88 results on '"Tavolaro, S."'
Search Results
2. Transition zone and anterior stromal prostate cancers: Evaluation of discriminant location criteria using multiparametric fusion-guided biopsy
- Author
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Tavolaro, S., Mozer, P., Roupret, M., Comperat, E., Rozet, F., Barret, E., Drouin, S., Vaessen, C., Lucidarme, O., Cussenot, O., Boudghène, F., and Renard-Penna, R.
- Published
- 2018
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3. Genetic landscape of ultra-stable chronic lymphocytic leukemia patients
- Author
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Raponi, S., Del Giudice, I., Marinelli, M., Wang, J., Cafforio, L., Ilari, C., Piciocchi, A., Messina, M., Bonina, S., Tavolaro, S., Bordyuh, M., Mariglia, P., Peragine, N., Mauro, F.R., Chiaretti, S., Molica, S., Gentile, M., Visentin, A., Trentin, L., Rigolin, G.M., Cuneo, A., Diop, F., Rossi, D., Gaidano, G., Guarini, A., Rabadan, R., and Foà, R.
- Published
- 2018
- Full Text
- View/download PDF
4. Evidence for X(3872) in Pb-Pb Collisions and Studies of its Prompt Production at root s(NN)=5.02 TeV
- Author
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Sirunyan, A. M., Tumasyan, A., Adam, W., Ambrogi, F., Bergauer, T., Dragicevic, M., Ero, J., Del, Valle, Escalante, A., Flechl, M., Fruhwirth, R., Jeitler, M., Krammer, N., Kratschmer, I, Liko, D., Madlener, T., Mikulec, I, Rad, N., Schieck, J., Schofbeck, R., Spanring, M., Waltenberger, W., Wulz, C-E, Zarucki, M., Drugakov, V, Mossolov, V, Gonzalez, Suarez, J., Darwish, M. R., Wolf, De, E. A., Croce, Di, Janssen, D., Kello, X., Lelek, T., Pieters, A., Sfar, M., Rejeb, H., Van, Haevermaet, Van, Mechelen, Van, Putte, Van, Remortel, Blekman, N., Bols, F., Chhibra, E. S., D'Hondt, S. S., Clercq, De, Lontkovskyi, J., Lowette, D., Marchesini, S., Moortgat, I, Python, S., Tavernier, Q., Van, Doninck, Van, Mulders, Beghin, P., Bilin, D., Clerbaux, B., Lentdecker, De, Delannoy, G., Dorney, H., Favart, B., Grebenyuk, L., Kalsi, A., Moureaux, A. K., Popov, L., Postiau, A., Starling, N., Thomas, E., L. V., Velde, Er, Vanlaer, C., Vannerom, P., Cornelis, D., Dobur, T., Khvastunov, D., Niedziela, I, Roskas, M., Skovpen, C., Tytgat, K., Verbeke, M., Vermassen, W., Vit, B., Bruno, M., Caputo, G., David, C., Delaere, P., Delcourt, C., Giammanco, M., Lemaitre, A., Prisci, V, Aro, J., Saggio, A., Vischia, P., Zobec, J., Alves, G. A., Silva, Correia, G., Hensel, C., Moraes, A., Batista Das Chagas, Belchior, E., Carvalho, W., Chinellato, J., Coelho, E., Costa, Da, E. M., Silveira, Da, Damiao, G. G., De Jesus, D., Martins, De Oliveira, C., Souza, De, Fonseca, S., Malbouisson, H., Martins, J., Figueiredo, Matos, D., Jaime, Medina, M., Almeida, De, Melo, M., Herrera, Mora, C., Mundim, L., Nogima, H., Prado Da Silva, Teles, W. L., Rebello, P., Rosas, Sanchez, L. J., Santoro, A., Sznajder, A., Thiel, M., Tonelli, Manganote, E. J., Da Silva De Araujo, Torres, F., Pereira, Vilela, A., Bernardes, C. A., Calligaris, L., Fern, ez Perez Tomei, Gregores, T. R., Lemos, E. M., Mercadante, D. S., Novaes, P. G., Padula, S. F., S, Ra, S., Aleks, Rov, Antchev, A., Hadjiiska, G., Iaydjiev, R., Misheva, P., Rodozov, M., Shopova, M., Sultanov, M., Bonchev, G., Dimitrov, M., Ivanov, A., Litov, T., Pavlov, L., Petkov, B., Petrov, P., Fang, A., Gao, W., Yuan, X., Ahmad, L., Hu, M., Wang, Z., Chen, Y., Chen, G. M., Chen, H. S., Jiang, M., Leggat, C. H., Liao, D., Liu, H., Spiezia, Z., Tao, A., Yazgan, J., Zhang, E., Zhang, H., Zhao, S., Agapitos, J., Ban, A., Levin, G., Li, A., Li, J., Li, L., Mao, Q., Qian, Y., Wang, S. J., Wang, D., Xiao, Q., Avila, M., Cabrera, C., Florez, A., Gonzalez, Hern, C. F., Ez, Segura, Delgado, M. A., Mejia, Guisao, Ruiz, Alvarez, J. D., Salazar, Gonzalez, C. A., Vanegas, Arbelaez, Godinovic, N., Lelas, N., Puljak, D., Sculac, I, Antunovic, T., Kovac, Z., Brigljevic, M., Ferencek, V, Kadija, D., Mesic, K., Roguljic, B., Starodumov, M., Susa, A., Ather, T., Attikis, M. W., Erodotou, A., Ioannou, E., Kolosova, A., Konstantinou, M., Mavromanolakis, S., Mousa, G., Nicolaou, J., Ptochos, C., Razis, F., Rykaczewski, P. A., Saka, H., Tsiakkouri, H., Finger, D., Finger, M., r. M., J, Kveton, A., Tomsa, J., Ayala, E., Jarrin, Carrera, E., Mahmoud, M. A., Mohammed, Y., Bhowmik, S., Antunes De Oliveira, Carvalho, A., Dewanjee, R. K., Ehataht, K., Kadastik, M., Raidal, M., Veelken, C., Eerola, P., Forthomme, L., Kirschenmann, H., Osterberg, K., Voutilainen, M., Garcia, F., Havukainen, J., Heikkila, J. K., Karimaki, V, Kim, M. S., Kinnunen, R., Lampen, T., Lassila-Perini, K., Laurila, S., Lehti, S., Linden, T., Siikonen, H., Tuominen, E., Tuominiemi, J., Luukka, P., Tuuva, T., Besancon, M., Couderc, F., Dejardin, M., Denegri, D., Fabbro, B., Faure, J. L., Ferri, F., Ganjour, S., Givernaud, A., Gras, P., Monchenault, De, Hamel, G., Jarry, P., Leloup, C., Lenzi, B., Locci, E., Malcles, J., R, Er, Rosowsky, J., Sahin, A., Savoy-Navarro, M. O., Titov, A., Yu, M., Ahuja, G. B., Amendola, S., Beaudette, C., Bonanomi, F., Busson, M., Charlot, P., Diab, C., Falmagne, B., Cassagnac, De, Granier, R., Kucher, I, Lobanov, A., Perez, Martin, C., Nguyen, M., Och, O, Paganini, C., Rembser, P., Salerno, J., Sauvan, R., Sirois, J. B., Zabi, Y., Zghiche, A., Agram, A., J-L, Rea, Bloch, J., Bourgatte, D., Brom, G., J-M, Chabert, Collard, E. C., Conte, C., Fontaine, E., J-C, Gele, Goerlach, D., Grimault, U., Bihan, Le, A-C, Tonon, Van, Hove, Gadrat, P., Beauceron, S., Bernet, S., Boudoul, C., Camen, G., Carle, C., Chanon, A., Chierici, N., Contardo, R., Depasse, D., Mamouni, El, Fay, H., Gascon, J., Gouzevitch, S., Ille, M., Jain, B., Laktineh, Sa, Lattaud, I. B., Lesauvage, H., Lethuillier, A., Mirabito, M., Perries, L., Sordini, S., Torterotot, V, Touquet, L., G. V., Donckt, Er, Viret, M., Toriashvili, S., Tsamalaidze, T., Autermann, Z., Feld, C., Klein, L., Lipinski, K., Meuser, M., Pauls, D., Preuten, A., Rauch, M., Schulz, M. P., Teroerde, J., Erdmann, M., Fischer, M., Ghosh, B., Hebbeker, S., Hoepfner, T., Keller, K., Mastrolorenzo, H., Merschmeyer, L., Meyer, M., Millet, A., Mocellin, P., Mondal, G., Mukherjee, S., Noll, S., Novak, D., Pook, A., Pozdnyakov, T., Quast, A., Radziej, T., Rath, M., Reithler, Y., Roemer, H., Schmidt, J., Schuler, A., Sharma, S. C., Wiedenbeck, A., Zaleski, S., Flugge, S., Ahmad, G., Haj, W., Hlushchenko, O., Kress, T., Muller, T., Nowack, A., Pistone, C., Pooth, O., Roy, D., Sert, H., Stahl, A., Martin, Aldaya, M., Asmuss, P., Babounikau, I, Bakhshiansohi, H., Beernaert, K., Behnke, O., Martinez, Bermudez, A., Bin, Anuar, Borras, A. A., Botta, K., Campbell, V, Cardini, A., Connor, A., Rodriguez, P., Consuegra, S., Contreras-Campana, C., Danilov, V, Wit, De, Defranchis, A., Pardos, M. M., Diez, C., Damiani, Dominguez, D., Eckerlin, G., Eckstein, D., Eichhorn, T., Elwood, A., Eren, E., Banos, Estevez, L. I., Gallo, E., Geiser, A., Grohsjean, A., Guthoff, M., Haranko, M., Harb, A., Jafari, A., Jomhari, N. Z., Jung, H., Kasem, A., Kasemann, M., Kaveh, H., Keaveney, J., Kleinwort, C., Knolle, J., Krucker, D., Lange, W., Lenz, T., Lidrych, J., Lipka, K., Lohmann, W., Mankel, R., Melzer-Pellmann, I-A, Meyer, A. B., Missiroli, M., Mnich, J., Mussgiller, A., Myronenko, V, Adan, Perez, D., Pflitsch, S. K., Pitzl, D., Raspereza, A., Saibel, A., Savitskyi, M., Scheurer, V, Schutze, P., Schwanenberger, C., Shevchenko, R., Singh, A., Ricardo, Sosa, R. E., Tholen, H., Turkot, O., Vagnerini, A., Van De Klundert, Walsh, M., Wen, R., Wichmann, Y., Wissing, K., Zenaiev, C., Zlebcik, O., Aggleton, R., Bein, R., Benato, S., Benecke, L., Dreyer, A., Ebrahimi, T., Feindt, A., Frohlich, F., Garbers, A., Garutti, C., Gonzalez, E., Gunnellini, D., Haller, P., Hinzmann, J., Karavdina, A., Kasieczka, A., Klanner, G., Kogler, R., Kovalchuk, R., Kurz, N., Kutzner, S., Lange, V, Lange, J., Malara, T., Multhaup, A., Niemeyer, J., Reimers, C. E. N., Rieger, A., Schleper, O., Schumann, P., Schw, S., T, J., Sonneveld, J., Stadie, H., Steinbruck, G., Vormwald, B., Zoi, I, Akbiyik, M., Baselga, M., Baur, S., Berger, T., Butz, E., Caspart, R., Chwalek, T., Boer, De, Dierlamm, W., Morabit, El, Faltermann, K., Giffels, N., Gottmann, M., Hartmann, A., Heidecker, F., Husemann, C., Iqbal, U., Kudella, M. A., Maier, S., Mitra, S., Mozer, S., Muller, M. U., Muller, D., Musich, Th, Nurnberg, M., Rabbertz, G., Savoiu, K., Schafer, D., Schnepf, D., Schroder, M., Shvetsov, M., Simonis, I, Ulrich, H. J., Wassmer, R., Weber, M., Wohrmann, M., Wolf, C., Wozniewski, R., Anagnostou, S., Asenov, G., Daskalakis, P., Geralis, G., Kyriakis, T., Loukas, A., Paspalaki, D., Stakia, G., Diamantopoulou, A., Karathanasis, M., Kontaxakis, G., Manousakis-katsikakis, P., Panagiotou, A., Papavergou, A., Saoulidou, I, Theofilatos, N., Vellidis, K., Vourliotis, K., Bakas, E., Kousouris, G., Papakrivopoulos, K., Tsipolitis, I, Zacharopoulou, G., Evangelou, A., Foudas, I, Gianneios, C., Katsoulis, P., Kokkas, P., Mallios, P., Manitara, S., Manthos, K., Papadopoulos, N., Strologas, I, Triantis, J., Tsitsonis, F. A., Bartok, D., Chudasama, M., Csanad, R., Major, M., P. M., Al, K., Mehta, A., Pasztor, G., Suranyi, O., Veres, I, Bencze, G., Hajdu, G., Horvath, C., Sikler, D., Veszpremi, F., Vesztergombi, V., Beni, G., Czellar, N., Karancsi, S., Molnar, J., Szillasi, J., Raics, Z., Teyssier, P., Trocsanyi, D., Ujvari, Z. L., Csorgo, B., Metzger, T., Nemes, W. J., Novak, F., Choudhury, T., Komaragiri, S., Tiwari, J. R., Bahinipati, P. C., Kar, S., Kole, C., Mal, G., Bindhu, P., Muraleedharan Nair, V. K., Nayak, A., Sahoo, D. K., Swain, S. K., Bansal, S., Beri, S. B., Bhatnagar, V, Chauhan, S., Dhingra, N., Gupta, R., Kaur, A., Kaur, M., Kaur, S., Kumari, P., Lohan, M., Meena, M., Eep, S, Sharma, K., Singh, S., Virdi, J. B., Walia, A. K., Bhardwaj, G., Choudhary, A., Garg, B. C., Gola, R. B., Keshri, M., Kumar, S., Ashok, Naimuddin, Priyanka, M., Ranjan, P., Shah, K., Aashaq, Sharma, Bhardwaj, R., Bharti, R., Bhattacharya, M., Bhattacharya, R., Bhaw, S., Eep, U., Bhowmik, D., Dutta, S., Ghosh, S., Gomber, B., Maity, M., Mondal, K., N, An, Purohit, S., Rout, A., Saha, P. K., Sarkar, G., Sharan, S., Singh, M., Thakur, B., Behera, S., Behera, P. K., Kalbhor, S. C., Muhammad, P., Pujahari, A., Sharma, P. R., Sikdar, A., Dutta, A. K., Jha, D., Mishra, V, Netrakanti, D. K., Pant, P. K., Shukla, L. M., Aziz, P., Bhat, T., Dugad, M. A., Mohanty, S., Sur, G. B., Verma, N., Ravindra, Kumar, Banerjee, S., Bhattacharya, S., Chatterjee, S., Das, P., Guchait, M., Karmakar, S., Majumder, G., Mazumdar, K., Sahoo, N., Sawant, S., Dube, S., Kansal, B., Kapoor, A., Kothekar, K., P, Ey, Rane, S., Rastogi, A., Sharma, A., Chenarani, S., Etesami, S., Khakzad, S. M., Najafabadi, M., Mohammadi, M., Naseri, M., Hosseinabadi, Rezaei, F., Felcini, M., Grunewald, M., Abbrescia, M., Aly, R., Calabria, C., Colaleo, A., Creanza, D., Cristella, L., Filippis, De, Palma, De, Florio, Di, Elmetenawee, A., Fiore, W., Gelmi, L., Iaselli, A., Ince, G., Lezki, M., Maggi, S., Maggi, G., Merlin, M., Miniello, J. A., My, G., Nuzzo, S., Pompili, S., Pugliese, A., Radogna, G., Ranieri, R., Selvaggi, A., Silvestris, G., Simone, L., Venditti, F. M., Verwilligen, R., Abbiendi, P., Battilana, G., Bonacorsi, C., Borgonovi, D., Braibant-Giacomelli, L., Campanini, S., Capiluppi, R., Castro, P., Cavallo, A., Codispoti, F. R., Cuffiani, G., Dallavalle, M., Fabbri, G. M., Fanfani, F., Fontanesi, A., Giacomelli, E., Giommi, P., Gr, L., I, C., Guiducci, L., Iemmi, F., Meo, Lo, Marcellini, S., Masetti, S., Navarria, G., Perrotta, F. L., Primavera, A., Rossi, F., Rovelli, A. M., Siroli, T., Tosi, G. P., Albergo, N., Costa, S., Mattia, Di, Potenza, A., Tricomi, R., Tuve, A., Barbagli, C., Cassese, G., Ceccarelli, A., Ciulli, R., Civinini, V, D'Aless, C., Ro, R., Fiori, F., Focardi, E., Latino, G., Lenzi, P., Meschini, M., Paoletti, S., Sguazzoni, G., Viliani, L., Benussi, L., Bianco, S., Piccolo, D., Bozzo, M., Ferro, F., Mulargia, R., Robutti, E., Tosi, S., Benaglia, A., Beschi, A., Brivio, F., Ciriolo, V, Dinardo, M. E., Dini, P., Gennai, S., Ghezzi, A., Govoni, P., Guzzi, L., Malberti, M., Malvezzi, S., Menasce, D., Monti, F., Moroni, L., Paganoni, M., Pedrini, D., Ragazzi, S., Fatis, De, Tabarelli, T., Valsecchi, D., Zuolo, D., Buontempo, S., Cavallo, N., Iorio, De, Crescenzo, Di, Fabozzi, A., Fienga, F., Galati, F., Iorio, G., Layer, A. O. M., Lista, L., Meola, L., Paolucci, S., Rossi, P., Sciacca, B., Voevodina, C., Azzi, E., Bacchetta, P., Bisello, N., Boletti, D., Bragagnolo, A., Carlin, A., Checchia, R., Manzano, P., De Castro, P., Dorigo, T., Dosselli, U., Gasparini, F., Gasparini, U., Gozzelino, A., Hoh, S. Y., Margoni, M., Meneguzzo, A. T., Pazzini, J., Presilla, M., Ronchese, P., Rossin, R., Simonetto, F., Tiko, A., Tosi, M., Zanetti, M., Zotto, P., Zucchetta, A., Zumerle, G., Braghieri, A., Fiorina, D., Montagna, P., Ratti, S. P., Re, V, Ressegotti, M., Riccardi, C., Salvini, P., Vai, I, Vitulo, P., Biasini, M., Bilei, G. M., Ciangottini, D., Fano, L., Lariccia, P., Leonardi, R., Manoni, E., Mantovani, G., Mariani, V, Menichelli, M., Rossi, A., Santocchia, A., Spiga, D., Rosov, K., Azzurri, P., Bagliesi, G., Bertacchi, V, Bianchini, L., Boccali, T., Castaldi, R., Ciocci, M. A., Dell'Orso, R., Donato, S., Giannini, L., Giassi, A., Grippo, M. T., Ligabue, F., Manca, E., Orli, M, Messineo, G., Palla, A., Rizzi, F., Rol, A., I, G., Chowdhury, Roy, S., Scribano, A., Spagnolo, P., Tenchini, R., Tonelli, G., Turini, N., Venturi, A., Verdini, P. G., Cavallari, F., Cipriani, M., Del, Re, Marco, Di, Diemoz, E., Longo, M., Meridiani, E., Organtini, P., G. P., Olfi, F., Paramatti, R., Quaranta, C., Rahatlou, S., Rovelli, C., Santanastasio, F., Soffi, L., Tramontano, R., Amapane, N., Arcidiacono, R., Argiro, S., Arneodo, M., Bartosik, N., Bellan, R., Bellora, A., Biino, C., Cappati, A., Cartiglia, N., Cometti, S., Costa, M., Covarelli, R., Demaria, N., Fern, Ez, Gonzalez, J. R., Kiani, B., Legger, F., Mariotti, C., Maselli, S., Migliore, E., Monaco, V, Monteil, E., Monteno, M., Obertino, M. M., Ortona, G., Pacher, L., Pastrone, N., Pelliccioni, M., Angioni, Pinna, G. L., Romero, A., Ruspa, M., Salvatico, R., Sola, V, Solano, A., Soldi, D., Staiano, A., Trocino, D., Belforte, S., Elise, C, Casarsa, V, Cossutti, M., Rold, Da, Della, Ricca, Vazzoler, G., Zanetti, F., Kim, A., Kim, B., Kim, D. H., Lee, G. N., Lee, J., Moon, S. W., C. S., Oh, Pak, Y. D., I, S., Sekmen, S., Son, D. C., Yang, Y. C., Kim, H., Moon, D. H., Francois, B., Kim, T. J., Park, J., Cho, S., Choi, S., Go, Y., Ha, S., Hong, B., Lee, K., Lee, K. S., Lim, J., Park, S. K., Roh, Y., Yoo, J., Goh, J., Kim, H. S., Almond, J., Bhyun, J. H., Choi, J., Jeon, S., Kim, J., Kim, J. S., Lee, H., Lee, S., Nam, K., Oh, M., S. B., Oh, Radburn-Smith, B. C., Yang, U. K., Yoo, H. D., Yoon, I, Jeon, D., Kim, J. H., Lee, J. S. H., Park, I. C., Watson, I. J., Choi, Y., Hwang, C., Jeong, Y., Lee, Y., Yu, I, Veckalns, V., Dudenas, V, Juodagalvis, A., Rinkevicius, A., Tamulaitis, G., Vaitkus, J., Idris, Mohamad, F., Abdullah, Wan, W. A. T., Yusli, M. N., Zolkapli, Z., Benitez, J. F., Hern, Ez, Castaneda, A., Quijada, Murillo, J. A., Palomo, Valencia, L., Castilla-Valdez, H., De La Cruz-Burelo, Heredia-De La Cruz, Lopez-Fern, I, Ez, R., Sanchez-Hern, Ez, Moreno, A., Carrillo, S., Oropeza, Barrera, Ramirez-Garcia, C., Vazquez, Valencia, Eysermans, F., Pedraza, J., I, Salazar, Ibarguen, H. A., Uribe, Estrada, Pineda, C., Morelos, A., Mijuskovic, J., Raicevic, N., Krofcheck, D., Bheesette, S., Butler, P. H., Lujan, P., Ahmad, A., Ahmad, M., Awan, M. I. M., Hassan, Q., Hoorani, H. R., Khan, W. A., Shah, M. A., Shoaib, M., Waqas, M., Avati, V, Grzanka, L., Malawski, M., Bialkowska, H., Bluj, M., Boimska, B., Gorski, M., Kazana, M., Szleper, M., Zalewski, P., Bunkowski, K., Byszuk, A., Doroba, K., Kalinowski, A., Konecki, M., Krolikowski, J., Olszewski, M., Walczak, M., Araujo, M., Bargassa, P., Bastos, D., Francesco, Di, Faccioli, A., Galinhas, P., Gallinaro, B., Hollar, M., Leonardo, J., Niknejad, N., Seixas, T., Shchelina, J., Strong, K., Toldaiev, G., Varela, O., Afanasiev, J., Bunin, S., Ershov, P., Golutvin, Y., Gorbunov, I, Kamenev, I, Karjavine, A., Korenkov, V, Lanev, V, Malakhov, A., Matveev, A., Mitsyn, V, Moisenz, V. V., Palichik, P., Perelygin, V, Shmatov, V, Skatchkov, S., Yuldashev, N., Zarubin, B. 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M., Rik, P., Petrov, V, Ryutin, R., Slabospitskii, S., Sobol, A., Troshin, S., Tyurin, N., Uzunian, A., Volkov, A., Babaev, A., Iuzhakov, A., Okhotnikov, V, Borchsh, V, Ivanchenko, V, Tcherniaev, E., Adzic, P., Cirkovic, P., Dordevic, M., Milenovic, P., Milosevic, J., Stojanovic, M., Aguilar-Benitez, M., Alcaraz, Maestre, Alvarez, Fern, Ez, A., Bachiller, I, Barrio, Luna, Bedoya, M., Cristina, F., Brochero, Cifuentes, J. A., Carrillo, Montoya, Cepeda, C. A., Cerrada, M., Colino, M., De la Cruz, Delgado, Peris, Fern, A., Ramos, Ez, Flix, J. P., Fouz, J., M. C., Gonzalez, Lopez, Goy, Lopez, Hern, S., J. M., Ez, Josa, I, Moran, M., Navarro, Tobar, Perez-Calero, Yzquierdo, Puerta, Pelayo, Redondo, J., Romero, I, Sanchez, Navas, Soares, S., Triossi, M. S., Willmott, A., Albajar, C., Troconiz, De, Reyes-Almanza, J. 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E., Sturdy, N., Thapa, J., Black, P., Bose, K., Buchanan, T., Caillol, J., Carlsmith, C., Dasu, D., Bruyn, De, Dodd, I, Galloni, L., He, C., Herndon, H., Herve, M., Hussain, A., Lanaro, U., Loeliger, A., Loveless, A., Sreekala, R., Madhusudanan, J., Mallampalli, A., Pinna, D., Ruggles, T., Savin, A., Sharma, V, Smith, W. H., Teague, D., Trembath-reichert, S., and Cms, Collaboration
- Subjects
MODEL ,Physics and Astronomy ,High Energy Physics::Experiment ,QUARK-GLUON PLASMA ,Nuclear Experiment - Abstract
The first evidence for X(3872) production in relativistic heavy ion collisions is reported. The X(3872) production is studied in lead-lead (Pb-Pb) collisions at a center-of-mass energy of root s(NN) = 5.02 TeV per nucleon pair, using the decay chain X(3872) -> J/psi pi(+)pi(-) -> mu(+) mu(-) pi(+)pi(-). The data were recorded with the CMS detector in 2018 and correspond to an integrated luminosity of 1.7 nb(-1). The measurement is performed in the rapidity and transverse momentum ranges vertical bar y vertical bar < 1.6 and 15 < p(T) < 50 GeV/c. The significance of the inclusive X(3872) signal is 4.2 standard deviations. The prompt X(3872) to psi 2S yield ratio is found to be rho(Pb-Pb) = 1.08 +/- 0.49(stat) +/- 0.52(syst), to be compared with typical values of 0.1 for pp collisions. This result provides a unique experimental input to theoretical models of the X(3872) production mechanism, and of the nature of this exotic state.
- Published
- 2022
5. Percutaneous CT-guided cyanoacrylate glue plugging for fluid leakage after interventional oncologic procedure
- Author
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Tavolaro, S., Ben Ammar, M., Nouri-Neuville, M., and Cornelis, F.H.
- Published
- 2019
- Full Text
- View/download PDF
6. Multimodal image-guided electrochemotherapy of unresectable liver metastasis from renal cell cancer
- Author
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Cornelis, F.H., Korenbaum, C., Ben Ammar, M., Tavolaro, S., Nouri-Neuville, M., and Lotz, J.P.
- Published
- 2019
- Full Text
- View/download PDF
7. P2.19 Comparison of Brachial and Central Blood Pressures from 2 Sphygmocor Xcel Systems Equipped with a 2M and 6M-Long Hose
- Author
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Stoer, S., Soulat, G., Tavolaro, S., Millasseau, S., Khettab, H., Boutouyrie, P., Laurent, S., and Mousseaux, E.
- Published
- 2015
- Full Text
- View/download PDF
8. P8.3 Aortic Flow Alterations in Dilated and Hypertrophic Cardiomyopathy: New Insight from Quantitative Flow MRI
- Author
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Bargiotas, I., Bollache, E., De Cesare, A., Besson-Hajji, L., Tavolaro, S., Redheuil, A., Mousseaux, E., and Kachenoura, N.
- Published
- 2014
- Full Text
- View/download PDF
9. Characterization of small (<4 cm) solid renal masses by computed tomography and magnetic resonance imaging: Current evidence and further development
- Author
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Schieda, N., primary, Lim, R.S., additional, McInnes, M.D.F., additional, Thomassin, I., additional, Renard-Penna, R., additional, Tavolaro, S., additional, and Cornelis, F.H., additional
- Published
- 2018
- Full Text
- View/download PDF
10. Refined karyotype-based prognostic stratification of chronic lymphocytic leukemia with a low-and very-low-risk genetic profile
- Author
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Giudice, I Del, Rigolin, G. M., Raponi, S., Cafforio, L., Ilari, C., Wang, Jiguang, Bordyuh, M., Piciocchi, A., Marinelli, M., Nanni, M., Tavolaro, S., Filetti, M., Bardi, A., Tammiso, E., Volta, E., Negrini, M., Saccenti, E., Mauro, F. R., Rossi, D., Gaidano, G., Guarini, A., Rabadan, R., Cuneo, A., Foà, R., Giudice, I Del, Rigolin, G. M., Raponi, S., Cafforio, L., Ilari, C., Wang, Jiguang, Bordyuh, M., Piciocchi, A., Marinelli, M., Nanni, M., Tavolaro, S., Filetti, M., Bardi, A., Tammiso, E., Volta, E., Negrini, M., Saccenti, E., Mauro, F. R., Rossi, D., Gaidano, G., Guarini, A., Rabadan, R., Cuneo, A., and Foà, R.
- Published
- 2018
11. Refined karyotype-based prognostic stratification of chronic lymphocytic leukemia with a low- and very-low-risk genetic profile
- Author
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Giudice, I Del, primary, Rigolin, G M, additional, Raponi, S, additional, Cafforio, L, additional, Ilari, C, additional, Wang, J, additional, Bordyuh, M, additional, Piciocchi, A, additional, Marinelli, M, additional, Nanni, M, additional, Tavolaro, S, additional, Filetti, M, additional, Bardi, A, additional, Tammiso, E, additional, Volta, E, additional, Negrini, M, additional, Saccenti, E, additional, Mauro, F R, additional, Rossi, D, additional, Gaidano, G, additional, Guarini, A, additional, Rabadan, R, additional, Cuneo, A, additional, and Foà, R, additional
- Published
- 2017
- Full Text
- View/download PDF
12. Chromosome aberrations detected by conventional karyotyping using novel mitogens in chronic lymphocytic leukemia: Clinical and biologic correlations
- Author
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Gian Matteo Rigolin, Del Giudice, I., Formigaro, L., Saccenti, E., Martinelli, S., Cavallari, M., Lista, E., Tammiso, E., Volta, E., Lupini, L., Bassi, C., Bardi, A., Sofritti, O., Daghia, G., Cavazzini, F., Marinelli, M., Tavolaro, S., Guarini, A., Negrini, M., Foa, R., and Cuneo, A.
- Subjects
Adult ,Male ,Cancer Research ,Oligonucleotides ,Chromosome Disorders ,leucemia linfatica cronica ,NO ,Time-to-Treatment ,Cytogenetics ,FISH ,Genetics ,Humans ,Receptor, Notch1 ,In Situ Hybridization, Fluorescence ,Aged ,Aged, 80 and over ,CLL, karyotype ,Chromosomes, Human, Pair 13 ,Middle Aged ,Ribonucleoprotein, U2 Small Nuclear ,Phosphoproteins ,Prognosis ,Leukemia, Lymphocytic, Chronic, B-Cell ,Recombinant Proteins ,karyotype ,citogenetica, FISH, prognosi, leucemia linfatica cronica ,Karyotyping ,Multivariate Analysis ,Mutation ,Interleukin-2 ,Female ,RNA Splicing Factors ,Chromosome Deletion ,Mitogens ,Tumor Suppressor Protein p53 ,Immunoglobulin Heavy Chains ,citogenetica ,prognosi ,CLL ,Chromosomes, Human, Pair 17 - Abstract
To clarify whether karyotype aberrations (KA) involving regions not covered by the standard fluorescence in situ hybridization (FISH) panel have independent prognostic relevance, we evaluated KA by conventional cytogenetics in a learning cohort (LC; n = 166) and a validation cohort (VC; n = 250) of untreated chronic lymphocytic leukemia (CLL) patients. In the VC, novel mitogens were used to improve metaphase generation and TP53, NOTCH1, and SF3B1 mutations were assessed. KA undetected by FISH were found in 35 and 35% of the cases in the LC and VC, respectively. In addition to FISH, KA allowed reclassification of 23 and 26% of cases in the LC and VC, respectively, into a higher cytogenetic risk group. By multivariate analysis, both in the LC and VC, KA other than isolated 13q deletion correlated with a shorter time to first treatment (TFT; P0.001 and 0.003, respectively), while a complex karyotype predicted a worse overall survival (OS, P = 0.015 and 0.010, respectively). In the VC, where a comprehensive biologic assessment was performed, a shorter TFT was also predicted by stage (P0.001), IGHV mutational status (P = 0.05), and del(17p)/TP53 mutations (P = 0.033) while stage (P = 0.023) and del(17p)/TP53 mutations (P = 0.024) independently predicted a shorter OS. FISH results did not independently impact on TFT and OS, in the LC and VC cohorts; this was also the case for NOTCH1 and SF3B1 mutations in the VC. We suggest that in CLL, conventional karyotyping with novel mitogens could be more effective than FISH for the detection of KA allowing for a more precise refinement of prognosis.
- Published
- 2015
13. Chlorambucil plus rituximab with or without maintenance rituximab as first-line treatment for elderly chronic lymphocytic leukemia patients
- Author
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Foà, R, Del Giudice, I, Cuneo, Antonio, Del Poeta, G, Ciolli, S, Di Raimondo, F, Lauria, F, Cencini, E, Rigolin, Gian Matteo, Cortelezzi, A, Nobile, F, Callea, V, Brugiatelli, M, Massaia, M, Molica, S, Trentin, L, Rizzi, R, Specchia, G, Di Serio, F, Orsucci, L, Ambrosetti, A, Montillo, M, Luigi Zinzani, P, Ferrara, F, Morabito, F, Angela Mura, M, Soriani, S, Peragine, N, Tavolaro, S, Bonina, S, Marinelli, M, Stefania De Propris, M, Della Starza, I, Piciocchi, A, Alietti, A, Runggaldier, Ej, Gamba, E, Romana Mauro, F, Chiaretti, S, Guarini, A., R. Foà, I. D. Giudice, A. Cuneo, G. D. Poeta, S. Ciolli, F. D. Raimondo, F. Lauria, E. Cencini, G. M. Rigolin, A. Cortelezzi, F. Nobile, V. Callea, M. Brugiatelli, M. Massaia, S. Molica, L. Trentin, R. Rizzi, G. Specchia, F. D. Serio, L. Orsucci, A. Ambrosetti, M. Montillo, P. L. Zinzani, F. Ferrara, F. Morabito, M. A. Mura, S. Soriani, N. Peragine, S. Tavolaro, S. Bonina, M. Marinelli, M. S. De, I. D. Starza, A. Piciocchi, A. Alietti, E. J. Runggaldier, E. Gamba, F. R. Mauro, S. Chiaretti, and A. Guarini
- Subjects
Male ,Murine-Derived ,drug therapy/pathology, Male, Survival Analysis, Treatment Outcome ,Antibodies ,Disease-Free Survival ,Drug Administration Schedule ,Antibodies, Monoclonal, Murine-Derived ,Antineoplastic Combined Chemotherapy Protocols ,Monoclonal ,80 and over ,80 and over, Antibodie ,Humans ,therapeutic use, Chlorambucil ,Chronic ,Aged ,Aged, 80 and over ,Aged, Aged ,Leukemia ,Chlorambucil ,Female ,Induction Chemotherapy ,Leukemia, Lymphocytic, Chronic, B-Cell ,Rituximab ,Survival Analysis ,Treatment Outcome ,Hematology ,B-Cell ,Lymphocytic ,CLL ,chlorambucil ,administration /&/ dosage, Antineoplastic Combined Chemotherapy Protocol ,administration /&/ dosage, Disease-Free Survival, Drug Administration Schedule, Female, Humans, Induction Chemotherapy, Leukemia ,Settore MED/15 - Malattie del Sangue - Abstract
In a phase II trial, we evaluated chlorambucil and rituximab (CLB-R) as first-line induction treatment with or without R as maintenance for elderly chronic lymphocytic leukemia (CLL) patients. Treatment consisted of eight 28-day cycles of CLB (8 mg/m(2) /day, days 1-7) and R (day 1 of cycle 3, 375 mg/m(2) ; cycles 4-8, 500 mg/m(2) ). Responders were randomized to 12 8-week doses of R (375 mg/m(2) ) or observation. As per intention-to-treat analysis, 82.4\% (95\% CI, 74.25-90.46\%) of 85 patients achieved an overall response (OR), 16.5\% a complete response (CR), 2.4\% a CR with incomplete bone marrow recovery. The OR was similar across Binet stages (A 86.4\%, B 81.6\%, and C 78.6\%) and age categories (60-64 years, 92.3\%; 65-69, 85.2\%; 70-74, 75.0\%; ≥75, 81.0\%). CLB-R was well tolerated. After a median follow-up of 34.2 months, the median progression-free survival (PFS) was 34.7 months (95\% CI, 33.1-39.5). TP53 abnormalities, complex karyotype, and low CD20 gene expression predicted lack of response; SF3B1 mutation and BIRC3 disruption low CR rates. IGHV mutations significantly predicted PFS. R maintenance tended towards a better PFS than observation and was safe and most beneficial for patients in partial response and for unmutated IGHV cases. CLB-R represents a promising option for elderly CLL patients.
- Published
- 2014
14. Stress tests sur le système bancaire et les organismes d’assurance en France
- Author
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Martin v., Tavolaro S., and Viol S.
- Abstract
Au premier semestre 2012, le Secrétariat général de l’Autorité de contrôle prudentiel (SGACP) a procédé à l’examen de la stabilité du système financier français dans le cadre du programme FSAP (Financial Sector Assessment Program) du Fonds Monétaire International (FMI). - Commencée en mars 2012, sur la base des comptes à fin décembre 2011, cette évaluation a comporté un exercice de stress test réalisé à partir, d’une part, des modèles internes des banques et assurances (exercice dit « bottom-up ») et, d’une part, des modèles de stress du SGACP pour les banques (exercice dit « top-down »). L’objectif était de juger la résistance des banques et des assurances à l’apparition d’un certain nombre de chocs hypothétiques, d’ordre macro-économiques et financiers. Cet exercice de stress a été conduit dans des conditions macro-économiques et financières particulièrement dégradées, au coeur de la crise des dettes souveraines européennes. - En ce qui concerne le secteur bancaire, 8 groupes (BNP Paribas, Société Générale, Groupe Crédit Agricole, Groupe BPCE, Groupe Crédit Mutuel, La Banque Postale, HSBC France, Caisse des Dépôts et Consignations) ont pris part au stress « bottom-up » (représentant plus de 97% du total actif des banques françaises). Sur le plan méthodologique, l’exercice s’est appuyé sur deux scénarios – un scénario central et un scénario « défavorable » – et sur une analyse en sensibilité. L’exercice s’est articulé autour de trois types d’indicateurs : des indicateurs de solvabilité qui incluaient un stress souverain, des indicateurs de liquidité et des indicateurs de contagion. Sur le plan réglementaire, cet exercice, qui intègre la réglementation prudentielle effectivement en vigueur sur l’horizon de simulation (2012-2016), s’est inscrit dans un cadre en pleine évolution avec la mise en place progressive de la CRDIV. - Les résultats des stress de solvabilité témoignent de la capacité des banques françaises à résister à une détérioration significative de l’environnement économique, tout en étant capable de se conformer aux nouvelles exigences de la CRD IV : l’ensemble des banques affichent, dans le scénario central, un ratio supérieur à 9% sur tout l’horizon considéré, et supérieur à 8% dans le scénario adverse. Par ailleurs, en simulant un dysfonctionnement partiel des marchés interbancaires (« wholesale funding »), les stress de liquidité ont permis de mesurer, la vulnérabilité que constitue cette source de financement de marché pour le secteur bancaire et, d’autre part, l’existence d’importantes réserves de collatéraux éligibles à la BCE leur permettant de faire face durablement (plus d’un an) à un épisode de crise, en ayant recours à la BCE. Enfin, les stress tests sur les expositions interbancaires ont montré la forte résilience du système bancaire français aux risques de contagion. - S’agissant du secteur de l’assurance, les 25 entités de l’échantillon retenu couvrent 70% du marché de l’assurance vie et 50% du marché de l’assurance non vie, avec respectivement 12 et 13 assureurs. Les assureurs ont évalué l’impact à l’horizon d’un an des scénarios central et défavorable dans le cadre de la réglementation actuelle Solvabilité 1 en utilisant leurs propres modèles. Ils ont ainsi été amenés à calculer l’impact des stress de liquidité, de marché et assurantiels sur leur marge de solvabilité en tenant compte des mécanismes d’absorption des pertes, c’est-à-dire des impôts différés et de la participation aux bénéfices. - Les résultats montrent que les assureurs vie ne sont que faiblement atteints par le scénario défavorable en raison de capacités importantes d’absorption des pertes par la participation aux bénéfices. Quant aux assureurs non vie, qui ne disposent pas de ce mécanisme, l’effet plus important du scénario défavorable ne met pas en péril leur solvabilité, en raison du niveau généralement élevé de leurs ratios de solvabilité initiaux. Au cours de l’année 2011, les assureurs vie et non vie ont fortement augmenté leurs disponibilités qui représentent en fin d’année respectivement 4% et 3,6% de leurs placements. Ce comportement prudent a été essentiellement motivé par deux phénomènes : la situation de décollecte en assurance vie mais aussi la perception d’un risque accru sur tous les types de placement. - Ce numéro d’Analyses et Synthèses aborde successivement les enjeux des stress tests institutionnels, les caractéristiques de l’exercice FSAP France et les principaux résultats et enseignements.
- Published
- 2013
15. Domino Effects when Banks Hoard Liquidity: The French network
- Author
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Fourel, V., Héam, J-C., Salakhova, D., and Tavolaro, S.
- Subjects
Liquidity hoarding, solvency and funding contagion, financial networks, systemic risk ,jel:G28 ,jel:G01 ,jel:G21 - Abstract
We investigate the consequences of banks' liquidity hoarding behaviour for the stability of the financial system by proposing a new model of banking contagion through two channels, bilateral exposures and funding shortage. Inspired by the key role of liquidity hoarding in the 2007-2009 financial crisis, we incorporate banks' hoarding behaviour in a standard Iterative Default Cascade algorithm to compute the propagation of a common market shock through a banking system. In addition to potential solvency contagion, a market shock leads to banks liquidity hoarding that may generate problems of short-term funding for other banks. As an empirical exercise, we apply this model to the French banking system. Relying on data on banks bilateral exposures collected by France' Prudential Supervisory Authority, the French banking sector appears resilient to the combination of an initial market shock (losses on marked-to-market assets) and the resulting solvency and liquidity contagion. Moreover, the model gauges the relative weight of the various factors in the total loss.
- Published
- 2013
16. TP53 mutations in adult acute lymphoblastic leukemia (ALL) are relatively frequent in molecularly negative case of both B- and T-lineage and correlate with poor response to induction therapy
- Author
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Chiaretti, S., Brugnoletti, F., Tavolaro, S., Bonina, S., Paoloni, F., Marinelli, M., Della Starza, I., Negulici, A., Vitale, A., De Propris MS, Elia, L., Vignetti, M., Massimiliano BONIFACIO, Kropp, M., Sica, M., La Starza, R., Pizzolo, G., Molica, S., Leone, G., Meloni, G., Testi, Am, Guarini, A., and Foà, R.
- Subjects
acute lymphoblastic leukemia ,TP53 - Published
- 2012
17. BCR stimulation induces a differential microRNA (MIR) profiling between B lymphocytes derived from chronic lymphocytic leukemia (CLL) patients and healthy donors
- Author
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Tavolaro, S., Chiaretti, Sabina, Peragine, Nadia, Bonina, Silvia, Brugnoletti, Fulvia, Santangelo, S., Marinelli, Marilisa, DEL GIUDICE, Ilaria, Mauro, F., Guarini, A., and Foa, Roberto
- Published
- 2011
18. Genomic and functional analyses of chronic lymphocytic leukemia (CLL) cells following IgD stimulation
- Author
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Tavolaro, S., Peragine, Nadia, Chiaretti, Sabina, Ricciardi, Maria Rosaria, Messina, M., Santangelo, S., Marinelli, Marilisa, Di Maio, V., DEL GIUDICE, Ilaria, Mauro, Francesca Romana, Foà, R., and Guarini, A.
- Published
- 2011
19. TP53 GENE SEQUENCING IDENTIFIES A PECULIAR MUTATION PROFILE AND CORRELATION WITH P53 PROTEIN DYSFUNCTIONS IN CHRONIC LYMPHOCYTIC LEUKEMIA PATIENTS AT DIFFERENT PHASES OF THE DISEASE
- Author
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Marinelli, M., Peragine, N., Santangelo, S., Ghia, E. M., Di Maio, V., DEL GIUDICE, Ilaria, Mauro, Francesca Romana, Tavolaro, S., Guarini, Anna, and Foa, Roberto
- Published
- 2010
20. GENOMIC PROFILE OF NON-NODAL MANTLE CELL LYMPHOMA IS CHARACTERIZED BY A DOWN-MODULATION OF GENES INVOLVED IN TUMOR INVASION
- Author
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Messina, M, DEL GIUDICE, Ilaria, Chiaretti, Sabina, Santangelo, S, Tavolaro, S, De Propris MS, Nanni, M, Pescarmona, E, Mancini, F, Pulsoni, Alessandro, Martelli, Maurizio, Cavalieri, E, Finolezzi, E, Cuneo, A, Mauro, Francesca Romana, Guarini, Anna, and Foa, Roberto
- Published
- 2010
21. EVALUATION OF TP53 MUTATIONS WITH THE AMPLICHIP P53 ARRAY IN CHRONIC LYMPHOCYTIC LEUKEMIA (CLL): HIGHER SENSITIVITY AND CORRELATION WITH CLINICAL OUTCOME
- Author
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Chiaretti, Sabina, Tavolaro, S., Marinelli, M., Messina, M., DEL GIUDICE, Ilaria, Mauro, Francesca Romana, Santangelo, S., Di Maio, V., Piciocchi, A., Magliozzi, M., Peragine, N., Truong, S., Patten, N., Lawrence, J., Ghia, E. M., Nanni, M., Guarini, Anna, and Foa, Roberto
- Published
- 2010
22. NODAL AND NON-NODAL MANTLE CELL LYMPHOMAS DISPLAY A DIFFERENT GENOMIC PROFILE AND IGHV MUTATIONAL STATUS
- Author
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DEL GIUDICE, Ilaria, Messina, M., Chiaretti, Sabina, Santangelo, S., Tavolaro, S., Maria Stefania De Propris, Nanni, M., Pescarmona, Edoardo, Mancini, F., Pulsoni, A., Russo, E., Cavalieri, E., Finolezzi, E., Cuneo, A., Mauro, F., Guarini, A., and Foa, R.
- Published
- 2010
23. Preclinical development of MEK inhibition-based therapeutic strategies in Acute Myeloid Leukemia
- Author
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Maria Rosaria RICCIARDI, Bergamo, P., Chiaretti, S., Scerpa, M. C., Tavolaro, S., Petrucci, M. T., Gervasoni, J., Ciuffreda, L., Decandia, S., Libotte, F., Abrams, S., Steelman, L., Konopleva, M., Cognetti, F., Foa, R., Andreeff, M., Mccubrey, J., Tafuri, A., and Milella, M.
- Published
- 2008
24. CD52 antigen expression and gene profile in lymphoproliferative disorders: therapeutic implications
- Author
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De Propris MS, Chiaretti, Sabina, Attolico, I, Tavolaro, S, Messina, M, Intoppa, S, Milani, Ml, Vitale, A, Perbellini, O, Mauro, Francesca Romana, DEL GIUDICE, Ilaria, Foa, R, and Guarini, A.
- Published
- 2008
25. P53 EVALUATION IN CLL BY P53 ARRAY: A SIMPLE, SENSITIVE AND SPECIFIC METHOD THAT UNRAVELS A HIGH PERCENTAGE OF POLYMORPHISMS AND MUTATIONS
- Author
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Chiaretti, Sabina, Tavolaro, S., Messina, M., Marinelli, M., DEL GIUDICE, Ilaria, Mauro, Francesca Romana, Santangelo, S., Peragine, N., Truong, S., De Propris, M. S., Nanni, M., Guarini, Anna, and Foa, Roberto
- Published
- 2008
26. SPONTANEOUS CLINICAL REMISSION IN CHRONIC LYMPHOCYTIC LEUKEMIA: CLINICAL AND BIOLOGIC FEATURES OF 9 CASES
- Author
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DEL GIUDICE, Ilaria, Mauro, Francesca Romana, Chiaretti, Sabina, Tavolaro, S., Santangelo, S., Marinelli, M., Maggio, R., De Propris, M. S., Mancini, F., Quattrocchi, L., Armiento, D., Guarini, Anna, and Foa, Roberto
- Published
- 2008
27. IgV(H) germline and mutated chronic lymphocytic leukemia (CLL) cases exert a diverse responsiveness upon BCR ligation
- Author
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Tavolaro, S., Maggio, R., Peragine, N., Messina, M., Citarella, Franca, Santangelo, S., Marinelli, M., Ricciardi, Maria Rosaria, De Propris, M. S., DEL GIUDICE, Ilaria, Mauro, Francesca Romana, Chiaretti, Sabina, Foa, Roberto, and Guarini, Anna
- Published
- 2007
28. Effective targeting of MEK/ERK signalling by the highly selective small molecule inhibitor of MEK, PD0325901, in hematopoietic and solid tumors
- Author
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Ricciardi, Maria Rosaria, Scerpa, Mc, Ciuffreda, L, Chiaretti, S, Tavolaro, S, Gervasoni, J, De Cave, F, Gregorj, C, Petrucci, Mt, Cognetti, F, Andreeff, M, Zupi, G, Foà, R, Tafuri, Agostino, and Milella, M.
- Published
- 2006
29. MRI evaluation of coronary anatomy and myocardial perfusion after arterial switch for transposition of great arteries
- Author
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Raimondi, F., primary, Tavolaro, S., additional, Khraiche, D., additional, Boudjemline, Y., additional, and Bonnet, D., additional
- Published
- 2014
- Full Text
- View/download PDF
30. TP53 mutations are frequent in adult acute lymphoblastic leukemia cases negative for recurrent fusion genes and correlate with poor response to induction therapy
- Author
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Chiaretti, S, Brugnoletti, F, Tavolaro, S, Bonina, S, Paoloni, F, Marinelli, M, Patten, N, Bonifacio, M, Kropp, Mg, Sica, Simona, Guarini, A, Foà, R., Sica, Simona (ORCID:0000-0003-2426-3465), Chiaretti, S, Brugnoletti, F, Tavolaro, S, Bonina, S, Paoloni, F, Marinelli, M, Patten, N, Bonifacio, M, Kropp, Mg, Sica, Simona, Guarini, A, Foà, R., and Sica, Simona (ORCID:0000-0003-2426-3465)
- Abstract
Acute lymphoblastic leukemia (ALL) is a disease of either B-cell (80–85%) or T-cell (20–25%) derivation. Several molecular aberrations (i.e. BCR-ABL1, MLL/AFF1, SIL/TAL1 and E2A/PBX1) confer an overall poor outcome.1,2 However, a proportion of patients do not carry known genetic abnormalities and have a heterogeneous clinical course. P53 plays a crucial role in cell cycle regulation and apoptosis after DNA damage, and its role in tumorigenesis is well-recognized in solid and hematologic malignancies, particularly acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL), in which its deregulation represents an important predictor of poor outcome.3–10
- Published
- 2013
31. NOTCH1 mutations in +12 chronic lymphocytic leukemia (CLL) confer an unfavorable prognosis, induce a distinctive transcriptional profiling and refine the intermediate prognosis of +12 CLL
- Author
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Del Giudice, I, Rossi, D, Chiaretti, S, Marinelli, M, Tavolaro, S, Gabrielli, S, Laurenti, Luca, Marasca, R, Rasi, S, Fangazio, M, Guarini, A, Gaidano, G, Foà, R., Laurenti, Luca (ORCID:0000-0002-8327-1396), Del Giudice, I, Rossi, D, Chiaretti, S, Marinelli, M, Tavolaro, S, Gabrielli, S, Laurenti, Luca, Marasca, R, Rasi, S, Fangazio, M, Guarini, A, Gaidano, G, Foà, R., and Laurenti, Luca (ORCID:0000-0002-8327-1396)
- Abstract
Trisomy 12, the third most frequent chromosomal aberration in chronic lymphocytic leukemia (CLL), confers an intermediate prognosis. In our cohort of 104 untreated patients carrying +12, NOTCH1 mutations occurred in 24% of cases and were associated to unmutated IGHV genes (P=0.003) and +12 as a sole cytogenetic abnormality (P=0.008). NOTCH1 mutations in +12 CLL associated with an approximately 2.4 fold increase in the risk of death, a significant shortening of survival (P<0.01) and proved to be an independent predictor of survival in multivariate analysis. Analogous to +12 CLL with TP53 disruption or del(11q), NOTCH1 mutations in +12 CLL conferred a significantly worse survival compared to that of +12 CLL with del(13q) or +12 only. The overrepresentation of cell cycle/proliferation related genes of +12 CLL with NOTCH1 mutations suggests the biological contribution of NOTCH1 mutations to determine a poor outcome. NOTCH1 mutations refine the intermediate prognosis of +12 CLL.
- Published
- 2012
32. Somatically acquired JAK1 mutations in adult acute lymphoblastic leukemia
- Author
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Flex, E, Petrangeli, V, Stella, L, Chiaretti, S, Hornakova, T, Knoops, L, Ariola, C, Fodale, V, Clappier, E, Paoloni, F, Martinelli, S, Fragale, A, Sanchez, M, Tavolaro, S, Messina, M, Cazzaniga, G, Camera, A, Pizzolo, G, Tornesello, A, Vignetti, M, Battistini, A, Cavé, H, Gelb, B, Renauld, J, Biondi, A, Constantinescu, S, Foà, R, Tartaglia, M, Gelb, BD, Constantinescu, SN, Tartaglia, M., BIONDI, ANDREA, Flex, E, Petrangeli, V, Stella, L, Chiaretti, S, Hornakova, T, Knoops, L, Ariola, C, Fodale, V, Clappier, E, Paoloni, F, Martinelli, S, Fragale, A, Sanchez, M, Tavolaro, S, Messina, M, Cazzaniga, G, Camera, A, Pizzolo, G, Tornesello, A, Vignetti, M, Battistini, A, Cavé, H, Gelb, B, Renauld, J, Biondi, A, Constantinescu, S, Foà, R, Tartaglia, M, Gelb, BD, Constantinescu, SN, Tartaglia, M., and BIONDI, ANDREA
- Abstract
Aberrant signal transduction contributes substantially to leukemogenesis. The Janus kinase 1 (JAK1) gene encodes a cytoplasmic tyrosine kinase that noncovalently associates with a variety of cytokine receptors and plays a nonredundant role in lymphoid cell precursor proliferation, survival, and differentiation. We report that somatic mutations in JAK1 occur in individuals with acute lymphoblastic leukemia (ALL). JAK1 mutations were more prevalent among adult subjects with the T cell precursor ALL, where they accounted for 18% of cases, and were associated with advanced age at diagnosis, poor response to therapy, and overall prognosis. All mutations were missense, and some were predicted to destabilize interdomain interactions controlling the activity of the kinase. Three mutations that were studied promoted JAK1 gain of function and conferred interleukin (IL)-3-independent growth in Ba/F3 cells and/or IL-9-independent resistance to dexamethasone-induced apoptosis in T cell lymphoma BW5147 cells. Such effects were associated with variably enhanced activation of multiple downstream signaling pathways. Leukemic cells with mutated JAK1 alleles shared a gene expression signature characterized by transcriptional up-regulation of genes positively controlled by JAK signaling. Our findings implicate dysregulated JAK1 function in ALL, particularly of T cell origin, and point to this kinase as a target for the development of novel antileukemic drugs.
- Published
- 2008
33. TP53 mutations are frequent in adult acute lymphoblastic leukemia cases negative for recurrent fusion genes and correlate with poor response to induction therapy
- Author
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Chiaretti, S., primary, Brugnoletti, F., additional, Tavolaro, S., additional, Bonina, S., additional, Paoloni, F., additional, Marinelli, M., additional, Patten, N., additional, Bonifacio, M., additional, Kropp, M. G., additional, Sica, S., additional, Guarini, A., additional, and Foa, R., additional
- Published
- 2013
- Full Text
- View/download PDF
34. Identification of molecular and functional patterns of p53 alterations in chronic lymphocytic leukemia patients in different phases of the disease
- Author
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Marinelli, M., primary, Peragine, N., additional, Di Maio, V., additional, Chiaretti, S., additional, De Propris, M. S., additional, Raponi, S., additional, Tavolaro, S., additional, Mauro, F. R., additional, Giudice, I. D., additional, Guarini, A., additional, and Foa, R., additional
- Published
- 2012
- Full Text
- View/download PDF
35. NOTCH1 mutations in +12 chronic lymphocytic leukemia (CLL) confer an unfavorable prognosis, induce a distinctive transcriptional profiling and refine the intermediate prognosis of +12 CLL
- Author
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Del Giudice, I., primary, Rossi, D., additional, Chiaretti, S., additional, Marinelli, M., additional, Tavolaro, S., additional, Gabrielli, S., additional, Laurenti, L., additional, Marasca, R., additional, Rasi, S., additional, Fangazio, M., additional, Guarini, A., additional, Gaidano, G., additional, and Foa, R., additional
- Published
- 2011
- Full Text
- View/download PDF
36. ATM gene alterations in chronic lymphocytic leukemia patients induce a distinct gene expression profile and predict disease progression
- Author
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Guarini, A., primary, Marinelli, M., additional, Tavolaro, S., additional, Bellacchio, E., additional, Magliozzi, M., additional, Chiaretti, S., additional, De Propris, M. S., additional, Peragine, N., additional, Santangelo, S., additional, Paoloni, F., additional, Nanni, M., additional, Del Giudice, I., additional, Mauro, F. R., additional, Torrente, I., additional, and Foa, R., additional
- Published
- 2011
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37. Gene expression profiling identifies a subset of adult T-cell acute lymphoblastic leukemia with myeloid-like gene features and over-expression of miR-223
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Chiaretti, S., primary, Messina, M., additional, Tavolaro, S., additional, Zardo, G., additional, Elia, L., additional, Vitale, A., additional, Fatica, A., additional, Gorello, P., additional, Piciocchi, A., additional, Scappucci, G., additional, Bozzoni, I., additional, Fozza, C., additional, Candoni, A., additional, Guarini, A., additional, and Foa, R., additional
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- 2010
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38. Characterization of ABL1 expression in adult T-cell acute lymphoblastic leukemia by oligonucleotide array analysis
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Chiaretti, S., primary, Tavolaro, S., additional, Ghia, E. M., additional, Ariola, C., additional, Matteucci, C., additional, Elia, L., additional, Maggio, R., additional, Messina, M., additional, Ricciardi, M. R., additional, Vitale, A., additional, Ritz, J., additional, Mecucci, C., additional, Guarini, A., additional, and Foa, R., additional
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- 2007
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39. Apport du bootstrap à la régression PLS : application à la prédiction de la qualité des gazoles
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Aji, S., primary, Tavolaro, S., additional, Lantz, F., additional, and Faraj, A., additional
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- 2003
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40. Comparison of brachial and central blood pressures from 2 SphygmoCor XCEL systems equipped with a 2m and 6m-long hose.
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Stoer, S., Soulat, G., Tavolaro, S., Millasseau, S., Khettab, H., Boutouyrie, P., Laurent, S., and Mousseaux, E.
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- 2015
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41. Aortic flow alterations in dilated and hypertrophic cardiomyopathy: New insight from quantitative flow MRI.
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Bargiotas, I., Bollache, E., De Cesare, A., Besson-Hajji, L., Tavolaro, S., Redheuil, A., Mousseaux, E., and Kachenoura, N.
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- 2014
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42. Somatically acquired JAK1 mutations in adult acute lymphoblastic leukemia
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Stefan N. Constantinescu, Andrea Camera, Robin Foà, Marco Tartaglia, Hélène Cavé, Laurent Knoops, Simone Martinelli, Lorenzo Stella, Francesca Paoloni, Valentina Petrangeli, Valentina Fodale, Simona Tavolaro, Angela Battistini, Cristina Ariola, Giovanni Cazzaniga, Emmanuelle Clappier, Alessandra Fragale, Sabina Chiaretti, Marco Vignetti, Andrea Biondi, Jean-Christophe Renauld, Assunta Tornesello, Bruce D. Gelb, Giovanni Pizzolo, Massimo Sanchez, Monica Messina, Tekla Hornakova, Elisabetta Flex, Flex, E, Petrangeli, V, Stella, L, Chiaretti, S, Hornakova, T, Knoops, L, Ariola, C, Fodale, V, Clappier, E, Paoloni, F, Martinelli, S, Fragale, A, Sanchez, M, Tavolaro, S, Messina, M, Cazzaniga, G, Camera, A, Pizzolo, G, Tornesello, A, Vignetti, M, Battistini, A, Cavé, H, Gelb, B, Renauld, J, Biondi, A, Constantinescu, S, Foà, R, Tartaglia, M, UCL - Cliniques universitaires Saint-Luc, and UCL - MD/MIGE - Département de microbiologie, d'immunologie et de génétique
- Subjects
Models, Molecular ,Somatic cell ,DNA Mutational Analysis ,animal cell ,medicine.disease_cause ,T cell lymphoma ,Mice ,Mutant Protein ,Models ,JAK1 ,ALL ,MUTATIONS ,T lymphocyte ,Immunology and Allergy ,gene mutation ,Settore CHIM/02 - Chimica Fisica ,Leukemic ,child ,Mutation ,Tumor ,Janus kinase 1 ,Gene Expression Regulation, Leukemic ,Kinase ,adult ,allele ,apoptosis ,article ,protein domain ,Precursor Cell Lymphoblastic Leukemia-Lymphoma ,enzyme activity ,medicine.anatomical_structure ,leukemia cell ,priority journal ,Signal transduction ,signal transduction ,mutational analysis ,lymphoma cell ,alleles ,animals ,base sequence ,cell line ,dna mutational analysis ,enzymology/genetics/pathology ,gene expression profiling ,gene expression regulation ,genetics ,humans ,janus kinase 1 ,leukemic ,metabolism ,mice ,models ,molecular ,molecular sequence data ,mutant proteins ,mutation ,precursor cell lymphoblastic leukemia-lymphoma ,tumor ,T cell ,prevalence ,Molecular Sequence Data ,Immunology ,dexamethasone ,acute lymphoblastic leukemia ,protein localization ,Biology ,leukemogenesis ,interleukin 3 ,Cell Line ,Cell Line, Tumor ,Acute lymphocytic leukemia ,medicine ,Animals ,Humans ,controlled study ,human ,mouse ,Alleles ,nonhuman ,Base Sequence ,Animal ,gene interaction ,missense mutation ,Gene Expression Profiling ,genetic transcription ,Brief Definitive Report ,treatment response ,Molecular ,Janus Kinase 1 ,medicine.disease ,Molecular biology ,cyclosporin A ,gene function ,Gene Expression Regulation ,interleukin 9 ,adolescent ,gene expression ,Adult Acute Lymphoblastic Leukemia ,Brief Definitive Reports ,Mutant Proteins ,prognosis ,molecular model ,upregulation - Abstract
Aberrant signal transduction contributes substantially to leukemogenesis. The Janus kinase 1 (JAK1) gene encodes a cytoplasmic tyrosine kinase that noncovalently associates with a variety of cytokine receptors and plays a nonredundant role in lymphoid cell precursor proliferation, survival, and differentiation. We report that somatic mutations in JAK1 occur in individuals with acute lymphoblastic leukemia (ALL). JAK1 mutations were more prevalent among adult subjects with the T cell precursor ALL, where they accounted for 18% of cases, and were associated with advanced age at diagnosis, poor response to therapy, and overall prognosis. All mutations were missense, and some were predicted to destabilize interdomain interactions controlling the activity of the kinase. Three mutations that were studied promoted JAK1 gain of function and conferred interleukin (IL)-3–independent growth in Ba/F3 cells and/or IL-9–independent resistance to dexamethasone-induced apoptosis in T cell lymphoma BW5147 cells. Such effects were associated with variably enhanced activation of multiple downstream signaling pathways. Leukemic cells with mutated JAK1 alleles shared a gene expression signature characterized by transcriptional up-regulation of genes positively controlled by JAK signaling. Our findings implicate dysregulated JAK1 function in ALL, particularly of T cell origin, and point to this kinase as a target for the development of novel antileukemic drugs.
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- 2008
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43. AICDA expression in BCR/ABL1-positive acute lymphoblastic leukaemia is associated with a peculiar gene expression profile
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Loredana Elia, Robin Foà, Giovanni Martinelli, Simona Tavolaro, Francesca Paoloni, Annalisa Lonetti, Cristina Papayannidis, Ilaria Iacobucci, Sabina Chiaretti, Simona Santangelo, Antonella Vitale, Monica Messina, Anna Guarini, Messina M, Chiaretti S, Iacobucci I, Tavolaro S, Lonetti A, Santangelo S, Elia L, Papayannidis C, Paoloni F, Vitale A, Guarini A, Martinelli G, and Foà R.
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Adult ,Male ,Transcription, Genetic ,DNA repair ,Fusion Proteins, bcr-abl ,Somatic hypermutation ,Biology ,bcr ,Leukocyte Count ,hemic and lymphatic diseases ,Cytidine Deaminase ,Precursor B-Cell Lymphoblastic Leukemia-Lymphoma ,Activation-induced (cytidine) deaminase ,Humans ,abl1+b-all ,aicda ,bcr/abl1+ b-all ,gene expression profiling ,Gene ,Oligonucleotide Array Sequence Analysis ,ABL ,Gene Expression Profiling ,breakpoint cluster region ,Hematology ,Cytidine deaminase ,Gene expression profiling ,ACUTE LYMPHOBLASTIC LEUKEMIA (ALL) ,biology.protein ,Cancer research ,Female - Abstract
Activation-induced cytidine deaminase (AICDA) initiates somatic hypermutation and class-switch recombination of immunoglobulin (Ig) genes and induces mutations also in non-Ig genes. AICDA aberrant expression was detected in B-lineage acute lymphoblastic leukaemia (B-ALL), particularly BCR/ABL1+ B-ALL; patients expressing AICDA carried more copy number alterations than 'AICDA-negative' cases. To determine the role of AICDA, AICDA expression and gene expression profiling were studied in adult BCR/ABL1+ B-ALL. Patients displaying the full-length isoform AICDA are characterized by up-regulation of DNA repair/replication and cell cycle genes, suggesting their involvement in the genetic instability of BCR/ABL1+ B-ALL.
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- 2011
44. Diagnosis Yield and Safety of Surgical Biopsy in Interstitial Lung Diseases: A Prospective Study.
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Radu D, Freynet O, Kambouchner M, Boubaya M, Nunes H, Uzunhan Y, Brillet PY, Guiraudet P, Noorah MZ, Israël-Biet D, Le Pimpec-Barthes F, Juvin K, Charpentier A, Gibault L, Assouad J, Naccache JM, Antoine M, Tavolaro S, Alifano M, Honoré I, L'Huillier JP, Debrosse D, Dupin C, Pradère P, Debray MP, Cazes A, Mordant P, Castier Y, Beloucif S, Crestani B, Lévy V, Martinod E, and Valeyre D
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- Humans, Prospective Studies, Retrospective Studies, Biopsy methods, Lung pathology, Thoracic Surgery, Video-Assisted adverse effects, Lung Diseases, Interstitial diagnosis, Lung Diseases, Interstitial surgery
- Abstract
Background: Surgical lung biopsy is essential in the diagnostic algorithm of interstitial lung disease (ILD) of unknown cause. Safety concerns have been recently reiterated. This study prospectively assessed the yield of diagnosis and safety of video-assisted thoracoscopic surgical lung biopsy (VATS-LB) for ILD diagnosis., Methods: This prospective study, conducted in 6 ILD-referral Paris hospitals, included 103 patients with ILD. VATS-LB was proposed after initial multidisciplinary discussion. A final diagnosis was made after the procedure, during a second multidisciplinary discussion. The main outcome was to determine the final diagnoses and their proportion after VATS-LB. Other outcomes were the percentage of change in diagnosis and treatment propositions after VATS-LB and adverse events during 3 months after the operation, postoperative pulmonary function, quality of life, and pain., Results: A definite diagnosis was reached in 87 patients (84.4%), and 16 remained unclassifiable (15.6%). After VATS-LB, the hypothesized diagnosis changed in 65 patients (63.1%) and treatment changed in 41 patients (39.8%). One patient died of acute exacerbation. In-hospital complications were predicted by a shorter preoperative 6-minute walking test distance and by forced vital capacity lower than 77%. Postoperative quality of life was not modified at 3 months, whereas forced vital capacity decreased slightly. Postoperative neuropathic pain was revealed in 5% of patients at 1 month and in 2% at 3 months., Conclusions: VATS-LB dramatically changed preoperative hypothetical diagnoses and treatment in ILD of unknown cause, with good patient survival in ILD referral centers., (Copyright © 2022 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)
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- 2022
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45. The dark side of histones: genomic organization and role of oncohistones in cancer.
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Amatori S, Tavolaro S, Gambardella S, and Fanelli M
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- Epigenesis, Genetic, Humans, Mutation, Carcinogenesis genetics, Genome, Histones genetics, Neoplasms genetics, Neoplasms physiopathology
- Abstract
Background: The oncogenic role of histone mutations is one of the most relevant discovery in cancer epigenetics. Recurrent mutations targeting histone genes have been described in pediatric brain tumors, chondroblastoma, giant cell tumor of bone and other tumor types. The demonstration that mutant histones can be oncogenic and drive the tumorigenesis in pediatric tumors, led to the coining of the term "oncohistones." The first identified histone mutations were localized at or near residues normally targeted by post-translational modifications (PTMs) in the histone N-terminal tails and suggested a possible interference with histone PTMs regulation and reading., Main Body: In this review, we describe the peculiar organization of the multiple genes that encode histone proteins, and the latter advances in both the identification and the biological role of histone mutations in cancer. Recent works show that recurrent somatic mutations target both N-terminal tails and globular histone fold domain in diverse tumor types. Oncohistones are often dominant-negative and occur at higher frequencies in tumors affecting children and adolescents. Notably, in many cases the mutations target selectively only some of the genes coding the same histone protein and are frequently associated with specific tumor types or, as documented for histone variant H3.3 in pediatric glioma, with peculiar tumors arising from specific anatomic locations., Conclusion: The overview of the most recent advances suggests that the oncogenic potential of histone mutations can be exerted, together with the alteration of histone PTMs, through the destabilization of nucleosome and DNA-nucleosome interactions, as well as through the disruption of higher-order chromatin structure. However, further studies are necessary to fully elucidate the mechanism of action of oncohistones, as well as to evaluate their possible application to cancer classification, prognosis and to the identification of new therapies.
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- 2021
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46. Echocardiographic features in antiphospholipid-negative Sneddon's syndrome and potential association with severity of neurological symptoms or recurrence of strokes: a longitudinal cohort study.
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Assan F, de Zuttere D, Bottin L, Tavolaro S, Courvoisier DS, Barbaud A, Alamowitch S, Francès C, and Chasset F
- Subjects
- Cohort Studies, Echocardiography, Female, Humans, Longitudinal Studies, Middle Aged, Recurrence, Antiphospholipid Syndrome, Lupus Erythematosus, Systemic, Stroke diagnostic imaging, Stroke epidemiology, Stroke etiology
- Abstract
Aims: Sneddon's syndrome (SS) may be classified as antiphospholipid positive (aPL+) or negative (aPL- SS). An association between Libman-Sacks (LS) endocarditis and strokes has been described in aPL+ patients. To describe cardiac involvement in aPL- SS and assess the potential association between LS endocarditis and severity or recurrence of neurological symptoms., Methods and Results: This longitudinal cohort study included aPL- SS patients followed in our departments between 1991 and June 2018. All patients underwent transthoracic 2D and Doppler echocardiography at diagnosis. Follow-up echocardiography was performed annually and the potential relationship between LS endocarditis development and neurovascular relapse as well as long-term cardiac worsening was prospectively assessed. We included 61 patients [52 women; median age 45 (range 24-60)]. For valvular involvement, 36 (59%) patients showed leaflet thickening; 18 (29.5%) had LS endocarditis at baseline. During a median follow-up of 72 months, LS endocarditis developed in eight (17.4%) patients, and 13 (28.3%) showed significant worsening of their cardiac status, including two who needed valvular replacement. After adjusting for baseline antithrombotic treatment regimen, neither the presence of LS endocarditis at baseline nor development during follow-up was associated with neurological relapse [hazard ratio (HR): 1.06, 95% confidence interval (CI): 0.33-4.74, P = 0.92] and [HR: 0.38, 95% CI: 0.02-1.89, P = 0.31], respectively., Conclusion: A long-term follow-up is needed to detect cardiac complications in aPL- SS. No change in neurological relapse was observed in patients presenting LS endocarditis occurrence during follow-up without any modification in antithrombotic treatment. Further research is necessary to assess the usefulness of treatment escalation in these patients., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email: journals.permissions@oup.com.)
- Published
- 2021
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47. Pyogenic lung abscess in an infectious disease unit: a 20-year retrospective study.
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Maitre T, Ok V, Calin R, Lassel L, Canestri A, Denis M, Hamidi M, Tavolaro S, Verdet C, Parrot A, Cadranel J, and Pialoux G
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- Hospital Units, Humans, Retrospective Studies, Risk Factors, Liver Abscess, Pyogenic epidemiology, Liver Abscess, Pyogenic therapy
- Abstract
Background: Pyogenic lung abscesses are rare and poorly described infections. This study aimed to describe their prognostic factors., Methods: We retrospectively included all patients hospitalized between 1 January 1998 and 1 June 2018, with an International Classification of Diseases, version 10 (IDC-10) diagnosis of pyogenic lung abscess, from the Diamm based medical records (Micro6, Nancy, France). Parasitic, fungal, or mycobacterial lung abscesses were excluded., Results: A total of 64 patients were included. Abscesses were associated with immunosuppression in 28 patients, including HIV infection and immunosuppressive therapy for eight and 12 patients, respectively. Bacterial identification was obtained for 36 patients. Nine patients (14%) developed lung abscesses after hematogenous dissemination. They differed from bronchogenic abscesses by their younger age ( p = 0.03), the absence of smoking or emphysema ( p = 0.05), Staphylococcus aureus ( p = 0.001) or Streptococcus spp. ( p = 0.05) isolation, and the smaller size of their abscess ( p = 0.02). Overall, evolution was marked by radiological sequelae (46.9%), relapse (12.5%), and death (4.8%). Radiological sequelae occurred more frequently during the course of bronchogenic abscesses ( p = 0.02), particularly when they spontaneously discharged ( p = 0.04). Relapses were more frequent in patients with emphysema ( p = 0.04) and when Haemophilus influenzae was isolated ( p = 0.04). In multivariate analysis, poor outcomes, including death, sequelae, and relapse occurred more frequently in patients who had bronchogenic abscess ( p = 0.02), and in those who received antibiotics during less than 6 weeks ( p = 0.05)., Conclusion: A duration of antibiotic treatment of less than 6 weeks and bronchogenic presentation were globally associated with poor outcome of pyogenic lung abscesses. These data should be considered when proposing guidelines for the care of pyogenic lung abscesses. The reviews of this paper are available via the supplemental material section .
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- 2021
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48. Bronchial Dieulafoy's Disease: Visualization of Embolization Particles in Bronchial Aspirate.
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Bonnefoy V, Garnier M, Tavolaro S, Antoine M, Assouad J, Fartoukh M, and Gibelin A
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- Aged, Bronchial Arteries pathology, Bronchoscopy methods, Combined Modality Therapy methods, Critical Illness, Follow-Up Studies, Hemoptysis etiology, Hemoptysis therapy, Humans, Intensive Care Units, Male, Pulmonary Disease, Chronic Obstructive diagnostic imaging, Radiography, Thoracic methods, Recurrence, Risk Assessment, Treatment Outcome, Bronchial Arteries diagnostic imaging, Computed Tomography Angiography methods, Embolization, Therapeutic methods, Hemoptysis diagnostic imaging, Pneumonectomy methods, Pulmonary Disease, Chronic Obstructive complications
- Published
- 2018
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49. Refined karyotype-based prognostic stratification of chronic lymphocytic leukemia with a low- and very-low-risk genetic profile.
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Giudice ID, Rigolin GM, Raponi S, Cafforio L, Ilari C, Wang J, Bordyuh M, Piciocchi A, Marinelli M, Nanni M, Tavolaro S, Filetti M, Bardi A, Tammiso E, Volta E, Negrini M, Saccenti E, Mauro FR, Rossi D, Gaidano G, Guarini A, Rabadan R, Cuneo A, and Foà R
- Subjects
- Female, Genetic Profile, Humans, Karyotype, Karyotyping methods, Male, Mutation genetics, Prognosis, Risk Factors, Leukemia, Lymphocytic, Chronic, B-Cell genetics, Leukemia, Lymphocytic, Chronic, B-Cell pathology
- Published
- 2018
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50. Chlorambucil plus rituximab with or without maintenance rituximab as first-line treatment for elderly chronic lymphocytic leukemia patients.
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Foà R, Del Giudice I, Cuneo A, Del Poeta G, Ciolli S, Di Raimondo F, Lauria F, Cencini E, Rigolin GM, Cortelezzi A, Nobile F, Callea V, Brugiatelli M, Massaia M, Molica S, Trentin L, Rizzi R, Specchia G, Di Serio F, Orsucci L, Ambrosetti A, Montillo M, Zinzani PL, Ferrara F, Morabito F, Mura MA, Soriani S, Peragine N, Tavolaro S, Bonina S, Marinelli M, De Propris MS, Starza ID, Piciocchi A, Alietti A, Runggaldier EJ, Gamba E, Mauro FR, Chiaretti S, and Guarini A
- Subjects
- Aged, Aged, 80 and over, Antibodies, Monoclonal, Murine-Derived administration & dosage, Chlorambucil administration & dosage, Disease-Free Survival, Drug Administration Schedule, Female, Humans, Induction Chemotherapy, Leukemia, Lymphocytic, Chronic, B-Cell pathology, Male, Rituximab, Survival Analysis, Treatment Outcome, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Leukemia, Lymphocytic, Chronic, B-Cell drug therapy
- Abstract
In a phase II trial, we evaluated chlorambucil and rituximab (CLB-R) as first-line induction treatment with or without R as maintenance for elderly chronic lymphocytic leukemia (CLL) patients. Treatment consisted of eight 28-day cycles of CLB (8 mg/m(2) /day, days 1-7) and R (day 1 of cycle 3, 375 mg/m(2) ; cycles 4-8, 500 mg/m(2) ). Responders were randomized to 12 8-week doses of R (375 mg/m(2) ) or observation. As per intention-to-treat analysis, 82.4% (95% CI, 74.25-90.46%) of 85 patients achieved an overall response (OR), 16.5% a complete response (CR), 2.4% a CR with incomplete bone marrow recovery. The OR was similar across Binet stages (A 86.4%, B 81.6%, and C 78.6%) and age categories (60-64 years, 92.3%; 65-69, 85.2%; 70-74, 75.0%; ≥75, 81.0%). CLB-R was well tolerated. After a median follow-up of 34.2 months, the median progression-free survival (PFS) was 34.7 months (95% CI, 33.1-39.5). TP53 abnormalities, complex karyotype, and low CD20 gene expression predicted lack of response; SF3B1 mutation and BIRC3 disruption low CR rates. IGHV mutations significantly predicted PFS. R maintenance tended towards a better PFS than observation and was safe and most beneficial for patients in partial response and for unmutated IGHV cases. CLB-R represents a promising option for elderly CLL patients., (Copyright © 2014 Wiley Periodicals, Inc.)
- Published
- 2014
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