meneses, R. T., additional, Bernard, A., additional, Hernandez, A. I., additional, Reynaud, A., additional, Lerclercq, C., additional, Daubert, J., additional, Donal, E., additional, Arjan Singh, R., additional, Sivarani, S., additional, Lim, S., additional, Azman, W., additional, Almeida, M., additional, Cardim, N., additional, Fonseca, V., additional, Carmelo, V., additional, Santos, S., additional, Santos, T., additional, Toste, J., additional, Kosmala, W., additional, Orda, A., additional, Karolko, B., additional, Mysiak, A., additional, Przewlocka-Kosmala, M., additional, Farsalinos, K., additional, Tsiapras, D., additional, Kyrzopoulos, S., additional, Avramidou, E., additional, Vassilopoulou, D., additional, Voudris, V., additional, Hayrapetyan, H., additional, Adamyan, K., additional, Montero Cabezas, J., additional, Granda Nistal, C., additional, Garcia Aranda, B., additional, Sanchez Sanchez, V., additional, Sestito, A., additional, Lamendola, P., additional, Di Franco, A., additional, Lauria, C., additional, Lanza, G., additional, Kukucka, M., additional, Unbehaun, A., additional, Buz, S., additional, Mladenow, A., additional, Kuppe, H., additional, Pasic, M., additional, Habazettl, H., additional, Gemma, D., additional, Montoro Lopez, N., additional, De Celix, M. G. R., additional, Lopez Fernandez, T., additional, De Torres Alba, F., additional, Del Valle, D. I., additional, Ramirez, U., additional, Mesa, J., additional, Moreno Yanguela, M., additional, Lopez Sendon, J., additional, Eveborn, G. 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additional, Unger, P., additional, Mornos, C., additional, Cozma, D., additional, Ionac, A., additional, Mornos, A., additional, Valcovici, M., additional, Pescariu, S., additional, Petrescu, L., additional, Hu, K., additional, Liu, D., additional, Niemann, M., additional, Herrmann, S., additional, Cikes, M., additional, Stoerk, S., additional, Knop, S., additional, Ertl, G., additional, Bijnens, B., additional, Weidemann, F., additional, De Knegt, M., additional, Biering-Sorensen, T., additional, Sogaard, P., additional, Sivertsen, J., additional, Jensen, J., additional, Mogelvang, R., additional, Lam, W., additional, Tang, M., additional, Chan, K., additional, Yang, Y., additional, Fang, F., additional, Sun, J., additional, Yu, C., additional, Lam, Y., additional, Panoulas, V., additional, Sulemane, S., additional, Bratsas, A., additional, Konstantinou, K., additional, Francone, M., additional, Schau, T., additional, Seifert, M., additional, Ridjab, D., additional, Schoep, M., 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additional, Van Camp, G., additional, and Cosyns, B., additional

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2012
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40. Poster Session 2: Thursday 8 December 2011, 14:00-18:00 * Location: Poster Area

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Luo, X., primary, Fang, F., additional, Sun, J., additional, Xie, J., additional, Lee, A., additional, Zhang, Q., additional, Yu, C., additional, Breithardt, O., additional, Schiessl, S., additional, Schmid, M., additional, Seltmann, M., additional, Klinghammer, L., additional, Zeissler, C., additional, Kuechle, M., additional, Daniel, W., additional, Ege, M., additional, Guray, U., additional, Guray, Y., additional, Demirkan, B., additional, Kisacik, H., additional, Kim, S.-E., additional, Hong, J.-Y., additional, Lee, J.-H., additional, Park, D.-G., additional, Han, K.-R., additional, Oh, D.-J., additional, Tufekcioglu, O., additional, Cozma, D. C., additional, Mornos, C., additional, Ionac, A., additional, Petrescu, L., additional, Tutuianu, C., additional, Dragulescu, S. I., additional, Guimaraes, L., additional, Tavares, G., additional, Rodrigues, A., additional, Nagamatsu, C., additional, Fischer, C., additional, Vieira, M., additional, Oliveira, W., additional, Wilberg, T., additional, Cordovil, A., additional, Morhy, S., additional, Muraru, D., additional, Peluso, M., additional, Dal Bianco, L., additional, Beraldo, M., additional, Solda', E., additional, Tuveri, M., additional, Cucchini, U., additional, Al Mamary, A., additional, Badano, L., additional, Iliceto, S., additional, Pizzuti, A., additional, Mabritto, B., additional, Derosa, C., additional, Tomasello, A., additional, Rovere, M., additional, Parrini, I., additional, Conte, M., additional, Lareva, N., additional, Govorin, A., additional, Cooper, R., additional, Sharif, J., additional, Somauroo, J. D., additional, Hung, J. D., additional, Porcelli, V., additional, Skevington, R., additional, Shahzad, A., additional, Scott, S., additional, Lindqvist, P., additional, Soderberg, S., additional, Gonzalez, M., additional, Tossavainen, E., additional, Henein, M., additional, Nciri, N., additional, Saad, H., additional, Nawas, S., additional, Ali, A., additional, Youssufzay, A., additional, Safi, A., additional, Faruk, S., additional, Yurdakul, S., additional, Erdemir, V., additional, Tayyareci, Y., additional, Yildirimturk, O., additional, Memic, K., additional, Aytekin, V., additional, Gurel, M., additional, Aytekin, S., additional, Przewlocka-Kosmala, M., additional, Cielecka-Prynda, M., additional, Mysiak, A., additional, Kosmala, W., additional, Pescariu, S., additional, Cozma, D., additional, Mornos, A., additional, Dragulescu, S., additional, Maurea, N., additional, Tocchetti, C. 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Published
2011
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46. c-FLIPL enhances anti-apoptotic Akt functions by modulation of Gsk3β activity.

Author

Quintavalle, C., Incoronato, M., Puca, L., Acunzo, M., Zanca, C., Romano, G., Garofalo, M., Iaboni, M., Croce, C. M., and Condorelli, G.

Subjects
*SERINE proteinases, *PROTEIN kinases, *APOPTOSIS, *DNA, *TUMOR necrosis factors, *CANCER cells
Abstract

Akt is a serine-threonine kinase that has an important role in transducing survival signals. Akt also regulates a number of proteins involved in the apoptotic process. To find new Akt interactors, we performed a two-hybrid screening in yeast using full-length Akt cDNA as bait and a human cDNA heart library as prey. Among 200 clones obtained, two of them were identified as coding for the c-FLIPL protein. c-FLIPL is an endogenous inhibitor of death receptor-induced apoptosis through the caspase-8 pathway. Using co-immunoprecipitation experiments of either transfected or endogenous proteins, we confirmed the interaction between Akt and c-FLIPL. Furthermore, we observed that c-FLIPL overexpression interferes with Gsk3-β phosphorylation levels. Moreover, through its effects on Gsk3β, c-FLIPL overexpression in cancer cells induced resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). This effect was mediated by the regulation of p27Kip1 and caspase-3 expression. These results indicate the existence of a new mechanism of resistance to TRAIL in cancer cells, and unexpected functions of c-FLIPL. [ABSTRACT FROM AUTHOR]

Published
2010
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48. Evaluation on 'real life' prescriptions of antifungal prophylaxis in high risk patients: preliminary results from a prospective survey Evaluation on 'real life' prescriptions of antifungal prophylaxis in high risk patients: preliminary results from a prospective survey

Author

Caira, M., Busca, A., Melillo, L., Candoni, A., Caramatti, C., Specchia, G., Fanci, R., Rossi, G., Cattaneo, C., Vacca, A., Quintavalle, C., Picardi, M., Mitra, M. E., Delia, M., Landini, B., Gasbarrino, C., Invernizzi, R., Salutari, P., Martino, B., Garzia, M. G., Chierichini, A., Venditti, A., Nadali, G., Luppi, M., Leone, G., Nosari, A. M., Aversa, F., Livio PAGANO, and Vianelli, N.

50. Urinary Dickkopf-3 and Contrast-Associated Kidney Damage

Author

Giuseppina Roscigno, Giuseppe Biondi-Zoccai, Carlo Briguori, Cristina Quintavalle, Gerolama Condorelli, Giacomo Frati, Francesca De Micco, Alessandra Affinito, Silvia Nuzzo, Roscigno, G., Quintavalle, C., Biondi-Zoccai, G., De Micco, F., Frati, G., Affinito, A., Nuzzo, S., Condorelli, G., and Briguori, C.

Subjects
Male, kidney, medicine.medical_specialty, Urinary system, Urology, Contrast Media, Renal function, 030204 cardiovascular system & hematology, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Iodinated contrast, medicine, Humans, 030212 general & internal medicine, Renal Insufficiency, Chronic, Wnt Signaling Pathway, Adaptor Proteins, Signal Transducing, Aged, Aged, 80 and over, Creatinine, Kidney, urogenital system, business.industry, Acute kidney injury, Biomarker, Acute Kidney Injury, medicine.disease, 3. Good health, medicine.anatomical_structure, chemistry, Biomarker (medicine), Female, Cardiology and Cardiovascular Medicine, business, Biomarkers, Human, Kidney disease
Abstract

Background: Administration of iodinated contrast medium (CM) during invasive cardiovascular procedures may be associated with impairment of kidney function. Objectives: Urinary dickkopf-3 (DKK3), a stress-induced renal tubular epithelium–derived glycoprotein, has been identified as a biomarker predicting both acute kidney injury (AKI) and persistent kidney dysfunction. Methods: Urinary DKK3/creatinine ratio (uDKK3/uCr), urine and serum neutrophil gelatinase-associated lipocalin (uNGAL, sNGAL) and serum cystatin C (sCyC) were assessed in 458 patients with chronic kidney disease scheduled for invasive cardiovascular procedures requiring CM administration with universal adoption of nephroprotective interventions. Contrast-associated AKI (CA-AKI) was defined as serum creatinine increase ≥0.3 mg/dl at 48 h after CM administration. Persistent kidney dysfunction was defined as persistent estimated glomerular filtration rate reduction ≥25% at 1 month compared with baseline. Results: CA-AKI occurred in 64 or the 458 patients (14%), and baseline uDKK3/uCr ≥491 pg/mg was the best threshold for its prediction. Net reclassification improvement (NRI) was significantly increased by adding baseline uDKK3/uCr to the Mehran, Gurm, and National Cardiovascular Data Registry (NCDR) scores (all p < 0.05), and the same applied to integrated discrimination improvement (IDI) when adding uDKK3/uCr to the Gurm and NCDR scores (p < 0.001). Persistent kidney dysfunction occurred in 57 of the 458 patients (12%) and baseline uDKK3/uCr ≥322 pg/mg appeared as the best threshold for its prediction. Adding baseline uDKK3/uCr to the Mehran, Gurm, and NCDR scores significantly increased IDI and NRI (all p < 0.001). Conclusions: Baseline uDKK3/uCr seems to be a reliable marker for improving the identification of patients with chronic kidney disease undergoing invasive coronary and peripheral procedures at risk for AKI and persistent kidney dysfunction.

Published
2021

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