68 results on '"Poi M"'
Search Results
2. Associations of High‐Dose Melphalan Pharmacokinetics and Outcomes in the Setting of a Randomized Cryotherapy Trial
- Author
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Cho, YK, Sborov, DW, Lamprecht, M, Li, J, Wang, J, Hade, EM, Gao, Y, Tackett, K, Williams, N, Benson, DM, Efebera, YA, Rosko, AE, Devine, SM, Poi, M, Hofmeister, CC, and Phelps, MA
- Published
- 2017
- Full Text
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3. Erlotinib in African Americans With Advanced Non-Small Cell Lung Cancer: A Prospective Randomized Study With Genetic and Pharmacokinetic Analyses
- Author
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Phelps, M A, Stinchcombe, T E, Blachly, J S, Zhao, W, Schaaf, L J, Starrett, S L, Wei, L, Poi, M, Wang, D, Papp, A, Aimiuwu, J, Gao, Y, Li, J, Otterson, G A, Hicks, W J, Socinski, M A, and Villalona-Calero, M A
- Published
- 2014
- Full Text
- View/download PDF
4. Production of leading charged particles and leading charged-particle jets at small transverse momenta in pp collisions at <tex>\sqrt{s}$</tex>=8 TeV
- Author
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Khachatryan, V., Sirunyan, A. M., Tumasyan, A., Adam, W., Bergauer, T., Dragicevic, M., Eroe, J., Friedl, M., Fruehwirth, R., Ghete, V. M., Hartl, C., Hoermann, N., Hrubec, J., Jeitler, M., Kiesenhofer, W., Knuenz, V., Krammer, M., Kraetschmer, I., Liko, D., Mikulec, I., Rabady, D., Rahbaran, B., Rohringer, H., Schoefbeck, R., Strauss, J., Treberer-Treberspure, W., Waltenberger, W., Wulz, C-E., Mossolov, V., Shumeiko, N., Gonzalez, J. Suarez, Alderweireldt, Sara, Bansal, Sunil, Cornelis, Tom, de Wolf, Eddi, Janssen, Xavier, Knutsson, Albert, Lauwers, Jasper, Luyckx, Sten, Ochesanu, S., Rougny, Romain, van de Klundert, Merijn, van Haevermaet, Hans, Van Mechelen, Pierre, Van Remortel, Nick, Van Spilbeeck, Alex, Blekman, F., Blyweert, S., D'Hondt, J., Daci, N., Heracleous, N., Keaveney, J., Lowette, S., Maes, M., Olbrechts, A., Python, Q., Strom, D., Tavernier, S., Van Doninck, W., Van Mulders, P., Van Onsem, G. P., Villella, I., Caillol, C., Clerbaux, B., De Lentdecker, G., Dobur, D., Favart, L., Gay, A. P. R., Grebenyuk, A., Leonard, A., Mohammadi, A., Pernie, L., Randle-conde, A., Reis, T., Seva, T., Thomas, L., Vander Velde, C., Vanlaer, P., Wang, J., Zenoni, F., Adler, V., Beernaert, K., Benucci, L., Cimmino, A., Costantini, S., Crucy, S., Fagot, A., Garcia, G., Mccartin, J., Rios, A. A. Ocampo, Poyraz, D., Ryckbosch, D., Salva, S., Sigamani, M., Strobbe, N., Thyssen, F., Tytgat, M., Yazgan, E., Zaganidis, N., Basegmez, S., Beluffi, C., Bruno, G., Castello, R., Caudron, A., Ceard, L., Da Silveira, G. G., Delaere, C., du Pree, T., Favart, D., Forthomme, L., Giammanco, A., Hollar, J., Jafari, A., Jez, P., Komm, M., Lemaitre, V., Nuttens, C., Pagano, D., Perrini, L., Pin, A., Piotrzkowski, K. K., Popov, A., Quertenmont, L. L., Selvaggi, M., Marono, M. Vidal, Garcia, J. M. Vizan, Beliy, N., Caebergs, T., Daubie, E., Hammad, G. H., Aida Junior, W. L., Alves, G. A., Brito, L., Correa Martins Junior, M., Dos Reis Martins, T., Molina, J., Mora Herrera, C., Poi, M. E., Rebello Teles, P., Carvalho, W., Chinellato, J., Custodio, A., Da Costa, E. M., De Jesus Damiao, D., De Oliveira Martins, C., Fonseca De Souza, S., Malbouisson, H., Matos Figueiredo, D., Mundim, L., Nogima, H., Prado Da Silva, W. L., Santaolalla, J., Santoro, A., Sznajder, A., Tonelli Manganote, E. J., Vilela Pereira, A., Bernardes, C. A., Dogra, S., Fernandez Perez Tomei, T. R., Gregores, E. M., Mercadante, P. G., Novaes, S. F., Padula, Sandra S., Aleksandrov, A., Genchey, V., Hadjiiska, R., Iaydjiev, P., Marinov, A., Piperov, S., Rodozov, M., Stoykova, S., Sultanov, G., Vutova, M., Dimitrov, A., Glushkov, I., Litov, L., Pavlov, B., Petkov, P., Bian, J. G., Chen, G. M., Chen, H. S., Chen, M., Cheng, T., Du, R., Jiang, C. H., Plestina, R., Romeo, F., Tao, J., Wang, Z., Asawatangtrakuldee, C., Ban, Y., Liu, S., Mao, Y., Qian, S. J., Wang, D., Xu, Z., Zhang, F., Zhang, L., Zou, W., Avila, C., Cabrera, A., Chaparro Sierra, L. F., Florez, C., Gomez, J. P., Gomez Moreno, B., Sanabria, J. C., Godinovic, N., Lelas, D., Polic, D., Puljak, I., Antunovic, Z., Kovac, M., Brigljevic, V., Kadija, K., Luetic, J., Mekterovic, D., Sudic, L., Attikis, A., Mavromanolakis, G., Mousa, J., Nicolaou, C., Ptochos, F., Razis, P. A., Rykaczewski, H., Bodlak, M., Finger, M., Finger, M., Jr., Assran, Y., Elgammal, S., Kamel, A. Ellithi, Mahmoud, M. A., Kadastik, M., Murumaa, M., Raidal, M., Tiko, A., Eerola, P., Voutilainen, M., Haerkoenen, J., Karimaeki, V., Kinnunen, R., Kortelainen, M. J., Lampen, T., Lassila-Perini, K., Lehti, S., Linden, T., Luukka, P., Maeenpaeae, T., Peltola, T., Tuominen, E., Tuominiemi, J., Tuovinen, E., Wendland, L., Talvitie, J., Tuuva, T., Besancon, M., Couderc, F., Dejardin, M., Denegri, D., Fabbro, B., Faure, J. L., Favaro, C., Ferri, F., Ganjour, S., Givemaud, A., Gras, P., de Monchenault, G. Hamel, Jarry, P., Locci, E., Malcles, J., Rander, J., Rosowsky, A., Titov, M., Baffioni, S., Beaudette, F., Busson, P., Chapon, E., Chariot, C., Dahms, T., Dobrzyns, L., Filipovic, N., Florent, A., de Cassagnac, R. Granier, Mastrolorenzo, L., Mine, P., Naranjo, I. N., Nguyen, M., Ochando, C., Ortona, G., Paganini, P., Regnard, S., Salerno, R., Sauvan, J. B., Sirois, Y., Veelken, C., Yilmaz, Y., Zabi, A., Agram, J-L., Andrea, J., Aubin, A., Bloch, D., Brom, J-M., Chabert, E. C., Collard, C., Conte, E., Fontaine, J-C., Gele, D., Goerlach, U., Goetzmann, C., Le Bilian, A-C., Skovpen, K., Van Hove, P., Gadrat, S., Beauceron, S., Beaupere, N., Bernet, C., Boudou, G., Bouvier, E., Brochet, S., Montoya, C. A. Carrillo, Chasserat, J., Chierici, R., Contardo, D., Courbon, B., Depasse, P., El Mamouni, H., Fan, J., Fay, J., Gascon, S., Gouzevitch, M., Ille, B., Kurca, T., Lethuillier, M., Mirabito, L., Pequegnot, A. L., Perries, S., Alvarez, J. D. Ruiz, Sabes, D., Sgandurra, L., Sordini, V., Vander Donckt, M., Verdier, P., Viret, S., Xiao, H., Tsamalaidze, Z., Autermann, C., Beranek, S., Bontenackels, M., Edelhoff, M., Feld, L., Heister, A., Klein, K., Lipinski, M., Ostapchuk, A., Preuten, M., Raupach, F., Sammet, J., Schael, S., Schulte, J. F., Weber, H., Wittmer, B., Zhukov, V., Ata, M., Brodski, M., Dietz-Laursonn, E., Duchardt, D., Erdmann, M., Fischer, R., Gueth, A., Hebbeker, T., Heidemann, C., Hoepfner, K., Klingebiel, D., Knutzen, S., Kreuzer, P., Merschmeyer, M., Meyer, A., Millet, P., Olschewski, M., Padeken, K., Papacz, P., Reithler, H., Schmitz, S. A., Sonnenschein, L., Teyssier, D., Thueer, S., Cherepanov, V., Erdogan, Y., Fluegge, G., Geenen, H., Geisler, M., Ahmad, W. Haj, Hoehle, F., Kargoll, B., Kress, T., Kuessel, Y., Kuensken, A., Lingemann, J., Nowack, A., Nugent, I. M., Pistone, C., Pooth, O., Stahl, A., Martin, M. Aldaya, Asin, I., Bartosik, N., Behr, J., Behrens, U., Bell, A. J., Bethani, A., Borras, K., Burgmeier, A., Cakir, A., Calligaris, L., Campbell, A., Choudhury, S., Costanza, F., Pardos, C. Diez, Dolinska, G., Dooling, S., Dorland, T., Eckerlin, G., Eckstein, D., Eichhorn, T., Flucke, G., Garcia, J. Garay, Geiser, A., Gizhko, A., Gunnellini, P., Hauk, J., Hempel, M., Jung, H. H., Kalogeropoulos, A., Karacheban, O., Kasemann, M., Katsas, P., Kieseler, J., Kleinwort, C., Korol, I., Kruecker, D., Lange, W., Leonard, J., Lipka, K., Lobanov, A., Lohmann, W., Lutz, B., Mankel, R., Marfin, I., Melzer-Pellmann, I-A., Meyer, A. B., Mittag, G., Mnich, J., Mussgiller, A., Naumann-Emme, S., Nayak, A., Ntomari, E., Perrey, H., Pitzl, D., Placakyte, R., Raspereza, A., Cipriano, P. M. Ribeiro, Roland, B., Ron, E., Sahin, M. Oe., Salfeld-Nebgen, J., Saxena, P., Schoerner-Sadenius, T., Schroeder, M., Seitz, C., Spannage, S., Trevino, A. D. R. Vargas, Walsh, R., Wissing, C., Blobel, V., Vignali, M. Centis, Draeger, A. R., Erfle, J., Garutti, E., Goebel, K., Goerner, M., Haller, J., Hoffmann, M., Hoeing, R. S., Junkes, A., Kirschenmann, H., Klanner, R., Kogler, R., Lapsien, T., Lenz, T., Marchesini, I., Marconi, D., Ott, J., Peiffer, T., Perieanu, A., Pietsch, N., Poehlsen, J., Poehlsen, T., Rathjens, D., Sander, C., Schettler, H., Schleper, P., Schlieckau, E., Schmidt, A., Seidel, M., Sola, V., Stadie, H., Steinbrueck, G., Troendle, D., Usai, E., Vanelderen, L., Vanhoefer, A., Barth, C., Baus, C., Berger, J., Boeser, C., Butz, E., Chwalek, T., De Boer, W., Descroix, A., Dierlamm, A., Feindt, M., Frensch, F., Giffels, M., Gilbert, A., Hartmann, F., Hauth, T., Husenciann, U., Katkov, I., Kornnriayer, A., Pardo, P. Lobelle, Mozer, M. U., Mueller, T., Mueller, Th., Nuernberg, A., Quast, G., Rabbertz, K., Roecker, S., Simonis, H. J., Stober, F. M., Ulrich, R., Wagner-Kuhr, J., Wayand, S., Weiler, T., Wolf, R., Anagnostou, G., Daskalakis, G., Geralis, T., Giakoumopoulou, V. A., Kyriakis, A., Loukas, D., Markou, A., Markou, C., Psallidas, A., Topsis-Giotis, I., Agapitos, A., Kesisoglou, S., Panagiotou, A., Saoulidou, N., Stiliaris, E., Tziaferi, E., Aslanoglou, X., Evangelou, I., Flouris, G., Foudas, C., Kokkas, P., Manthos, N., Papadopoulos, I., Paradas, E., Strologas, J., Bencze, G., Hajdu, C., Hidas, P., Horvath, D., Sikler, F. F., Veszpremi, V., Vesztergombi, G., Zsigmond, A. J., Beni, N., Czellar, S., Karancsi, J., Molnar, J., Palinkas, J., Szillasi, Z., Makovec, A., Raics, P., Trocsanyi, Z. L., Ujvari, B., Swain, S. K., Beri, S. B., Bhatnagar, V., Gupta, R., Bhawandeep, U., Kalsi, A. K., Kaur, M., Kumar, R., Mitta, M., Nishu, N., Singh, J. B., Kumar, Ashok, Kumar, Arun, Ahuja, S., Bhardwaj, A., Choudhary, B. C., Kumar, A., Malhotra, S., Naimuddin, M., Ranjan, K., Sharma, V., Banerjee, S., Bhattacharya, S., Chatterjee, K., Dutta, S., Gomber, B., Jam, Sa, Jain, Sh, Khurana, R., Modak, A., Mukherjee, S., Roy, D., Sarkar, S., Sharan, M., Abdulsalam, A., Dutta, D., Kumar, V., Mohanty, A. K., Pant, L. M., Shukla, P., Topkar, A., Aziz, T., Bhowmik, S., Chatterjee, R. M., Dewanjee, R. K., Dugad, S., Ganguly, S., Ghosh, S., Guchait, M., Gurtu, A., Kole, G., Kumar, S., Maity, M., Majumder, G., Mazumdar, K., Mohanty, G. B., Parida, B., Sudhakar, K., Wickramage, N., Sharma, S., Bakhshiansohi, H., Behnamian, H., Etesami, S. M., Fahim, A., Goldouzian, R., Khakzad, M., Najafabadi, M. Mohammadi, Naseri, M., Mehdiabadi, S. Paktinat, Hosseinabadi, F. Rezaei, Safarzadeh, B., Zeinali, M., Felcini, M., Grunewald, M., Abbrescia, M., Calabria, C., Chhibra, S. S., Colaleo, A., Creanza, D., Cristella, L., De Filippis, N., De Palma, M., Fiore, L., Iaselli, G., Maggi, G., Maggi, M., My, S., Nuzzo, S., Pompili, A., Pugliese, G., Radogna, R., Selvaggi, G., Sharma, A., Silvestris, L., Venditti, R., Verwilligen, P., Abbiendi, G., Benvenuti, A. C., Bonacorsi, D., Braibant-Giacomelli, S., Brigliadori, L., Campanini, R., Capiluppi, P., Castro, A., Cavallo, F. R., Codispoti, G., Cuffiani, M., Dallavalle, G. M., Fabbri, F., Fanfani, A., Fasanella, D., Giacomelli, P., Grandi, C., Guiducci, L., Marcellini, S., Masetti, G., Montanari, A., Navarria, F. L., Perrotta, A., Rossi, A. M., Rovelli, T., Siroli, G. P., Tosi, N., Travaglini, R., Albergo, S., Cappello, G., Chiorboli, M., Costa, S., Giordano, F., Potenza, R., Tricomi, A., Tuve, C., Barbagli, G., Ciulli, V., Civinini, C., D'Alessandro, R., Focardi, E., Gallo, E., Gonzi, S., Gori, V., Lenzi, P., Meschini, M., Paoletti, S., Sguazzoni, G., Tropiano, A., Benussi, L., Bianco, S., Piccolo, D., Ferretti, R., Ferro, F., Lo Vetere, M., Robutti, E., Tosi, S., Dinardo, M. E., Fiorendi, S., Gennai, S., Gerosa, R., Ghezzi, A., Govoni, P., Lucchini, M. T., Malvezzi, S., Manzoni, R. A., Martelli, A., Marzocchi, B., Menasce, D., Moroni, L., Paganoni, M., Pedrini, D., Ragazzi, S., Redaelli, N., de Fatis, T. Tabarelli, Buontempo, S., Cavallo, N., Di Guida, S., Fabozzi, F., Iorio, A. O. M., Lista, L., Meola, S., Merola, M., Paolucci, P., Azzi, P., Bacchetta, N., Bellato, M., Dall'Osso, M., Dorigo, T., Fantinel, S., Gonella, F., Gozzelino, A., Gulmini, M., Lacaprara, S., Margoni, M., Meneguzzo, A. T., Montecassiano, F., Pazzini, J., Pegoraro, M., Pozzobon, N., Ronchese, P., Sgaravatto, M., Simonetto, F., Torassa, E., Tosi, M., Vanini, S., Ventura, S., Zotto, P., Zucchetta, A., Gabusi, M., Ratti, S. P., Re, V., Riccardi, C., Salvini, P., Vitulo, P., Biasini, M., Bilei, G. M., Ciangottini, D., Fano, L., Lariccia, P., Mantovani, G., Menichelli, M., Saha, A., Santocchia, A., Spiezia, A., Androsov, K., Azzurri, P., Bagliesi, G., Bernardini, J., Boccali, T., Broccolo, G., Castaldi, R., Cioccia, M. A., Dell'Orso, R., Donato, S., Fedi, G., Fiori, F., Foa, L., Giassi, A., Grippo, M. T., Ligabue, F., Lomtadze, T., Martini, L., Messineo, A., Moon, C. S., Palla, F., Rizzi, A., Savoy-Navarro, A., Serban, A. T., Spagnolo, P., Squillacioti, P., Tenchini, R., Tonelli, G., Venturi, A., Verdini, P. G., Vernieri, C., Barone, L., Cavallari, F., D'imperio, G., Del Re, D., Diemoz, M., Joida, C., Longo, E., Margaroli, F., Meridiani, P., Micheli, F., Organtini, G., Paramatti, R., Rahatlou, S., Rovelli, C., Santanastasio, F., Soffi, L., Traczyk, P., Amapane, N., Arcidiacono, R., Argiro, S., Arneodo, M., Bellan, R., Biina, C., Cartiglia, N., Casasso, S., Costa, M., Covarelli, R., Dattola, D., Degano, A., Demaria, N., Finco, L., Mariotti, C., Maselli, S., Migliore, E., Monaco, V., Musich, M., Obertino, M. M., Pacher, L., Pastrone, N., Pelliccioni, M., Angioni, G. L. Pinna, Romero, A., Ruspa, M., Sacchi, R., Solano, A., Staiano, A., Tamponi, U., Belforte, S., Candelise, V., Casarsa, M., Cossutti, F., Della Ricca, G., Gobbo, B., La Licata, C., Marone, M., Schizzi, A., Umer, T., Zanetti, A., Chang, S., Kropivnitskaya, A., Nam, S. K., Kim, D. H., Kim, G. N., Kim, M. S., Kong, D. J., Lee, S., Oh, Y. D., Park, H., Sakharov, A., Son, D. C., Kim, T. J., Ryu, M. S., Kim, J. Y., Moon, D. H., Song, S., Choi, S., Gyun, D., Hong, B., Kim, H., Kim, Y., Lee, B., Lee, K. S., Park, S. K., Roh, Y., Yoo, H. D., Choi, M., Kim, J. H., Park, I. C., Ryu, G., Choi, Y., Choi, Y. K., Goh, J., Kim, D., Kwon, E., Lee, J., Yu, I., Juodagalvis, A., Komaragiri, J. R., Ali, M. A. B. Md, Abdullah, W. A. T. Wan, Linares, E. Casimiro, Castilla-Valdez, H., De La Cruz-Burelo, E., Heredia-de La Cruz, I., Hernandez-Almada, A., Lopez-Fernandez, R., Sanchez-Hernandez, A., Moreno, S. Carrillo, Valencia, F. Vazquez, Pedraza, I., Ibarguen, H. A. Salazar, Pineda, A. Morelos, Krofcheck, D., Butler, P. H., Reucroft, S., Ahmad, A., Ahmad, M., Hassan, Q., Hoorani, H. R., Khan, W. A., Khurshid, T., Shoaib, M., Bialkowska, H., Bluj, M., Boimska, B., Frueboes, T., Gorski, M., Kazana, M., Nawrocki, K., Romanowska-Rybinska, K., Szleper, M., Zalewski, P., Brona, G., Bunkowski, K., Cwiok, M., Dominik, W., Doroba, K., Kalinowski, A., Konecki, M., Krolikowski, J., Misiura, M., Olszewski, M., Bargassa, P., Beirao Da Cruz E Silva, C., Faccioli, P., Ferreira Parracho, P. G., Gallinaro, M., Lloret Iglesias, L., Nguyen, F., Rodrigues Antunes, J., Seixas, J., Varela, J., Vischia, P., Afanasiev, S., Bunin, P., Gavrilenko, M., Golutvin, I., Gorbunov, I., Kamenev, A., Karjavin, V., Konoplyanikov, V., Laney, A., Malakhov, A., Matveev, V., Moisenz, P., Palichik, V., Perelygin, V., Shmatov, S., Skatchkov, N., Smirnov, V., Zarubin, A., Golovtsov, V., Ivanov, Y., Kim, V., Kuznetsova, E., Levchenko, P., Murzin, V., Oreshkin, V., Smirnov, I., Sulimov, V., Uvarov, L., Vavilov, S., Vorobyev, A., Vorobyev, An., Andreev, Yu., Dermenev, A., Gninenko, S., Golubev, N., Kirsanov, M., Krasnikov, N., Pashenkov, A., Tlisov, D., Toropin, A., Epshteyn, V., Gavrilov, V., Lychkovskaya, N., Popov, V., Pozdnyakov, I., Safronov, G., Semenov, S., Spiridonov, A., Stolin, V., Vlasov, E., Zhokin, A., Andreev, V., Azarkin, M., Dremin, I., Kirakosyan, M., Leonidov, A., Mesyats, G., Rusakov, S. V., Vinogradov, A., Belyaev, A., Boos, E., Ershov, A., Gribushin, A., Khein, L., Klyukhin, V., Kodolova, O., Lokhtin, I., Lukina, O., Obraztsov, S., Petrushanko, S., Savrin, V., Snigirev, A., Azhgirey, I., Bayshev, I., Bitioukov, S., Kachanov, V., Kalinin, A., Konstantinov, D., Krychkine, V., Petrov, V., Ryutin, R., Sobo, A., Tourtchanovitch, L., Troshin, S., Tyurin, N., Uzunian, A., Volkov, A., Adzic, P., Ekmedzic, M., Milosevic, J., Rekovic, V., Alcaraz Maestre, J., Battilana, C., Calvo, E., Cerrada, M., Chamizo Llatas, M., Colino, N., De La Cruz, B., Delgado Peris, A., Dominguez Vazquez, D., Escalante Del Valle, A., Fernandez Bedoya, C., Fernandez Ramos, J. P., Flix, J., Fouz, M. C., Garcia-Abia, P., Gonzalez Lopez, O., Goy Lopez, S., Hernandez, J. M., Josa, M. I., Navarro De Martino, E., Perez-Calero Yzquierdo, A., Puerta Pelayo, J., Quintario Olmeda, A., Redondo, I., Romero, L., Soares, M. S., Albajar, C., de Troconiz, J. F., Missiroli, M., Moran, D., Brun, H., Cuevas, J., Fernandez Menendez, J., Folgueras, S., Gonzalez Caballero, I., Brochero Cifuentes, J. A., Cabrillo, I. J., Calderon, A., Duarte Campderros, J., Fernandez, M., Gomez, G., Graziano, A., Lopez Virto, A., Marco, J., Marco, R., Martinez Riven, C., Matorras, F., Munoz Sanchez, F. J., Piedra Gomez, J., Rodrigo, T., Rodriguez-Marrero, A. Y., Ruiz-Jimeno, A., Scodellaro, L., Vila, I., Vilar Cortabitarte, R., Abbaneo, D., Auffray, E., Auzinger, G., Bachtis, M., Baillon, P., Ball, A. H., Barney, D., Benaglia, A., Bendavid, J., Benhabib, L., Benitez, J. F., Bianchi, G., Bloch, P., Bocci, A., Bonato, A., Bondu, O., Botta, C., Breuker, H., Camporesi, T., Cerminara, G., Colafranceschi, S., D'Alfonso, M., d'Enterria, D., Dabrowski, A., David, A., De Guio, F., De Roeck, A., De Visscher, S., Di Marco, E., Dobson, M., Dordevic, M., Dorney, B., Dupont, N., Elliott-Peisert, A., Eugster, J., Franzoni, G., Funk, W., Gigi, D., Gill, K., Giordano, D., Girone, M., Glege, F., Guida, R., Gundacker, S., Guthoff, M., Hammer, J., Hansen, M., Harris, P., Hegeman, J., Innocente, V., Janot, P., Kousouris, K., Krajczar, K., Lecoq, P., Lourenco, C., Magini, N., Malgeri, L., Mannelli, M., Marrouche, J., Masetti, L., Meijers, F., Mersi, S., Meschi, E., Moortgat, F., Morovic, S., Mulders, M., Orfanelli, S., Orsini, L., Pape, L., Perez, E., Petrilli, A., Petrucciani, G., Pfeiffer, A., Pimilae, M., Piparo, D., Plagge, M., Racz, A., Rolandi, G., Rovere, M., Sakulin, H., Schaefer, C., Schwick, C., Siegrist, P., Silva, P., Simon, M., Sphicas, P., Spiga, D., Steggemann, J., Stieger, B., Stoye, M., Takahashi, Y., Treille, D., Tsirou, A., Veres, G. 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A., Akchurin, N., Cowden, C., Damgov, J., Dragoiu, C., Dudero, P. R., Faulkner, J., Kovitanggoon, K., Kunori, S., Lee, S. W., Libeiro, T., Volobouev, I., Appelt, E., Delannoy, A. G., Greene, S., Gurrola, A., Johns, W., Maguire, C., Melo, A., Sharma, M., Sheldon, P., Snook, B., Tuo, S., Velkovska, J., Arenton, M. W., Boutle, S., Cox, B., Francis, B., Goodell, J., Hirosky, R., Ledovskoy, A., Li, H., Lin, C., Neu, C., Wolfe, E., Wood, J., Clarke, C., Harr, R., Karchin, P. E., Don, C. Kottachchi Kankanamge, Lamichhane, P., Sturdy, J., Belknap, D. A., Carlsmith, D., Cepeda, M., Dasu, S., Dodd, L., Duric, S., Friis, E., Hall-Wilton, R., Herndon, M., Herve, A., Klabbers, P., Lanaro, A., Lazaridis, C., Levine, A., Loveless, R., Mohapatra, A., Ojalvo, I., Perry, T., Pierro, G. A., Polese, G., Ross, I., Sarangi, T., Savin, A., Smith, W. H., Taylor, D., Vuosalo, C., Woods, N., and CMS Collaboration
- Subjects
Physics ,High Energy Physics::Phenomenology ,High Energy Physics::Experiment ,Nuclear Experiment - Abstract
The per-event yield of the highest transverse momentum charged particle and charged-particle jet, integrated above a given p(T)(min) threshold starting at p(T)(min) = 0.8 and 1 GeV, respectively, is studied in pp collisions at root s = 8 TeV. The particles and the jets are measured in the pseudorapidity ranges vertical bar n vertical bar < 2.4 and 1.9, respectively. The data are sensitive to the momentum scale at which parton densities saturate in the proton, to multiple partonic interactions, and to other key aspects of the transition between the soft and hard QCD regimes in hadronic collisions.
- Published
- 2015
5. Production of leading charged particles and leading charged-particle jets at small transverse momenta in pp collisions at root s=8 TeV
- Author
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Khachatryan, V., Sirunyan, A. M., Tumasyan, A., Adam, W., Bergauer, T., Dragicevic, M., Eroe, J., Friedl, M., Fruehwirth, R., Ghete, V. M., Hartl, C., Hoermann, N., Hrubec, J., Jeitler, M., Kiesenhofer, W., Knuenz, V., Krammer, M., Kraetschmer, I., Liko, D., Mikulec, I., Rabady, D., Rahbaran, B., Rohringer, H., Schoefbeck, R., Strauss, J., Treberer Treberspure, W., Waltenberger, W., Wulz, C. E., Mossolov, V., Shumeiko, N., Gonzalez, J. Suarez, Alderweireldt, S., Bansal, S., Cornelis, T., De Wolf, E. A., Janssen, X., Knutsson, A., Lauwers, J., Luyckx, S., Ochesanu, S., Rougny, R., Van de Klundert, M., Van Haevermaet, H., Van Mechelen, P., Van Remortel, N., Van Spilbeeck, A., Blekman, F., Blyweert, S., D'Hondt, J., Daci, N., Heracleous, N., Keaveney, J., Lowette, S., Maes, M., Olbrechts, A., Python, Q., Strom, D., Tavernier, S., Van Doninck, W., Van Mulders, P., Van Onsem, G. P., Villella, I., Caillol, C., Clerbaux, B., De Lentdecker, G., Dobur, D., Favart, L., Gay, A. P. R., Grebenyuk, A., Leonard, A., Mohammadi, A., Pernie, L., Randle conde, A., Reis, T., Seva, T., Thomas, L., Vander Velde, C., Vanlaer, P., Wang, J., Zenoni, F., Adler, V., Beernaert, K., Benucci, L., Cimmino, A., Costantini, S., Crucy, S., Fagot, A., Garcia, G., Mccartin, J., Rios, A. A. Ocampo, Poyraz, D., Ryckbosch, D., Salva, S., Sigamani, M., Strobbe, N., Thyssen, F., Tytgat, M., Yazgan, E., Zaganidis, N., Basegmez, S., Beluffi, C., Bruno, G., Castello, R., Caudron, A., Ceard, L., Da Silveira, G. G., Delaere, C., du Pree, T., Favart, D., Forthomme, L., Giammanco, A., Hollar, J., Jafari, A., Jez, P., Komm, M., Lemaitre, V., Nuttens, C., Pagano, D., Perrini, L., Pin, A., Piotrzkowski, K. K., Popov, A., Quertenmont, L. L., Selvaggi, M., Marono, M. Vidal, Garcia, J. M. Vizan, Beliy, N., Caebergs, T., Daubie, E., Hammad, G. H., Aida Junior, W. L., Alves, G. A., Brito, L., Correa Martins Junior, M., Dos Reis Martins, T., Molina, J., Mora Herrera, C., Poi, M. 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PHYSICS ,MODEL ,Astrophysics::High Energy Astrophysical Phenomena ,FISICA DELLE PARTICELLE ,High Energy Physics::Phenomenology ,QCD ,High Energy Physics::Experiment ,Nuclear Experiment - Abstract
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No. of bitstreams: 0 Previous issue date: 2015-12-01 BMWFW (Austria) FWF (Austria) FNRS (Belgium) FWO (Belgium) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) MES (Bulgaria) CERN (China) CAS (China) MoST (China) NSFC (China) COLCIENCIAS (Colombia) MSES (Croatia) CSF (Croatia) RPF (Cyprus) MoER (Estonia) ERC IUT (Estonia) ERDF (Estonia) Academy of Finland (Finland) MEC (Finland) HIP (Finland) CEA (France) CNRS/IN2P3 (France) BMBF (Germany) DFG (Germany) HGF (Germany) GSRT (Greece) OTKA (Hungary) NIH (Hungary) DAE (India) DST (India) IPM (Iran) SFI (Ireland) INFN (Italy) MSIP (Republic of Korea) NRF (Republic of Korea) LAS (Lithuania) MOE (Malaysia) UM (Malaysia) CINVESTAV (Mexico) CONACYT (Mexico) SEP (Mexico) UASLP-FAI (Mexico) MBIE (New Zealand) PAEC (Pakistan) MSHE (Poland) NSC (Poland) FCT (Portugal) JINR (Dubna) MON (Russia) RosAtom (Russia) RAS (Russia) RFBR (Russia) MESTD (Serbia) SEIDI (Spain) CPAN (Spain) Swiss Funding Agencies (Switzerland) MST (Taipei) ThEPCenter (Thailand) IPST (Thailand) STAR (Thailand) NSTDA (Thailand) TUBITAK (Turkey) TAEK (Turkey) NASU (Ukraine) SFFR (Ukraine) STFC (United Kingdom) DOE (USA) NSF (USA) Marie-Curie program European Research Council (European Union) EPLANET (European Union) Leventis Foundation A. P. Sloan Foundation Alexander von Humboldt Foundation Belgian Federal Science Policy Office Fonds pour la Formation a la Recherche dans l'Industrie et dans l'Agriculture (FRIA-Belgium) Agentschap voor Innovatie door Wetenschap en Technologie (IWT-Belgium) Ministry of Education, Youth and Sports (MEYS) of the Czech Republic Council of Science and Industrial Research, India HOMING PLUS program of the Foundation for Polish Science European Union, Regional Development Fund Compagnia di San Paolo (Torino) Consorzio per la Fisica (Trieste) MIUR (Italy) Thalis program Aristeia program EU-ESF Greek NSRF National Priorities Research Program by Qatar National Research Fund Rachadapisek Sompot Fund for Postdoctoral Fellowship, Chulalongkorn University (Thailand) Science and Technology Facilities Council The per-event yield of the highest transverse momentum charged particle and charged-particle jet, integrated above a given p(T)(min) threshold starting at p(T)(min) = 0.8 and 1 GeV, respectively, is studied in pp collisions at root s = 8 TeV. The particles and the jets are measured in the pseudorapidity ranges vertical bar n vertical bar < 2.4 and 1.9, respectively. The data are sensitive to the momentum scale at which parton densities saturate in the proton, to multiple partonic interactions, and to other key aspects of the transition between the soft and hard QCD regimes in hadronic collisions. Yerevan Phys Inst, Yerevan 375036, Armenia Inst Hochenergiephys OeAW, Vienna, Austria Nat Ctr Particle & High Energy Phys, Minsk, Byelarus Univ Antwerp, B-2020 Antwerp, Belgium Vrije Univ Brussel, Brussels, Belgium Univ Libre Bruxelles, Brussels, Belgium Univ Ghent, B-9000 Ghent, Belgium Catholic Univ Louvain, Louvain La Neuve, Belgium Univ Mons, B-7000 Mons, Belgium Ctr Brasileiro Pesquisas Fis, Rio De Janeiro, Brazil Univ Estado Rio de Janeiro, BR-20550011 Rio De Janeiro, Brazil Univ Estadual Paulista, Sao Paulo, Brazil Univ Fed ABC, Sao Paulo, Brazil Bulgarian Acad Sci, Inst Nucl Res & Nucl Energy, Sofia, Bulgaria Univ Sofia, BU-1126 Sofia, Bulgaria Inst High Energy Phys, Beijing 100039, Peoples R China Peking Univ, State Key Lab Nucl Phys & Technol, Beijing 100871, Peoples R China Univ Los Andes, Bogota, Colombia Univ Split, Fac Elect Engn Mech Engn & Naval Architecture, Split, Croatia Univ Split, Fac Sci, Split, Croatia Rudjer Boskovic Inst, Zagreb, Croatia Univ Cyprus, CY-1678 Nicosia, Cyprus Charles Univ Prague, Prague, Czech Republic Egyptian Network High Energy Phys, Acad Sci Res & Technol Arab Republ Egypt, Cairo, Egypt NICPB, Tallinn, Estonia Univ Helsinki, Dept Phys, Helsinki, Finland Helsinki Inst Phys, Helsinki, Finland Lappeenranta Univ Technol, Lappeenranta, Finland CEA Saclay, DSM IRFU, F-91191 Gif Sur Yvette, France Ecole Polytech, CNRS, Lab Leprince Ringuet, IN2P3, F-91128 Palaiseau, France Univ Haute Alsace Mulhouse, Inst Pluridisciplinaire Hubert Curien, Univ Strasbourg, CNRS,IN2P3, Strasbourg, France CNRS, Ctr Calcul, Inst Natl Phys Nucl & Phys Particules, IN2P3, Villeurbanne, France Univ Lyon 1, CNRS, IN2P3, Inst Phys Nucl Lyon, F-69622 Villeurbanne, France Tbilisi State Univ, Inst High Energy Phys & Informatizat, GE-380086 Tbilisi, Rep of Georgia Rhein Westfal TH Aachen, Phys Inst 1, Aachen, Germany Rhein Westfal TH Aachen, Phys Inst A 3, Aachen, Germany Rhein Westfal TH Aachen, Phys Inst B 3, Aachen, Germany DESY, Hamburg, Germany Univ Hamburg, Hamburg, Germany Univ Karlsruhe, Inst Expt Kernphys, Karlsruhe, Germany NCSR Demokritos, INPP, Aghia Paraskevi, Greece Univ Athens, Athens, Greece Univ Ioannina, GR-45110 Ioannina, Greece Wigner Res Ctr Phys, Budapest, Hungary Inst Nucl Res ATOMKI, Debrecen, Hungary Univ Debrecen, Debrecen, Hungary Natl Inst Sci Educ & Res, Bhubaneswar, Orissa, India Panjab Univ, Chandigarh 160014, India Univ Delhi, Delhi 110007, India Saha Inst Nucl Phys, Kolkata, India Bhabha Atom Res Ctr, Bombay 400085, Maharashtra, India Tata Inst Fundamental Res, Bombay 400005, Maharashtra, India IISER, Pune, Maharashtra, India Inst Res Fundamental Sci IPM, Tehran, Iran Univ Coll Dublin, Dublin 2, Ireland Ist Nazl Fis Nucl, Sez Bari, I-70126 Bari, Italy Univ Bari, Bari, Italy Politecn Bari, Bari, Italy Ist Nazl Fis Nucl, Sez Bologna, I-40126 Bologna, Italy Univ Bologna, Bologna, Italy Ist Nazl Fis Nucl, Sez Catania, I-95129 Catania, Italy Univ Catania, Catania, Italy CSFNSM, Catania, Italy Ist Nazl Fis Nucl, Sez Firenze, I-50125 Florence, Italy Univ Florence, Florence, Italy Ist Nazl Fis Nucl, Lab Nazl Frascati, I-00044 Frascati, Italy Ist Nazl Fis Nucl, Sez Genova, I-16146 Genoa, Italy Univ Genoa, Genoa, Italy Ist Nazl Fis Nucl, Sez Milano Bicocca, I-20133 Milan, Italy Univ Milano Bicocca, Milan, Italy Ist Nazl Fis Nucl, Sez Napoli, I-80125 Naples, Italy Univ Naples Federico II, Naples, Italy Univ Basilicata, I-85100 Potenza, Italy Univ G Marconi, Rome, Italy Ist Nazl Fis Nucl, Sez Padova, Padua, Italy Univ Padua, Padua, Italy Univ Trento, Trento, Italy Ist Nazl Fis Nucl, Sez Pavia, I-27100 Pavia, Italy Univ Pavia, I-27100 Pavia, Italy Ist Nazl Fis Nucl, Sez Perugia, I-06100 Perugia, Italy Univ Perugia, I-06100 Perugia, Italy Ist Nazl Fis Nucl, Sez Pisa, Pisa, Italy Univ Pisa, Pisa, Italy Scuola Normale Super Pisa, Pisa, Italy Ist Nazl Fis Nucl, Sez Roma, Rome, Italy Univ Rome, Rome, Italy Ist Nazl Fis Nucl, Sez Torino, I-10125 Turin, Italy Univ Turin, Turin, Italy Univ Piemonte Orientate, Novara, Italy Ist Nazl Fis Nucl, Sez Trieste, Trieste, Italy Univ Trieste, Trieste, Italy Kangwon Natl Univ, Chunchon, South Korea Kyungpook Natl Univ, Taegu, South Korea Chonbuk Natl Univ, Jeonju 561756, South Korea Chonnam Natl Univ, Inst Universe & Elementary Particles, Kwangju, South Korea Korea Univ, Seoul, South Korea Seoul Natl Univ, Seoul, South Korea Univ Seoul, Seoul, South Korea Sungkyunkwan Univ, Suwon, South Korea Vilnius State Univ, Vilnius, Lithuania Univ Malaya, Natl Ctr Particle Phys, Kuala Lumpur, Malaysia IPN, Ctr Invest Estudios Avanzados, Mexico City 07738, DF, Mexico Univ Iberoamer, Mexico City, DF, Mexico Benemerita Univ Autonoma Puebla, Puebla, Mexico Univ Autonoma San Luis Potosi, San Luis Potosi, Mexico Univ Auckland, Auckland 1, New Zealand Univ Canterbury, Christchurch 1, New Zealand Quaid I Azam Univ, Natl Ctr Phys, Islamabad, Pakistan Natl Ctr Nucl Res, Otwock, Poland Univ Warsaw, Inst Expt Phys, Fac Phys, Warsaw, Poland Lab Instrumentacao & Fis Expt Particulas, Lisbon, Portugal Joint Inst Nucl Res, Dubna, Russia Petersburg Nucl Phys Inst, St Petersburg, Russia Russian Acad Sci, Inst Nucl Res, Moscow 117312, Russia Inst Theoret & Expt Phys, Moscow 117259, Russia PN Lebedev Phys Inst, Moscow 117924, Russia Moscow MV Lomonosov State Univ, Skobeltsyn Inst Nucl Phys, Moscow, Russia Inst High Energy Phys, State Res Ctr Russian Federat, Protvino, Russia Univ Belgrade, Fac Phys, Belgrade 11001, Serbia Vinca Inst Nucl Sci, Belgrade, Serbia CIEMAT, Madrid, Spain Univ Autonoma Madrid, Madrid, Spain Univ Oviedo, Oviedo, Spain Univ Cantabria, CSIC, Inst Fis Cantabria IFCA, E-39005 Santander, Spain CERN, European Org Nucl Res, CH-1211 Geneva, Switzerland Paul Scherrer Inst, Villigen, Switzerland ETH, Inst Particle Phys, Zurich, Switzerland Univ Zurich, Zurich, Switzerland Natl Cent Univ, Chungli 32054, Taiwan NTU, Taipei, Taiwan Chulalongkorn Univ, Fac Sci, Dept Phys, Bangkok, Thailand Cukurova Univ, Adana, Turkey Middle E Tech Univ, Dept Phys, TR-06531 Ankara, Turkey Bogazici Univ, Istanbul, Turkey Istanbul Tech Univ, TR-80626 Istanbul, Turkey Kharkov Inst Phys & Technol, Natl Sci Ctr, Kharkov, Ukraine Univ Bristol, Bristol, Avon, England Rutherford Appleton Lab, Didcot OX11 0QX, Oxon, England Univ London Imperial Coll Sci Technol & Med, London, England Brunel Univ, Uxbridge UB8 3PH, Middx, England Baylor Univ, Waco, TX 76798 USA Univ Alabama, Tuscaloosa, AL USA Boston Univ, Boston, MA 02215 USA Brown Univ, Providence, RI 02912 USA Univ Calif Davis, Davis, CA 95616 USA Univ Calif Los Angeles, Los Angeles, CA USA Univ Calif Riverside, Riverside, CA 92521 USA Univ Calif San Diego, La Jolla, CA 92093 USA Univ Calif Santa Barbara, Santa Barbara, CA 93106 USA CALTECH, Pasadena, CA 91125 USA Carnegie Mellon Univ, Pittsburgh, PA 15213 USA Univ Colorado, Boulder, CO 80309 USA Cornell Univ, Ithaca, NY USA Fairfield Univ, Fairfield, CT 06430 USA Fermilab Natl Accelerator Lab, Batavia, IL 60510 USA Univ Florida, Gainesville, FL 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Piscataway, NJ USA Univ Tennessee, Knoxville, TN USA Texas A&M Univ, College Stn, TX USA Texas Tech Univ, Lubbock, TX 79409 USA Vanderbilt Univ, Nashville, TN 37235 USA Univ Virginia, Charlottesville, VA USA Wayne State Univ, Detroit, MI USA Univ Wisconsin, Madison, WI 53706 USA Vienna Univ Technol, A-1040 Vienna, Austria Univ Estadual Campinas, Campinas, SP, Brazil Suez Univ, Suez, Egypt British Univ Egypt, Cairo, Egypt Cairo Univ, Cairo, Egypt Fayoum Univ, Al Fayyum, Egypt Univ Haute Alsace, Mulhouse, France Brandenburg Tech Univ Cottbus, Cottbus, Germany Eotvos Lorand Univ, Budapest, Hungary Visva Bharati Univ, Santini Ketan, W Bengal, India King Abdulaziz Univ, Jeddah 21413, Saudi Arabia Univ Ruhuna, Matara, Sri Lanka Isfahan Univ Technol, Esfahan, Iran Univ Tehran, Dept Engn Sci, Tehran, Iran Islamic Azad Univ, Sci & Res Branch, Plasma Phys Res Ctr, Tehran, Iran Ist Nazl Fis Nucl, Lab Nazl Legnaro, I-35020 Legnaro, Italy Univ Siena, I-53100 Siena, Italy IN2P3, CNRS, Paris, France Int Islamic Univ Malaysia, Kuala Lumpur, Malaysia St Petersburg State Polytech Univ, St Petersburg, VA, Russia Natl Res Nucl Univ Moscow Engn Phys Inst MEPhI, Moscow, Russia Univ Rome, Fac Ingn, Rome, Italy Sezione Ist Nazl Fis Nucl, Pisa, Italy Albert Einstein Ctr Fundamental Phys, Bern, Switzerland Gaziosmanpasa Univ, Tokat, Turkey Adiyam Univ, Adiyaman, Turkey Mersin Univ, Mersin, Turkey Cag Univ, Mersin, Turkey Piri Reis Univ, Istanbul, Turkey Anadolu Univ, Eskisehir, Turkey Ozyegin Univ, Istanbul, Turkey Izmir Inst Technol, Izmir, Turkey Necmettin Erbakan Univ, Konya, Turkey Mimar Sinan Univ, Istanbul, Istanbul, Turkey Marmara Univ, Istanbul, Turkey Kafkas Univ, Kars, Turkey Yildiz Tech Univ, Istanbul, Turkey Univ Southampton, Sch Phys & Astron, Southampton, Hants, England Argonne Natl Lab, Argonne, IL 60439 USA Erzincan Univ, Erzincan, Turkey Texas A&M Univ Qatar, Doha, Qatar Univ Estadual Paulista, Sao Paulo, Brazil MIUR (Italy): 20108T4XTM Science and Technology Facilities Council: ST/I005912/1 GRIDPP Science and Technology Facilities Council: ST/M005356/1 Science and Technology Facilities Council: ST/J50094X/1 Science and Technology Facilities Council: CMS Science and Technology Facilities Council: ST/J005479/1 Science and Technology Facilities Council: ST/I005912/1 Science and Technology Facilities Council: ST/K001604/1 Science and Technology Facilities Council: ST/J004871/1 Science and Technology Facilities Council: ST/M004775/1 GRIDPP Science and Technology Facilities Council: GRIDPP Science and Technology Facilities Council: ST/L00609X/1 Science and Technology Facilities Council: ST/K003542/1 GRIDPP Science and Technology Facilities Council: ST/J005665/1 Science and Technology Facilities Council: ST/K003844/1 GRIDPP Science and Technology Facilities Council: ST/M005356/1 GRIDPP Science and Technology Facilities Council: ST/K003844/1 Science and Technology Facilities Council: ST/K001256/1 Science and Technology Facilities Council: ST/K003542/1 GRID PP Science and Technology Facilities Council: ST/L00609X/1 GRIDPP Science and Technology Facilities Council: ST/M004775/1 Science and Technology Facilities Council: ST/K001639/1 Science and Technology Facilities Council: ST/J004901/1 Science and Technology Facilities Council: ST/N000250/1 Science and Technology Facilities Council: ST/K001531/1
- Published
- 2015
6. Erlotinib in African Americans With Advanced Non–Small Cell Lung Cancer: A Prospective Randomized Study With Genetic and Pharmacokinetic Analyses
- Author
-
Papp, A., Gao, Y., Wei, L., Li, J., Wang, D., Socinski, M. A., Aimiuwu, J., Hicks, W. J., Zhao, W., Otterson, G. A., Blachly, J. S., Stinchcombe, T. E., Poi, M., Villalona-Calero, M. A., Schaaf, L. J., Starrett, S. L., and Phelps, M. A.
- Subjects
neoplasms ,respiratory tract diseases - Abstract
Prospective studies focusing on EGFR inhibitors in African Americans with NSCLC have not been previously performed. In this phase II randomized study, 55 African Americans with NSCLC received erlotinib 150mg/day or a body weight adjusted dose with subsequent escalations to the maximum allowable, 200mg/day, to achieve rash. Erlotinib and OSI-420 exposures were lower compared to previous reports, consistent with CYP3A pharmacogenetics implying higher metabolic activity. Tumor genetics revealed only two EGFR mutations, EGFR amplification in 17/47 samples, 8 KRAS mutations and 5 EML4-ALK translocations. Although absence of rash was associated with shorter time to progression (TTP), disease control rate, TTP, and 1-year survival were not different between the two dose groups, indicating the dose-to-rash strategy failed to increase clinical benefit. Observed low incidence of toxicity and low erlotinib exposure suggest standardized and maximum allowable dosing may be suboptimal in African Americans.
- Published
- 2014
- Full Text
- View/download PDF
7. 461 A phase I trial of dabrafenib (BRAF inhibitor) and pazopanib in BRAF mutated advanced malignancies
- Author
-
Haraldsdottir, S., primary, Janku, F., additional, Timmers, C., additional, Geyer, S., additional, Schaaf, L.J., additional, Sexton, J., additional, Thurmond, J., additional, Velez-Bravo, V., additional, Stepanek, V.M., additional, Bertino, E., additional, Kendra, K., additional, Mortazavi, A., additional, Subbiah, V., additional, Villalona-Calero, M., additional, Poi, M., additional, Phelps, M., additional, and Shah, M.H., additional
- Published
- 2014
- Full Text
- View/download PDF
8. Suggestive evidence for the involvement of the second calcium and surface loop in interfacial binding: monoclinic and trigonal crystal structures of a quadruple mutant of phospholipase A2
- Author
-
Sekar, K., primary, Yogavel, M., additional, Kanaujia, Shankar Prasad, additional, Sharma, Alok, additional, Velmurugan, D., additional, Poi, M.-J., additional, Dauter, Z., additional, and Tsai, M.-D., additional
- Published
- 2006
- Full Text
- View/download PDF
9. Third calcium ion found in an inhibitor-bound phospholipase A2
- Author
-
Sekar, K., primary, Gayathri, D., additional, Velmurugan, D., additional, Jeyakanthan, J., additional, Yamane, T., additional, Poi, M.-J., additional, and Tsai, M.-D., additional
- Published
- 2006
- Full Text
- View/download PDF
10. Atomic resolution structure of the double mutant (K53,56M) of bovine pancreatic phospholipase A2
- Author
-
Sekar, K., primary, Yogavel, M., additional, Gayathri, D., additional, Velmurugan, D., additional, Krishna, R., additional, Poi, M.-J., additional, Dauter, Z., additional, Dauter, M., additional, and Tsai, M.-D., additional
- Published
- 2005
- Full Text
- View/download PDF
11. Atomic resolution (0.97 Å) structure of the triple mutant (K53,56,121M) of bovine pancreatic phospholipase A2
- Author
-
Sekar, K., primary, Rajakannan, V., additional, Gayathri, D., additional, Velmurugan, D., additional, Poi, M.-J., additional, Dauter, M., additional, Dauter, Z., additional, and Tsai, M.-D., additional
- Published
- 2004
- Full Text
- View/download PDF
12. Suggestive evidence for the involvement of the second calcium and surface loop in interfacial binding: monoclinic and trigonal crystal structures of a quadruple mutant of phospholipase A2.
- Author
-
Sekar, K., Yogavel, M., Kanaujia, Shankar Prasad, Sharma, Alok, Velmurugan, D., Poi, M.-J., Dauter, Z., and Tsai, M.-D.
- Subjects
PHOSPHOLIPASE A2 ,PHOSPHOLIPASES ,CALCIUM ,IONS ,PHYSICAL & theoretical chemistry - Abstract
The crystal structures of the monoclinic and trigonal forms of the quadruple mutant K53,56,120,121M of recombinant bovine pancreatic phospholipase A
2 (PLA2 ) have been solved and refined at 1.9 and 1.1 Å resolution, respectively. Interestingly, the monoclinic form reveals the presence of the second calcium ion. Furthermore, the surface-loop residues are ordered and the conformation of residues 62–66 is similar to that observed in other structures containing the second calcium ion. On the other hand, in the trigonal form the surface loop is disordered and the second calcium is absent. Docking studies suggest that the second calcium and residues Lys62 and Asp66 from the surface loop could be involved in the interaction with the polar head group of the membrane phospholipid. It is hypothesized that the two structures of the quadruple mutant, monoclinic and trigonal, represent the conformations of PLA2 at the lipid interface and in solution, respectively. A docked structure with a phospholipid molecule and with a transition-state analogue bound, one at the active site coordinating to the catalytic calcium and the other at the second calcium site, but both at the i-face, is presented. [ABSTRACT FROM AUTHOR]- Published
- 2006
- Full Text
- View/download PDF
13. Third calcium ion found in an inhibitor-bound phospholipase A2.
- Author
-
Sekar, K., Gayathri, D., Velmurugan, D., Jeyakanthan, J., Yamane, T., Poi, M.-J., and Tsai, M.-D.
- Subjects
PHOSPHOLIPASE A2 ,CALCIUM ions ,LIPID metabolism ,HYDROLYSIS ,FATTY acids ,ORGANIC compounds ,CRYSTALLOGRAPHY - Abstract
The lipolytic enzyme phospholipase A
2 plays a crucial role in lipid metabolism and catalyzes hydrolysis of the fatty-acid ester bond at the sn-2 position of phospholipids. Here, the crystal structure (1.7 Å resolution) of the triple mutant (K53,56,121M) of bovine pancreatic phospholipase A2 complexed with an organic molecule, p-methoxybenzoic acid (anisic acid), is reported. Residues 60–70 (the surface-loop residues) are ordered and adopt conformations which are different from those normally found in structures in which a second calcium ion is present. It is interesting to note that for the first time a third calcium ion has been identified. In addition, four Tris (2-amino-2-hydroxymethyl-1,3-propanediol) molecules were located. It is believed that one of the Tris molecules plays a role in clamping the third calcium ion and that another is involved in controlling the dynamics of the surface loop through hydrogen bonds. [ABSTRACT FROM AUTHOR]- Published
- 2006
- Full Text
- View/download PDF
14. Atomic resolution structure of the double mutant (K53,56M) of bovine pancreatic phospholipase A2.
- Author
-
Sekar, K., Yogavel, M., Gayathri, D., Velmurugan, D., Krishna, R., Poi, M.-J., Dauter, Z., Dauter, M., and Tsai, M.-D.
- Subjects
PHOSPHOLIPASES ,PANCREATIC duct ,GENETIC mutation ,SYNCHROTRON radiation ,ELECTROMAGNETIC waves ,CALCIUM ions - Abstract
The structure of the double mutant K53,56M has previously been refined at 1.9 Å resolution using room-temperature data. The present paper reports the crystal structure of the same mutant K53,56M refined against 1.1 Å data collected using synchrotron radiation. A total of 116 main-chain atoms from 29 residues and 44 side chains are modelled in alternate conformations. Most of the interfacial binding residues are found to be disordered and alternate conformations could be recognized. The second calcium ion-binding site residue Glu92 adopts two alternate conformations. The minor and major conformations of Glu92 correspond to the second calcium ion bound and unbound states. [ABSTRACT FROM AUTHOR]
- Published
- 2006
- Full Text
- View/download PDF
15. Third-trimester maternal toxicity with nevirapine use in pregnancy.
- Author
-
Joy S, Poi M, Hughes L, Brady MT, Koletar SL, Para MF, and Fan-Havard P
- Published
- 2005
- Full Text
- View/download PDF
16. Atomic resolution (0.97 Å) structure of the triple mutant (K53,56,121M) of bovine pancreatic phospholipase A2.
- Author
-
Sekar, K., Rajakannan, V., Gayathri, D., Velmurugan, D., Poi, M.-J., Dauter, M., Dauter, Z., and Tsaid, M.-D.
- Subjects
BOVINE anatomy ,PHOSPHOLIPASES ,ESTERASES ,FATTY acids ,CARBOXYLIC acids ,ACETIC acid - Abstract
The enzyme phospholipase A2 catalyzes the hydrolysis of the sn-2 acyl chain of phospholipids, forming fatty acids and lysophospholipids. The crystal structure of a triple mutant (K53,56,121M) of bovine pancreatic phospholipase A2 in which the lysine residues at positions 53, 56 and 121 are replaced recombinantly by methionines has been determined at atomic resolution (0.97 Å ). The crystal is monoclinic (space group P2), with unit-cell parameters a = 36.934, b = 23.863, c = 65.931 Å, β = 101.47°. The structure was solved by molecular replacement and has been refined to a final R factor of 10.6% (R
free = 13.4%) using 63 926 unique reflections. The final protein model consists of 123 amino-acid residues, two calcium ions, one chloride ion, 243 water molecules and six 2-methyl-2,4- pentanediol molecules. The surface-loop residues 60-70 are ordered and have clear electron density. [ABSTRACT FROM AUTHOR]- Published
- 2005
- Full Text
- View/download PDF
17. Neuroendocrine mediators up-regulate a~1~b- and a~1~d-adrenergic receptor subtypes in human monocytes
- Author
-
Voort, C. R. Van Der, Kavelaars, A., Poi, M. Van De, and Heijnen, C. J.
- Published
- 1998
- Full Text
- View/download PDF
18. Suggestive evidence for the involvement of the second calcium and surface loop in interfacial binding: monoclinic and trigonal crystal structures of a quadruple mutant of phospholipase A2.
- Author
-
Sekar, K., Yogavel, M., Kanaujia, Shankar Prasad, Sharma, Alok, Velmurugan, D., Poi, M.-J., Dauter, Z., and Tsai, M.-D.
- Subjects
- *
PHOSPHOLIPASE A2 , *PHOSPHOLIPASES , *CALCIUM , *IONS , *PHYSICAL & theoretical chemistry - Abstract
The crystal structures of the monoclinic and trigonal forms of the quadruple mutant K53,56,120,121M of recombinant bovine pancreatic phospholipase A2 (PLA2) have been solved and refined at 1.9 and 1.1 Å resolution, respectively. Interestingly, the monoclinic form reveals the presence of the second calcium ion. Furthermore, the surface-loop residues are ordered and the conformation of residues 62–66 is similar to that observed in other structures containing the second calcium ion. On the other hand, in the trigonal form the surface loop is disordered and the second calcium is absent. Docking studies suggest that the second calcium and residues Lys62 and Asp66 from the surface loop could be involved in the interaction with the polar head group of the membrane phospholipid. It is hypothesized that the two structures of the quadruple mutant, monoclinic and trigonal, represent the conformations of PLA2 at the lipid interface and in solution, respectively. A docked structure with a phospholipid molecule and with a transition-state analogue bound, one at the active site coordinating to the catalytic calcium and the other at the second calcium site, but both at the i-face, is presented. [ABSTRACT FROM AUTHOR]
- Published
- 2006
- Full Text
- View/download PDF
19. Third calcium ion found in an inhibitor-bound phospholipase A2.
- Author
-
Sekar, K., Gayathri, D., Velmurugan, D., Jeyakanthan, J., Yamane, T., Poi, M.-J., and Tsai, M.-D.
- Subjects
- *
PHOSPHOLIPASE A2 , *CALCIUM ions , *LIPID metabolism , *HYDROLYSIS , *FATTY acids , *ORGANIC compounds , *CRYSTALLOGRAPHY - Abstract
The lipolytic enzyme phospholipase A2 plays a crucial role in lipid metabolism and catalyzes hydrolysis of the fatty-acid ester bond at the sn-2 position of phospholipids. Here, the crystal structure (1.7 Å resolution) of the triple mutant (K53,56,121M) of bovine pancreatic phospholipase A2 complexed with an organic molecule, p-methoxybenzoic acid (anisic acid), is reported. Residues 60–70 (the surface-loop residues) are ordered and adopt conformations which are different from those normally found in structures in which a second calcium ion is present. It is interesting to note that for the first time a third calcium ion has been identified. In addition, four Tris (2-amino-2-hydroxymethyl-1,3-propanediol) molecules were located. It is believed that one of the Tris molecules plays a role in clamping the third calcium ion and that another is involved in controlling the dynamics of the surface loop through hydrogen bonds. [ABSTRACT FROM AUTHOR]
- Published
- 2006
- Full Text
- View/download PDF
20. Atomic resolution structure of the double mutant (K53,56M) of bovine pancreatic phospholipase A2.
- Author
-
Sekar, K., Yogavel, M., Gayathri, D., Velmurugan, D., Krishna, R., Poi, M.-J., Dauter, Z., Dauter, M., and Tsai, M.-D.
- Subjects
- *
PHOSPHOLIPASES , *PANCREATIC duct , *GENETIC mutation , *SYNCHROTRON radiation , *ELECTROMAGNETIC waves , *CALCIUM ions - Abstract
The structure of the double mutant K53,56M has previously been refined at 1.9 Å resolution using room-temperature data. The present paper reports the crystal structure of the same mutant K53,56M refined against 1.1 Å data collected using synchrotron radiation. A total of 116 main-chain atoms from 29 residues and 44 side chains are modelled in alternate conformations. Most of the interfacial binding residues are found to be disordered and alternate conformations could be recognized. The second calcium ion-binding site residue Glu92 adopts two alternate conformations. The minor and major conformations of Glu92 correspond to the second calcium ion bound and unbound states. [ABSTRACT FROM AUTHOR]
- Published
- 2006
- Full Text
- View/download PDF
21. Atomic resolution (0.97 Å) structure of the triple mutant (K53,56,121M) of bovine pancreatic phospholipase A2.
- Author
-
Sekar, K., Rajakannan, V., Gayathri, D., Velmurugan, D., Poi, M.-J., Dauter, M., Dauter, Z., and Tsaid, M.-D.
- Subjects
- *
BOVINE anatomy , *PHOSPHOLIPASES , *ESTERASES , *FATTY acids , *CARBOXYLIC acids , *ACETIC acid - Abstract
The enzyme phospholipase A2 catalyzes the hydrolysis of the sn-2 acyl chain of phospholipids, forming fatty acids and lysophospholipids. The crystal structure of a triple mutant (K53,56,121M) of bovine pancreatic phospholipase A2 in which the lysine residues at positions 53, 56 and 121 are replaced recombinantly by methionines has been determined at atomic resolution (0.97 Å ). The crystal is monoclinic (space group P2), with unit-cell parameters a = 36.934, b = 23.863, c = 65.931 Å, β = 101.47°. The structure was solved by molecular replacement and has been refined to a final R factor of 10.6% (Rfree = 13.4%) using 63 926 unique reflections. The final protein model consists of 123 amino-acid residues, two calcium ions, one chloride ion, 243 water molecules and six 2-methyl-2,4- pentanediol molecules. The surface-loop residues 60-70 are ordered and have clear electron density. [ABSTRACT FROM AUTHOR]
- Published
- 2005
- Full Text
- View/download PDF
22. CDK4/6 and autophagy inhibitors synergize to suppress the growth of human head and neck squamous cell carcinomas.
- Author
-
Duah E, Seligson ND, Persaud AK, Dam Q, Pabla N, Rocco JW, Li J, and Poi M
- Subjects
- Humans, Squamous Cell Carcinoma of Head and Neck drug therapy, Cyclin-Dependent Kinase 4 metabolism, Cyclin-Dependent Kinase 4 pharmacology, Apoptosis, Autophagy, Cell Line, Tumor, Head and Neck Neoplasms drug therapy, Papillomavirus Infections
- Abstract
Head and neck squamous cell carcinoma (HNSCC) accounts for over 10,000 deaths in the United States annually. Approximately 80% of HNSCC are human papillomavirus (HPV)-negative which have an overall poorer prognosis compared to the HPV-positive disease. Treatment options are mainly nontargeted chemotherapy, radiation, and surgery. The cyclin-d-CDK4/6-RB pathway, which regulates cell cycle progression, is often deregulated in HNSCC, making it an attractive therapeutic target. In the current study, we investigated the therapeutic effects of cyclin-dependent kinase 4/6 (CDK4/6) inhibitors in preclinical models of HNSCCs. Our results show that the specific CDK4/6 inhibitor, abemaciclib, inhibited cell growth, and induced apoptosis in HNSCC cell lines. We also demonstrated that both the pro-survival autophagy pathway and the ERK pathway in HNSCC cells were activated with abemaciclib treatment through the generation of reactive oxygen species (ROS). Coinhibition of CDK4/6 and autophagy synergistically decreased cell viability, induced apoptosis, and inhibited tumor growth in both in vitro and in vivo preclinical HNSCC models. These results reveal a potential therapeutic strategy that supports the rationale for further clinical development of a combination of CDK4/6 and autophagy inhibitors in HNSCC., (© 2023 Wiley Periodicals LLC.)
- Published
- 2023
- Full Text
- View/download PDF
23. Dabrafenib Versus Dabrafenib + Trametinib in BRAF -Mutated Radioactive Iodine Refractory Differentiated Thyroid Cancer: Results of a Randomized, Phase 2, Open-Label Multicenter Trial.
- Author
-
Busaidy NL, Konda B, Wei L, Wirth LJ, Devine C, Daniels GA, DeSouza JA, Poi M, Seligson ND, Cabanillas ME, Sipos JA, Ringel MD, Eisfeld AK, Timmers C, and Shah MH
- Subjects
- Humans, Adolescent, Adult, Proto-Oncogene Proteins B-raf genetics, Iodine Radioisotopes therapeutic use, Pyrimidinones adverse effects, Pyridones adverse effects, Antineoplastic Combined Chemotherapy Protocols adverse effects, Oximes adverse effects, Mutation, Melanoma drug therapy, Thyroid Neoplasms drug therapy, Thyroid Neoplasms genetics, Thyroid Neoplasms radiotherapy, Adenocarcinoma
- Abstract
Background: Oncogenic BRAF mutations are commonly found in advanced differentiated thyroid cancer (DTC), and reports have shown efficacy of BRAF inhibitors in these tumors. We investigated the difference in response between dabrafenib monotherapy and dabrafenib + trametinib therapy in patients with BRAF-mutated radioactive iodine refractory DTC. Methods: In this open-label randomized phase 2 multicenter trial, patients aged ≥18 years with BRAF-mutated radioactive iodine refractory DTC with progressive disease by Response Evaluation Criteria in Solid Tumors (RECIST) 1.1 within 13 months before enrollment were eligible. Patients were randomly assigned to receive dabrafenib alone or dabrafenib + trametinib. The primary endpoint was objective response rate by modified RECIST (minor response of -20% to -29%, partial and complete response) within the first 24 weeks of therapy. Trial Registration Number: NCT01723202. Results: A total of 53 patients were enrolled. The objective response rate (modified RECIST) was 42% (11/26 [95% confidence interval {CI} 23-63%]) with dabrafenib versus 48% (13/27 [CI 29-68%]) with dabrafenib + trametinib ( p = 0.67). Objective response rate (RECIST 1.1) was 35% (9/26 [CI 17-56%]) with dabrafenib and 30% (8/27 [CI 14-51%]) with dabrafenib + trametinib. Most common treatment-related adverse events included skin and subcutaneous tissue disorders (17/26, 65%), fever (13/26, 50%), hyperglycemia (12/26, 46%) with dabrafenib alone and fever (16/27, 59%), nausea, chills, fatigue (14/27, 52% each) with dabrafenib + trametinib. There were no treatment-related deaths. Conclusions: Combination dabrafenib + trametinib was not superior in efficacy compared to dabrafenib monotherapy in patients with BRAF-mutated radioiodine refractory progressive DTC.
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- 2022
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24. Factors Predicting Participation in the Prospective Genomic Sequencing Study, Total Cancer Care (TCC), in Kentucky.
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Riggs MJ, Huang B, Chen Q, Bocklage T, Schuh MR, Poi M, Villano JL, Cavnar MJ, Arnold SM, Miller RW, Ueland FR, and Kolesar JM
- Subjects
- Appalachian Region, Cohort Studies, Female, Genomics, Humans, Kentucky epidemiology, Male, Prospective Studies, Neoplasms genetics, Neoplasms therapy
- Abstract
Purpose: Large-scale genomic sequencing studies are driving oncology drug development. However, rural populations, like those residing in Appalachian Kentucky, are underrepresented in these efforts. In this study, we determined the frequency of participation, reasons for nonparticipation, and factors predicting the decision to participate in the Total Cancer Care (TCC) prospective genomic cohort study., Methods: A total of 1,188 patients were invited to enroll in the TCC prospective cohort from December 2018 to May 2019. Declining patients were queried for their rationale for nonparticipation and their patient data were obtained from the Kentucky Cancer Registry (KCR). Logistic regression was used to assess the association between characteristics and study participation. The association of study participation with survival was modeled with Cox proportional-hazards regression., Results: 90.9% (1,081) patients consented to participate. In multivariate analysis, factors significantly associated with participation were age, gender, treatment status, and race. Though overall more women participated in the study, men were more likely to participate than women when invited (OR 1.57). Younger, Caucasian individuals who had received chemotherapy, but not surgery, were also more likely to participate. Patients in the Kentucky Appalachian cohort were primarily rural, had less educational attainment, and lower socioeconomic status. Kentucky Appalachian patients were no less likely to enroll in TCC than non-Appalachian patients. Consented individuals had higher overall survival compared to those who declined., Conclusion: Though minorities, those with low socioeconomic status, and rural populations are underrepresented in genomic studies, they were no less likely to participate when given the opportunity, and participation was associated with better clinical outcomes., (© 2020 National Rural Health Association.)
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- 2022
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25. Phase I evaluation of lenvatinib and weekly paclitaxel in patients with recurrent endometrial, ovarian, fallopian tube, or primary peritoneal Cancer.
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Backes FJ, Wei L, Chen M, Hill K, Dzwigalski K, Poi M, Phelps M, Salani R, Copeland LJ, Fowler JM, Cohn DE, Bixel K, Cosgrove C, Hays J, and O'Malley D
- Subjects
- Aged, Antineoplastic Combined Chemotherapy Protocols adverse effects, Antineoplastic Combined Chemotherapy Protocols pharmacokinetics, Carcinoma, Ovarian Epithelial drug therapy, Dose-Response Relationship, Drug, Drug Administration Schedule, Drug Resistance, Neoplasm, Endometrial Neoplasms drug therapy, Endometrial Neoplasms metabolism, Fallopian Tube Neoplasms drug therapy, Fallopian Tube Neoplasms metabolism, Female, Genital Neoplasms, Female metabolism, Humans, Middle Aged, Ovarian Neoplasms drug therapy, Ovarian Neoplasms metabolism, Paclitaxel administration & dosage, Paclitaxel adverse effects, Paclitaxel pharmacokinetics, Peritoneal Neoplasms metabolism, Phenylurea Compounds administration & dosage, Phenylurea Compounds adverse effects, Phenylurea Compounds pharmacokinetics, Quinolines administration & dosage, Quinolines adverse effects, Quinolines pharmacokinetics, Antineoplastic Combined Chemotherapy Protocols administration & dosage, Genital Neoplasms, Female drug therapy, Peritoneal Neoplasms drug therapy
- Abstract
Objectives: To estimate the maximally tolerated dose (MTD) and describe toxicities associated with lenvatinib and weekly paclitaxel in patients with recurrent endometrial and platinum resistant epithelial ovarian cancer., Methods: Using a 3 + 3 design patients were given weekly paclitaxel 80 mg/m2 IV day 1, 8, 15 and oral levantinib daily on a 28-day cycle. Lenvatinib dose levels were 8 mg, 12 mg, 16 mg, 20 mg. Toxicities were recorded using CTCAE v4.03 and response was determined with imaging after cycle 2, then every 3rd cycle, using RECIST 1.1 criteria., Results: 26 patients were enrolled; 19 with ovarian cancer (14 high grade serous, 1 low grade serous, 2 clear cell, 1 endometrioid, and 1 carcinosarcoma), and 7 with endometrial cancer (3 serous, and 4 endometrioid). The MTD was established at lenvatinib 16 mg and weekly paclitaxel 80 mg/m2. Toxicities (all grades) occurring in ≥25% of patients included anemia, neutropenia, lymphopenia, mucositis, nausea, diarrhea, anorexia, hypertension, fatigue, proteinuria, epistaxis, hoarseness. Twenty-three patients were evaluable for response and PFS; 15 (65%) had a partial response, 7 (30%) stable, 1 (4%) progressive disease with an objective response rate of 65%; 71% in ovarian and 50% in endometrial cancer. Median progression free survival (PFS) is 12.4 months; 14.0 months in endometrial cancer, 7.2 months in ovarian cancer; 54% had a PFS > 6 months. The median duration of response for PR patients (n = 15) was 10.9 months., Conclusions: The regimen was tolerable with manageable side effects. Encouraging activity was observed in endometrial and ovarian cancer, and warrants further development., Competing Interests: Declaration of Competing Interest Dr. Backes reports grants and personal fees from Eisai, grants and personal fees from Merck, grants from Immunogen, grants and personal fees from Clovis, personal fees from Agenus, AstraZeneca, Genentech, GlaxoSmithKline, all outside the submitted work. Dr. O'Malley reports personal fees from AstraZeneca, Tesaro/GSK, Immunogen, Ambry, Janssen/J&J, Abbvie, Regeneron, Amgen, Novocure, Genentech/Roche, GOG Foundation, Iovance Biotherapeutics, Inc., Myriad Genetics, Eisai, Agenus, Tarveda, Merck, SeaGen, Novartis, Mersana, Clovis, Rubis, Elevar, outside the submitted work. Dr. Salani reports personal fees from Glaxo Smith Kline, Clovis, Iovance, Seattle Genetics, Merck, Astra Zeneca, outside the submitted work. Dr. Hays reports personal fees from Clovis, AstraZeneca, Merck, Tesaro, Ipsen, Seattle Genetics, outside the submitted work. Dr. Copeland reports personal fees from Myriad Genetics, GlaxoSmithKline, Elevar, Toray Therapeutics, Rubius Therapeutics, Sorrento Therapeutics, outside the submitted work. None of the other authors (KB, CC, MP, KD, KH, MC, DC, MP, JF) have a significant conflict of interest related to the current study., (Copyright © 2021 Elsevier Inc. All rights reserved.)
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- 2021
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26. Brigatinib causes tumor shrinkage in both NF2-deficient meningioma and schwannoma through inhibition of multiple tyrosine kinases but not ALK.
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Chang LS, Oblinger JL, Smith AE, Ferrer M, Angus SP, Hawley E, Petrilli AM, Beauchamp RL, Riecken LB, Erdin S, Poi M, Huang J, Bessler WK, Zhang X, Guha R, Thomas C, Burns SS, Gilbert TSK, Jiang L, Li X, Lu Q, Yuan J, He Y, Dixon SAH, Masters A, Jones DR, Yates CW, Haggarty SJ, La Rosa S, Welling DB, Stemmer-Rachamimov AO, Plotkin SR, Gusella JF, Guinney J, Morrison H, Ramesh V, Fernandez-Valle C, Johnson GL, Blakeley JO, and Clapp DW
- Subjects
- Animals, Mice, Humans, Neurofibromatosis 2 drug therapy, Neurofibromatosis 2 genetics, Neurofibromatosis 2 pathology, Cell Line, Tumor, Protein-Tyrosine Kinases antagonists & inhibitors, Protein-Tyrosine Kinases metabolism, Protein-Tyrosine Kinases genetics, Xenograft Model Antitumor Assays, Meningeal Neoplasms drug therapy, Meningeal Neoplasms pathology, Meningeal Neoplasms genetics, Pyrimidines pharmacology, Anaplastic Lymphoma Kinase antagonists & inhibitors, Anaplastic Lymphoma Kinase genetics, Anaplastic Lymphoma Kinase metabolism, Neurilemmoma drug therapy, Neurilemmoma pathology, Neurilemmoma genetics, Organophosphorus Compounds pharmacology, Meningioma drug therapy, Meningioma pathology, Meningioma genetics, Protein Kinase Inhibitors pharmacology, Neurofibromin 2 genetics, Neurofibromin 2 deficiency, Neurofibromin 2 metabolism
- Abstract
Neurofibromatosis Type 2 (NF2) is an autosomal dominant genetic syndrome caused by mutations in the NF2 tumor suppressor gene resulting in multiple schwannomas and meningiomas. There are no FDA approved therapies for these tumors and their relentless progression results in high rates of morbidity and mortality. Through a combination of high throughput screens, preclinical in vivo modeling, and evaluation of the kinome en masse, we identified actionable drug targets and efficacious experimental therapeutics for the treatment of NF2 related schwannomas and meningiomas. These efforts identified brigatinib (ALUNBRIG®), an FDA-approved inhibitor of multiple tyrosine kinases including ALK, to be a potent inhibitor of tumor growth in established NF2 deficient xenograft meningiomas and a genetically engineered murine model of spontaneous NF2 schwannomas. Surprisingly, neither meningioma nor schwannoma cells express ALK. Instead, we demonstrate that brigatinib inhibited multiple tyrosine kinases, including EphA2, Fer and focal adhesion kinase 1 (FAK1). These data demonstrate the power of the de novo unbiased approach for drug discovery and represents a major step forward in the advancement of therapeutics for the treatment of NF2 related malignancies., Competing Interests: No authors have competing interests.
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- 2021
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27. A phase 1 trial of the histone deacetylase inhibitor AR-42 in patients with neurofibromatosis type 2-associated tumors and advanced solid malignancies.
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Collier KA, Valencia H, Newton H, Hade EM, Sborov DW, Cavaliere R, Poi M, Phelps MA, Liva SG, Coss CC, Wang J, Khountham S, Monk P, Shapiro CL, Piekarz R, Hofmeister CC, Welling DB, and Mortazavi A
- Subjects
- Adult, Aged, Aged, 80 and over, Female, Humans, Male, Maximum Tolerated Dose, Middle Aged, Neoplasms mortality, Neurofibromatosis 2 mortality, Phenylbutyrates adverse effects, Phenylbutyrates pharmacokinetics, Young Adult, Histone Deacetylase Inhibitors therapeutic use, Neoplasms drug therapy, Neurofibromatosis 2 drug therapy, Phenylbutyrates therapeutic use
- Abstract
Purpose: Given clinical activity of AR-42, an oral histone deacetylase inhibitor, in hematologic malignancies and preclinical activity in solid tumors, this phase 1 trial investigated the safety and tolerability of AR-42 in patients with advanced solid tumors, including neurofibromatosis type 2-associated meningiomas and schwannomas (NF2). The primary objective was to define the maximum tolerated dose (MTD) and dose-limiting toxicities (DLTs). Secondary objectives included determining pharmacokinetics and clinical activity., Methods: This phase I trial was an open-label, single-center, dose-escalation study of single-agent AR-42 in primary central nervous system and advanced solid tumors. The study followed a 3 + 3 design with an expansion cohort at the MTD., Results: Seventeen patients were enrolled with NF2 (n = 5), urothelial carcinoma (n = 3), breast cancer (n = 2), non-NF2-related meningioma (n = 2), carcinoma of unknown primary (n = 2), small cell lung cancer (n = 1), Sertoli cell carcinoma (n = 1), and uveal melanoma (n = 1). The recommended phase II dose is 60 mg three times weekly, for 3 weeks of a 28-day cycle. DLTs included grade 3 thrombocytopenia and grade 4 psychosis. The most common treatment-related adverse events were cytopenias, fatigue, and nausea. The best response was stable disease in 53% of patients (95% CI 26.6-78.7). Median progression-free survival (PFS) was 3.6 months (95% CI 1.2-9.1). Among evaluable patients with NF2 or meningioma (n = 5), median PFS was 9.1 months (95% CI 1.9-not reached)., Conclusion: Single-agent AR-42 is safe and well tolerated. Further studies may consider AR-42 in a larger cohort of patients with NF2 or in combination with other agents in advanced solid tumors., Trial Registration: NCT01129193, registered 5/24/2010.
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- 2021
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28. A kinome-wide screen identifies a CDKL5-SOX9 regulatory axis in epithelial cell death and kidney injury.
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Kim JY, Bai Y, Jayne LA, Hector RD, Persaud AK, Ong SS, Rojesh S, Raj R, Feng MJHH, Chung S, Cianciolo RE, Christman JW, Campbell MJ, Gardner DS, Baker SD, Sparreboom A, Govindarajan R, Singh H, Chen T, Poi M, Susztak K, Cobb SR, and Pabla NS
- Subjects
- Animals, Cell Death, Epithelial Cells metabolism, Female, Green Fluorescent Proteins metabolism, Humans, Keratinocytes metabolism, Kidney metabolism, Kidney Tubules metabolism, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Neurons metabolism, RNA Interference, RNA, Small Interfering metabolism, Acute Kidney Injury metabolism, Epithelial Cells cytology, Protein Serine-Threonine Kinases metabolism, SOX9 Transcription Factor metabolism
- Abstract
Renal tubular epithelial cells (RTECs) perform the essential function of maintaining the constancy of body fluid composition and volume. Toxic, inflammatory, or hypoxic-insults to RTECs can cause systemic fluid imbalance, electrolyte abnormalities and metabolic waste accumulation- manifesting as acute kidney injury (AKI), a common disorder associated with adverse long-term sequelae and high mortality. Here we report the results of a kinome-wide RNAi screen for cellular pathways involved in AKI-associated RTEC-dysfunction and cell death. Our screen and validation studies reveal an essential role of Cdkl5-kinase in RTEC cell death. In mouse models, genetic or pharmacological Cdkl5 inhibition mitigates nephrotoxic and ischemia-associated AKI. We propose that Cdkl5 is a stress-responsive kinase that promotes renal injury in part through phosphorylation-dependent suppression of pro-survival transcription regulator Sox9. These findings reveal a surprising non-neuronal function of Cdkl5, identify a pathogenic Cdkl5-Sox9 axis in epithelial cell-death, and support CDKL5 antagonism as a therapeutic approach for AKI.
- Published
- 2020
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29. Cisplatin Induced the Expression of SEI1 ( TRIP-Br1 ) Oncogene in Human Oral Squamous Cancer Cell Lines.
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Li J, Vangundy Z, and Poi M
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- Apoptosis drug effects, Cell Line, Tumor, Cell Proliferation drug effects, Cell Survival, Dose-Response Relationship, Drug, Drug Resistance, Neoplasm, Fluorouracil pharmacology, Humans, Carcinoma, Squamous Cell genetics, Cisplatin pharmacology, Gene Expression Regulation, Neoplastic drug effects, Mouth Neoplasms genetics, Oncogenes, Transcription Factors genetics
- Abstract
Background/aim: Aberrant expression of the SEI1 oncogene has been prevalently found in a variety of human cancers, including oral squamous cell carcinoma (OSCC). Recent studies have shown that cisplatin up-regulates the expression of SEI1 in breast and bladder cancer cells, thus inhibiting apoptosis and cell death in these cells. In the present study, we investigated the impact of cisplatin on the expression of SEI1 in OSCC cells., Materials and Methods: Four OSCC cell lines, CAL27, SCC4, SCC15, and SCC22A were treated with cisplatin and 5-fluorouracil, and changes in SEI1 expression in these cells were evaluated using quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) analyses., Results: Cisplatin significantly induced SEI1 expression in the tested OSCC cells. Contrarily, cisplatin treatment did not affect the expression of gankyrin and BMI1, two oncogenes frequently overexpressed in a coordinate manner with SEI1 in OSCC. Additionally, 5-fluorouracil did not bring about any detectable changes in SEI1 expression in these cells., Conclusion: Cisplatin-induced up-regulation of SEI1 expression in OSCC is specific, and such induction could underlie the development of resistance to cisplatin in OSCC., (Copyright© 2020, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)
- Published
- 2020
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30. PTC209, a Specific Inhibitor of BMI1, Promotes Cell Cycle Arrest and Apoptosis in Cervical Cancer Cell Lines.
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Li J, Vangundy Z, and Poi M
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- Cell Line, Tumor, Cell Proliferation, Cell Survival drug effects, Female, Gene Expression Regulation drug effects, Humans, Neoplastic Stem Cells drug effects, Neoplastic Stem Cells metabolism, Polycomb Repressive Complex 1 genetics, Polycomb Repressive Complex 1 metabolism, Uterine Cervical Neoplasms metabolism, Uterine Cervical Neoplasms pathology, Apoptosis drug effects, Cell Cycle Checkpoints drug effects, Enzyme Inhibitors pharmacology, Polycomb Repressive Complex 1 antagonists & inhibitors
- Abstract
Background/aim: Aberrant expression of the BMI1 oncogene has been prevalently found in a variety of human cancers, including cervical cancer. Recent studies have shown that PTC209, a specific BMI1 inhibitor, exhibits high potency in inhibiting the growth of colon, breast, oral cancer cells and cancer-initiating cells, indicative of its chemotherapeutic potential. In the current study, we evaluated the inhibitory abilities of PTC209 in cervical cancer cells., Materials and Methods: Three cervical cell lines, C33A, HeLa, and SiHa were treated with PTC209. The impacts of PTC209 on BMI1 were investigated using quantitative reverse-transcription PCR assay (qRT-PCR) and western blotting; changes in cell viability, cell cycle distribution, and apoptosis were assessed using cell viability testing, colony formation assay and flow cytometry analyses, respectively., Results: PTC209 exhibited considerably high short-term and long-term cytotoxicities in all tested cervical cancer cell lines regardless of their HPV infection status, TP53 and pRb statuses. PTC209 significantly downregulated the expression of BMI1 in cervical cancer cell lines, and such downregulation led to G0/G1 arrest (p<0.05). Moreover, PTC209 drove more cells into apoptosis (p<0.05)., Conclusion: PTC209 (BMI1-targeting agents, in general) represents a novel chemotherapeutic agent with potential in cervical cancer therapy., (Copyright© 2020, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)
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- 2020
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31. Increasing Adherence to Adjuvant Hormone Therapy Among Patients With Breast Cancer: A Smart Phone App-Based Pilot Study.
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Krok-Schoen JL, Naughton MJ, Young GS, Moon J, Poi M, Melin SA, Wood ME, Hopkins JO, Paskett ED, and Post DM
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- Female, Humans, Medication Adherence, Middle Aged, Pilot Projects, Social Support, Breast Neoplasms drug therapy, Hormone Replacement Therapy methods, Quality of Life psychology, Smartphone standards
- Abstract
Purpose: This study tested the feasibility and efficacy of using a text-based intervention to increase initiation, decrease discontinuation, and improve adherence as prescribed to adjuvant hormone therapy (AHT) among hyphenate post-menopausal breast cancer survivors., Methods: The 3-month intervention consisted of daily text message reminders to take medication, coupled with a dynamic (eg, feedback on progress) tailored intervention using weekly interactive surveys delivered by a smartphone app. Five clinic sites within the Alliance for Clinical Trials in Oncology participated. Hormone levels were measured prior to AHT initiation and at study exit., Results: Of the 39 patients recruited to the pilot study, 27 (69.2%) completed all study requirements (completed both the baseline and the exit surveys, both blood draws, and did not miss more than 2 weekly surveys). Significant improvements were observed pre- to postintervention for self-reported medication adherence ( P = .015), mental health functioning ( P = .007), and perceived stress ( P = .04). Significant decreases in estradiol, estrogen, and estrone hormone levels were observed from baseline to study exit ( P < .001), indicating the accuracy of self-reported AHT adherence. Participants (91.9%) and physicians (100%) agreed that participant participation in the intervention was beneficial., Conclusions: The results of this pilot study established the general feasibility and efficacy of an app-based intervention to support patient AHT adherence. Larger controlled, randomized trials are needed to examine the effectiveness of the app-based intervention in improving AHT and quality of life among breast cancer survivors.
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- 2019
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32. Pharmacokinetic-Pharmacodynamic Model of Neutropenia in Patients With Myeloma Receiving High-Dose Melphalan for Autologous Stem Cell Transplant.
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Cho YK, Irby DJ, Li J, Sborov DW, Mould DR, Badawi M, Dauki A, Lamprecht M, Rosko AE, Fernandez S, Hade EM, Hofmeister CC, Poi M, and Phelps MA
- Subjects
- Antineoplastic Agents, Alkylating adverse effects, Antineoplastic Agents, Alkylating pharmacokinetics, Antineoplastic Agents, Alkylating pharmacology, Area Under Curve, Female, Granulocyte Colony-Stimulating Factor therapeutic use, Half-Life, Humans, Male, Melphalan adverse effects, Melphalan pharmacokinetics, Melphalan pharmacology, Middle Aged, Models, Biological, Neutropenia therapy, Antineoplastic Agents, Alkylating administration & dosage, Hematopoietic Stem Cell Transplantation, Melphalan administration & dosage, Multiple Myeloma drug therapy, Neutropenia chemically induced
- Abstract
High-dose melphalan (HDM) is part of the conditioning regimen in patients with multiple myeloma (MM) receiving autologous stem cell transplantation (ASCT). However, individual sensitivity to melphalan varies, and many patients experience severe toxicities. Prolonged severe neutropenia is one of the most severe toxicities and contributes to potentially life-threatening infections and failure of ASCT. Granulocyte-colony stimulating factor (G-CSF) is given to stimulate neutrophil proliferation after melphalan administration. The aim of this study was to develop a population pharmacokinetic/pharmacodynamic (PK/PD) model capable of predicting neutrophil kinetics in individual patients with MM undergoing ASCT with high-dose melphalan and G-CSF administration. The extended PK/PD model incorporated several covariates, including G-CSF regimen, stem cell dose, hematocrit, sex, creatinine clearance, p53 fold change, and race. The resulting model explained portions of interindividual variability in melphalan exposure, therapeutic effect, and feedback regulation of G-CSF on neutrophils, thus enabling simulation of various doses and prediction of neutropenia duration., (© 2018 The Authors CPT: Pharmacometrics & Systems Pharmacology published by Wiley Periodicals, Inc. on behalf of the American Society for Clinical Pharmacology and Therapeutics.)
- Published
- 2018
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33. Phase I Trial of Dabrafenib and Pazopanib in BRAF Mutated Advanced Malignancies.
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Haraldsdottir S, Janku F, Poi M, Timmers C, Geyer S, Schaaf LJ, Sexton J, Wei L, Thurmond J, Velez-Bravo V, Stepanek VM, Bertino EM, Kendra K, Mortazavi A, Subbiah V, Phelps M, and Shah MH
- Abstract
Purpose: Several tumor types carry BRAF mutations and vascular endothelial growth factor pathway upregulation. Resistance mechanisms to BRAF inhibitors can include platelet-derived growth factor-β upregulation. Dabrafenib, a BRAF inhibitor, and pazopanib, a multikinase inhibitor that targets vascular endothelial growth factor and platelet-derived growth factor, have not been combined previously. This phase I study was designed to evaluate the safety, pharmacokinetics, and pharmacodynamics of the combination., Patients and Methods: Patients with any advanced BRAF mutated malignancy with adequate organ function were eligible. Prior use of dabrafenib or pazopanib was not allowed. Dosages started at dabrafenib 50 mg twice a day and pazopanib 400 mg daily on dose level (DL) 1, with maximum dosages of 150 mg twice a day and 800 mg daily on DL5. Pharmacokinetics and BRAF V600E plasma clone were measured, and efficacy was evaluated by imaging and tumor markers every 8 weeks., Results: Twenty-three patients with 11 different tumor histologies were enrolled in five DLs. Two dose-limiting toxicities were observed-a grade 3 bowel perforation on DL3 and grade 3 arthralgia on DL5. Common drug-related adverse events included nausea (52%), skin papules (43%), diarrhea (39%), hand-foot syndrome (30%), anemia (26%), rash (22%), vomiting (22%), hypophosphatemia (22%), and transaminitis (22%). Five patients (22%) experienced a partial response, including low-grade ovarian serous carcinoma, thyroid cancer, and glioblastoma multiforme, and two patients (appendiceal and thyroid cancer) had stable disease > 6 months. Pharmacokinetic measurements revealed pazopanib levels < 17.5 μg/mL in 80% of treated patients at steady state, particularly at DL5. BRAF V600E plasma copies correlated with response and progression., Conclusion: Combination dabrafenib and pazopanib had no unexpected toxicities, and durable partial responses were observed at DL3 or greater. Dose escalation beyond DL5 may be considered as pazopanib levels were suboptimal as a result of drug interaction with dabrafenib.
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- 2018
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34. Quantification of miRNAs Co-Immunoprecipitated with Argonaute Proteins Using SYBR Green-Based qRT-PCR.
- Author
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Phan HD, Li J, Poi M, and Nakanishi K
- Subjects
- Antibodies immunology, Antibodies metabolism, Argonaute Proteins immunology, Computational Biology methods, DNA, Complementary, Data Interpretation, Statistical, Gene Expression, HEK293 Cells, Humans, Mutation, Workflow, Argonaute Proteins metabolism, Immunoprecipitation methods, MicroRNAs genetics, MicroRNAs metabolism, Real-Time Polymerase Chain Reaction methods
- Abstract
MicroRNAs (miRNAs) are small non-coding RNAs that trigger post-transcriptional gene silencing. These RNAs need to be associated with the Argonaute proteins to be functional. This assembly begins with loading of a miRNA duplex, followed by the ejection of one of the strands (passenger). The remaining strand (guide) together with the Argonaute protein forms a ribonucleoprotein effector complex (the RNA-induced silencing complex, RISC). Mutation on the Argonaute protein, if affecting either step of the RISC assembly, impacts the function of miRNAs. Therefore, any observation of decreased miRNA level of mutants will provide insights into the role of those amino acid residues in the mechanical function of the Argonaute protein. In this chapter, we introduce a method to relatively quantify a specific miRNA co-immunoprecipitated with wild type and mutant Argonaute proteins from HEK293T cells, using Real-Time Quantitative Reverse Transcription Polymerase Chain Reaction (qRT-PCR). Spiking a synthetic exogenous miRNA as an internal control with RNA extraction prior to cDNA synthesis will normalize the C
t values obtained from the qRT-PCR assays and enable us to quantify the relative level of Argonaute-bound miRNA.- Published
- 2018
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35. G-CSF improves safety when you start the day after autologous transplant in multiple myeloma.
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Sborov DW, Cho YK, Cottini F, Hade EM, Lamprecht M, Tackett K, Sharma N, Williams N, Li J, Devine S, Poi M, Phelps MA, and Hofmeister CC
- Subjects
- Adult, Aged, Autografts, Combined Modality Therapy, Female, Humans, Male, Middle Aged, Multiple Myeloma diagnosis, Multiple Myeloma mortality, Odds Ratio, Treatment Outcome, Granulocyte Colony-Stimulating Factor administration & dosage, Hematopoietic Stem Cell Transplantation adverse effects, Multiple Myeloma therapy
- Published
- 2017
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36. A phase 1 trial of the HDAC inhibitor AR-42 in patients with multiple myeloma and T- and B-cell lymphomas.
- Author
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Sborov DW, Canella A, Hade EM, Mo X, Khountham S, Wang J, Ni W, Poi M, Coss C, Liu Z, Phelps MA, Mortazavi A, Andritsos L, Baiocchi RA, Christian BA, Benson DM, Flynn J, Porcu P, Byrd JC, Pichiorri F, and Hofmeister CC
- Subjects
- Humans, Histone Deacetylase Inhibitors adverse effects, Histone Deacetylase Inhibitors therapeutic use, Lymphoma, B-Cell drug therapy, Multiple Myeloma drug therapy, Phenylbutyrates adverse effects, Phenylbutyrates therapeutic use
- Abstract
Histone deacetylase inhibitors (HDACi) have proven activity in hematologic malignancies, and their FDA approval in multiple myeloma (MM) and T-cell lymphoma highlights the need for further development of this drug class. We investigated AR-42, an oral pan-HDACi, in a first-in-man phase 1 dose escalation clinical trial. Overall, treatment was well tolerated, no DLTs were evident, and the MTD was defined as 40 mg dosed three times weekly for three weeks of a 28-day cycle. One patient each with MM and mantle cell lymphoma demonstrated disease control for 19 and 27 months (ongoing), respectively. Treatment was associated with reduction of serum CD44, a transmembrane glycoprotein associated with steroid and immunomodulatory drug resistance in MM. Our findings indicate that AR-42 is safe and that further investigation of AR-42 in combination regimens for the treatment of patients with lymphoma and MM is warranted., Trial Registration: http://clinicaltrials.gov/ct2/show/NCT01129193.
- Published
- 2017
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37. National survey of comprehensive pharmacy services provided in cancer clinical trials.
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Khandoobhai A, Poi M, Kelley K, Mirtallo J, Lopez B, and Griffith N
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- Clinical Trials as Topic organization & administration, Cross-Sectional Studies, Humans, National Cancer Institute (U.S.), Pharmacy Service, Hospital organization & administration, Professional Role, Surveys and Questionnaires, United States, Clinical Trials as Topic statistics & numerical data, Pharmacy Service, Hospital statistics & numerical data
- Abstract
Purpose: Pharmacy services provided in clinical trials at National Cancer Institute (NCI)-designated centers were assessed., Methods: This was a cross-sectional survey of 61 NCI-designated cancer centers. Directors of pharmacy were contacted and data were collected electronically via Qualtrics over 2 months. Trial participants were asked to estimate the frequency that their sites performed 26 services and the perceived importance of these services. Services were examined with respect to the difference between their reported performance and their reported importance. Eight of the 26 services showed a difference of at least 40% between the proportion of respondents performing the activities "often" or "almost always" and the proportion considering them "important" or "very important." Demographic information was collected, as well as perceived barriers., Results: Survey response rate was 59% (36 out of 61). The majority of services for clinical trials (19 out of 26) were viewed as important for pharmacists to perform; however, less than half (10 out of 26) were performed more than 50% of the time. Eight services had a gap of more than 40% when comparing the importance versus extent of implementation. Some of the largest gaps were reported in investigator-initiated trials development, medication reconciliation, therapeutic drug monitoring, and oral chemotherapy adherence assessment. Future studies can assist with cost justification by demonstrating the regulatory, safety, and financial benefits of pharmacist involvement in cancer trials., Conclusion: A survey of pharmacy directors at cancer centers revealed gaps between what respondents considered important pharmacist services in the provision of cancer clinical trials and the actual performance of those services in their institution., (Copyright © 2017 by the American Society of Health-System Pharmacists, Inc. All rights reserved.)
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- 2017
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38. Minocycline, a putative neuroprotectant, co-administered with doxorubicin-cyclophosphamide chemotherapy in a xenograft model of triple-negative breast cancer.
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Himmel LE, Lustberg MB, DeVries AC, Poi M, Chen CS, and Kulp SK
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- Animals, Apoptosis drug effects, Blotting, Western, Cell Line, Tumor, Cell Survival drug effects, Cognition Disorders prevention & control, Cyclophosphamide toxicity, DNA Damage drug effects, Doxorubicin toxicity, Female, Humans, Immunohistochemistry, Mice, Mice, Nude, Xenograft Model Antitumor Assays, Antineoplastic Combined Chemotherapy Protocols toxicity, Cognition Disorders chemically induced, Minocycline pharmacology, Neuroprotective Agents pharmacology, Triple Negative Breast Neoplasms
- Abstract
Minocycline is purported to have neuroprotective properties in experimental models of some human neurologic diseases, and has therefore been identified as a putative neuroprotectant for chemotherapy-induced cognitive impairment (CICI) in breast cancer patients. However, because its mechanism of action is believed to be mediated through anti-inflammatory, anti-apoptotic, and anti-oxidant pathways, co-administration of minocycline with chemotherapeutic agents has the potential to reduce the efficacy of anticancer drugs. The objective of this study is to evaluate the effect of minocycline on the activity of the AC chemotherapeutic regimen (Adriamycin [doxorubicin], Cytoxan [cyclophosphamide]) in in vitro and in vivo models of triple-negative breast cancer (TNBC). Clonogenic and methylthiazol tetrazolium (MTT) assays were used to assess survival and viability in two TNBC cell lines treated with increasing concentrations of AC in the presence or absence of minocycline. Biomarkers of apoptosis, cell stress, and DNA damage were evaluated by western blot. The in vivo effects of AC and minocycline, each alone and in combination, were assessed in a xenograft model of TNBC in female athymic nude mice by weekly tumor volume measurement, body and organ weight measurement, and histopathology. Apoptosis and proliferation were characterized by immunohistochemistry in the xenografts tumors. Brains from tumor-bearing mice were evaluated for microglial activation, glial scars, and the proportion of neural progenitor cells. Data from these in vitro and in vivo studies demonstrate that minocycline does not diminish the cytotoxic and tumor-suppressive effects of this chemotherapeutic drug combination in TNBC cells. Moreover, minocycline appeared to prevent the reduction in doublecortin-positive neural progenitor cells observed in AC-treated mice. We posit that minocycline may be useful clinically for its reported neuroprotective activity in breast cancer patients receiving AC without loss of chemotherapeutic efficacy., (Copyright © 2016 Elsevier GmbH. All rights reserved.)
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- 2016
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39. Molecular and Pharmacologic Properties of the Anticancer Quinolone Derivative Vosaroxin: A New Therapeutic Agent for Acute Myeloid Leukemia.
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Jamieson GC, Fox JA, Poi M, and Strickland SA
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- Aged, Aged, 80 and over, Animals, Antineoplastic Combined Chemotherapy Protocols, Cytarabine, Double-Blind Method, Haplorhini, Humans, Leukemia, Myeloid, Acute mortality, Mice, Middle Aged, Naphthyridines pharmacology, Rats, Thiazoles pharmacology, Leukemia, Myeloid, Acute drug therapy, Naphthyridines therapeutic use, Quinolones chemistry, Thiazoles therapeutic use
- Abstract
Vosaroxin is a first-in-class anticancer quinolone derivative that targets topoisomerase II and induces site-selective double-strand breaks in DNA, leading to tumor cell apoptosis. Vosaroxin has chemical and pharmacologic characteristics distinct from other topoisomerase II inhibitors due to its quinolone scaffold. The efficacy and safety of vosaroxin in combination with cytarabine were evaluated in patients with relapsed/refractory acute myeloid leukemia (AML) in a phase III, randomized, multicenter, double-blind, placebo-controlled study (VALOR). In this study, the addition of vosaroxin produced a 1.4-month improvement in median overall survival (OS; 7.5 months with vosaroxin/cytarabine vs. 6.1 months with placebo/cytarabine; hazard ratio [HR] 0.87, 95 % confidence interval [CI] 0.73-1.02; unstratified log-rank p [Formula: see text] 0.061; stratified log-rank p [Formula: see text]0.024), with the greatest OS benefit observed in patients ≥60 years of age (7.1 vs. 5.0 months; HR 0.75, 95 % CI 0.62-0.92; p [Formula: see text]0.003) and patients with early relapse (6.7 vs. 5.2 months; HR 0.77, 95 % CI 0.59-1.00; p [Formula: see text] 0.039), two AML patient groups that typically have poor prognosis. Here we review the chemical and pharmacologic properties of vosaroxin, how these properties are distinct from those of currently available topoisomerase II inhibitors, how they may contribute to the efficacy and safety profile observed in the VALOR trial, and the status of clinical development of vosaroxin for treatment of AML.
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- 2016
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40. A phase 1 clinical trial of flavopiridol consolidation in chronic lymphocytic leukemia patients following chemoimmunotherapy.
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Awan FT, Jones JA, Maddocks K, Poi M, Grever MR, Johnson A, Byrd JC, and Andritsos LA
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- Aged, Disease-Free Survival, Female, Humans, Immunotherapy methods, Male, Middle Aged, Treatment Outcome, Antineoplastic Agents therapeutic use, Flavonoids therapeutic use, Immunotherapy trends, Leukemia, Lymphocytic, Chronic, B-Cell diagnosis, Leukemia, Lymphocytic, Chronic, B-Cell drug therapy, Piperidines therapeutic use
- Abstract
Patients with chronic lymphocytic leukemia (CLL) who receive chemoimmunotherapy and do not achieve complete remission experience significantly shortened progression-free interval (PFS). Additionally, the majority of patients treated for relapsed disease demonstrate evidence of measurable disease. Eradication of minimal residual disease (MRD) results in improved PFS and overall survival. Maintenance therapy might result in eradication of MRD and improve response duration but might be associated with an increase in incidence of infectious complications. Flavopiridol is a broad cyclin-dependent kinase (CDK) inhibitor with established safety and efficacy in patients with relapsed CLL, particularly patients with high-risk cytogenetic features. A pharmacologically derived schedule was utilized as consolidation therapy in this phase I study to assess the safety and feasibility of outpatient therapy with flavopiridol in patients with low tumor burden. Flavopiridol was administered as a 30-min loading dose of 30 mg/m(2) followed by a 4-h infusion of 30 mg/m(2) once weekly for 3 weeks every 5 weeks (1 cycle) for planned 2 cycles in ten patients. Therapy was extremely well tolerated and no patient developed acute tumor lysis syndrome. The most common toxicities were gastrointestinal. Of the patients, 22 % improved their response from a PR to CR. Eighty-eight percent experienced a reduction in tumor burden as measured by extent of bone marrow involvement including patients with del17p and complex karyotype. The study establishes the safety and efficacy of flavopiridol as consolidation therapy after chemoimmunotherapy for patients with CLL. Further evaluation is required in larger trials for the utility of CDK inhibitors as consolidation or maintenance strategies.Registration number at ClinicalTrials.gov: NCT00377104.
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- 2016
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41. NK Cell-Mediated Antitumor Effects of a Folate-Conjugated Immunoglobulin Are Enhanced by Cytokines.
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Jaime-Ramirez AC, McMichael E, Kondadasula S, Skinner CC, Mundy-Bosse BL, Luedke E, Jones NB, Mani A, Roda J, Karpa V, Li H, Li J, Elavazhagan S, La Perle KM, Schmitt AC, Lu Y, Zhang X, Pan X, Mao H, Davis M, Jarjoura D, Butchar JP, Poi M, Phelps M, Tridandapani S, Byrd JC, Caligiuri MA, Lee RJ, and Carson WE 3rd
- Subjects
- Animals, Antibody-Dependent Cell Cytotoxicity immunology, Cell Line, Tumor, Disease Models, Animal, Female, Folate Receptor 1 genetics, Folate Receptor 1 metabolism, Gene Expression, Humans, Immunoglobulin G immunology, Immunomodulation, Interleukin-12 biosynthesis, Lymphocyte Activation immunology, Mice, Monocytes immunology, Monocytes metabolism, Neoplasms genetics, Neoplasms pathology, Tumor Burden immunology, Xenograft Model Antitumor Assays, Cytokines metabolism, Cytotoxicity, Immunologic drug effects, Folic Acid administration & dosage, Immunoconjugates immunology, Killer Cells, Natural immunology, Killer Cells, Natural metabolism, Neoplasms immunology, Neoplasms metabolism
- Abstract
Optimally effective antitumor therapies would not only activate immune effector cells but also engage them at the tumor. Folate conjugated to immunoglobulin (F-IgG) could direct innate immune cells with Fc receptors to folate receptor-expressing cancer cells. F-IgG bound to human KB and HeLa cells, as well as murine L1210JF, a folate receptor (FR)-overexpressing cancer cell line, as determined by flow cytometry. Recognition of F-IgG by natural killer (NK) cell Fc receptors led to phosphorylation of the ERK transcription factor and increased NK cell expression of CD69. Lysis of KB tumor cells by NK cells increased by about 5-fold after treatment with F-IgG, an effect synergistically enhanced by treatment with IL2, IL12, IL15, or IL21 (P< 0.001). F-IgG also enhanced the lysis of chronic lymphocytic leukemia cells by autologous NK cells. NK cells significantly increased production of IFNγ, MIP-1α, and RANTES in response to F-IgG-coated KB target cells in the presence of the NK cell-activating cytokine IL12, and these coculture supernatants induced significant T-cell chemotaxis (P< 0.001). F-IgG-coated targets also stimulated FcR-mediated monocyte effector functions. Studies in a murine leukemia model confirmed the intratumoral localization and antitumor activity of F-IgG, as well as enhancement of its effects by IL12 (P =0.05). The antitumor effect of this combination was dependent on NK cells and led to decreased tumor cell proliferation in vivo Thus, F-IgG can induce an immune response against FR-positive tumor cells that is mediated by NK cells and can be augmented by cytokine therapy., (©2016 American Association for Cancer Research.)
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- 2016
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42. Retracted: Reversal of Spinal Cord Ischemia Following Endovascular Thoracic Aortic Aneurysm Repair with Hyperbaric Oxygen and Therapeutic Hypothermia.
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Urquieta E, Jye Poi M, Varon J, and Lin PH
- Abstract
This article has been officially retracted. The senior author, Emmanuel Urquieta, of the article entitled, "Reversal of Spinal Cord Ischemia Following Endovascular Thoracic Aortic Aneurysm Repair with Hyperbaric Oxygen and Therapeutic Hypothermia," has requesed that the article, published online ahead of print (DOI: 10.1089/ther.2015.0025), be retracted because he discovered one of his coauthors mistakenly submitted the same article to the Journal of Vascular Surgery due to a miscommunication between them. The editorial leadership of Therapeutic Hypothermia and Temperature Management agree that the article must be retracted as a matter of proper scientific publishing protocol whereby an article may not be simultaneously submitted to two journals. The Editors commend Dr. Urquieta for willingly bringing this situation to their attention. Dr. Urquieta and his coauthors sincerely apologize to the Editors and the readership of Therapeutic Hypothermia and Temperature Management.
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- 2015
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43. The combination of milatuzumab, a humanized anti-CD74 antibody, and veltuzumab, a humanized anti-CD20 antibody, demonstrates activity in patients with relapsed and refractory B-cell non-Hodgkin lymphoma.
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Christian BA, Poi M, Jones JA, Porcu P, Maddocks K, Flynn JM, Benson DM Jr, Phelps MA, Wei L, Byrd JC, Wegener WA, Goldenberg DM, Baiocchi RA, and Blum KA
- Subjects
- Adult, Aged, Aged, 80 and over, Antibodies, Monoclonal, Humanized administration & dosage, Antibodies, Monoclonal, Humanized pharmacokinetics, Antineoplastic Combined Chemotherapy Protocols adverse effects, Female, Humans, Lymphoma, Non-Hodgkin diagnosis, Lymphoma, Non-Hodgkin mortality, Male, Middle Aged, Neoplasm Grading, Treatment Outcome, Antineoplastic Combined Chemotherapy Protocols therapeutic use, B-Lymphocytes pathology, Lymphoma, Non-Hodgkin drug therapy, Lymphoma, Non-Hodgkin pathology
- Abstract
As a result of the anti-tumour activity observed in vitro and in vivo with combined anti-CD20 and anti-CD74 antibodies, we initiated a phase I/II trial of veltuzumab and milatuzumab in patients with relapsed or refractory B-cell non-Hodgkin lymphoma (NHL). Patients received an induction of veltuzumab 200 mg/m(2) weekly combined with escalating doses of milatuzumab at 8, 16 and 20 mg/kg weekly for 4 weeks. Patients without disease progression could receive an extended induction with treatment on weeks 12, 20, 28 and 36. A total of 35 patients enrolled on the study. Median age was 63 years, median number of prior therapies was 3, and 63% of patients were rituximab refractory. No dose-limiting toxicities were observed in the phase I study. Related grade 3-4 toxicities included lymphopenia, leucopenia, neutropenia, anaemia, infusion reactions, hyperglycaemia, fatigue and atrial tachycardia. Median weeks of therapy was 12 and 29% of patients completed all 36 weeks of therapy. The overall response rate was 24%, median duration of response was 12 months, and responses were observed at all dose levels and in 50% of patients refractory to rituximab. Combination therapy with veltuzumab and milatuzumab demonstrated activity in a population of heavily pre-treated patients with relapsed or refractory indolent NHL., (© 2015 John Wiley & Sons Ltd.)
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- 2015
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44. A dose escalation feasibility study of lenalidomide for treatment of symptomatic, relapsed chronic lymphocytic leukemia.
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Maddocks K, Ruppert AS, Browning R, Jones J, Flynn J, Kefauver C, Gao Y, Jiang Y, Rozewski DM, Poi M, Phelps MA, Harper E, Johnson AJ, Byrd JC, and Andritsos LA
- Subjects
- Adult, Aged, Antineoplastic Agents adverse effects, Cohort Studies, Dose-Response Relationship, Drug, Feasibility Studies, Female, Humans, Lenalidomide, Leukemia, Lymphocytic, Chronic, B-Cell pathology, Male, Maximum Tolerated Dose, Middle Aged, Recurrence, Thalidomide administration & dosage, Thalidomide adverse effects, Treatment Outcome, Antineoplastic Agents administration & dosage, Leukemia, Lymphocytic, Chronic, B-Cell drug therapy, Thalidomide analogs & derivatives
- Abstract
Adequate dosing of lenalidomide in Chronic Lymphocytic Leukemia (CLL) remains unclear. This study determined maximum tolerated dose (MTD) in relapsed CLL patients (Cohort A) and patients achieving a partial response (PR) or better to recent therapy (Cohort B). Thirty-seven patients were enrolled. MTD was 2.5mg followed by 5.0mg continuous. In Cohort A, tumor flare grade 1-2 occurred in 15 patients (50%) and grade 3 in 1 patient (3%). Cohort A had 19 of 23 evaluable (83%) patients, 4 PR (17%) and 15 (65%) stable disease (SD), Cohort B had 6 of 7 patients (86%) with SD. Despite overall response rate not being high, many patients remained on therapy several months with SD., (Copyright © 2014 Elsevier Ltd. All rights reserved.)
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- 2014
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45. A phase I trial of flavopiridol in relapsed multiple myeloma.
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Hofmeister CC, Poi M, Bowers MA, Zhao W, Phelps MA, Benson DM, Kraut EH, Farag S, Efebera YA, Sexton J, Lin TS, Grever M, and Byrd JC
- Subjects
- Aged, Aged, 80 and over, Antineoplastic Agents adverse effects, Antineoplastic Agents blood, Antineoplastic Agents pharmacokinetics, Dose-Response Relationship, Drug, Flavonoids adverse effects, Flavonoids blood, Flavonoids pharmacokinetics, Humans, Middle Aged, Multiple Myeloma blood, Multiple Myeloma metabolism, Multiple Myeloma pathology, Piperidines adverse effects, Piperidines blood, Piperidines pharmacokinetics, Recurrence, Antineoplastic Agents administration & dosage, Flavonoids administration & dosage, Multiple Myeloma drug therapy, Piperidines administration & dosage
- Abstract
Purpose: Flavopiridol is primarily a cyclin-dependent kinase-9 inhibitor, and we performed a dose escalation trial to determine the maximum tolerated dose and safety and generate a pharmacokinetic (PK) profile., Methods: Patients with a diagnosis of relapsed myeloma after at least two prior treatments were included. Flavopiridol was administered as a bolus and then continuous infusion weekly for 4 weeks in a 6-week cycle., Results: Fifteen patients were treated at three dose levels (30 mg/m(2) bolus, 30 mg/m(2) CIV to 50 mg/m(2) bolus, and 50 mg/m(2) CIV). Cytopenias were significant, and elevated transaminases (grade 4 in 3 patients, grade 3 in 4 patients, and grade 2 in 3 patients) were noted but were transient. Diarrhea (grade 3 in 6 patients and grade 2 in 5 patients) did not lead to hospital admission. There were no confirmed partial responses although one patient with t(4;14) had a decrease in his monoclonal protein >50 % that did not persist. PK properties were similar to prior publications, and immunohistochemical staining for cyclin D1 and phospho-retinoblastoma did not predict response., Conclusions: Flavopiridol as a single agent given by bolus and then infusion caused significant diarrhea, cytopenias, and transaminase elevation but only achieved marginal responses in relapsed myeloma (ClinicalTrials.gov identifier NCT00112723).
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- 2014
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46. Flavopiridol can be safely administered using a pharmacologically derived schedule and demonstrates activity in relapsed and refractory non-Hodgkin's lymphoma.
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Jones JA, Rupert AS, Poi M, Phelps MA, Andritsos L, Baiocchi R, Benson DM, Blum KA, Christian B, Flynn J, Penza S, Porcu P, Grever MR, and Byrd JC
- Subjects
- Adult, Aged, Aged, 80 and over, Antineoplastic Agents pharmacology, Drug Administration Schedule, Female, Flavonoids pharmacology, Humans, Lymphoma, Non-Hodgkin diagnosis, Male, Maximum Tolerated Dose, Middle Aged, Piperidines pharmacology, Protein Kinase Inhibitors pharmacology, Recurrence, Treatment Outcome, Antineoplastic Agents therapeutic use, Flavonoids therapeutic use, Lymphoma, Non-Hodgkin drug therapy, Piperidines therapeutic use, Protein Kinase Inhibitors therapeutic use
- Abstract
Flavopiridol is a broad cyclin-dependent kinase inhibitor (CDKI) that induces apoptosis of malignant lymphocytes in vitro and in murine lymphoma models. We conducted a Phase I dose-escalation study to determine the maximum tolerated dose (MTD) for single-agent flavopiridol administered on a pharmacokinetically derived hybrid dosing schedule to patients with relapsed and refractory non-Hodgkin's lymphoma. Dose was escalated independently in one of four cohorts: indolent B-cell (Cohort 1), mantle cell (Cohort 2), intermediate-grade B-cell including transformed lymphoma (Cohort 3), and T-/NK-cell excluding primary cutaneous disease (Cohort 4). Forty-six patients were accrued. Grade 3 or 4 leukopenia was observed in the majority of patients (60%), but infection was infrequent. Common nonhematologic toxicities included diarrhea and fatigue. Biochemical tumor lysis was observed in only two patients, and no patients required hemodialysis for its management. Dose escalation was completed in two cohorts (indolent and aggressive B-cell). Dose-limiting toxicities were not observed, and the MTD was not reached in either cohort at the highest dose tested (50 mg/m(2) bolus + 50 mg/m(2) continuous infusion weekly for 4 consecutive weeks of a 6-week cycle). Clinical benefit was observed in 26% of 43 patients evaluable for response, including 14% with partial responses (two mantle cells, three indolent B-cells, and one diffuse large B-cell). The single-agent activity of this first-generation CDKI suggests that other agents in this class merit further study in lymphoid malignancies, both alone and in combination., (Copyright © 2013 Wiley Periodicals, Inc.)
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- 2014
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47. A pharmacokinetic/pharmacodynamic model of tumor lysis syndrome in chronic lymphocytic leukemia patients treated with flavopiridol.
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Ji J, Mould DR, Blum KA, Ruppert AS, Poi M, Zhao Y, Johnson AJ, Byrd JC, Grever MR, and Phelps MA
- Subjects
- Antineoplastic Agents pharmacokinetics, Female, Flavonoids pharmacokinetics, Follow-Up Studies, Humans, Leukemia, Lymphocytic, Chronic, B-Cell complications, Leukemia, Lymphocytic, Chronic, B-Cell pathology, Male, Maximum Tolerated Dose, Neoplasm Recurrence, Local, Piperidines pharmacokinetics, Prevalence, Prognosis, Tissue Distribution, Tumor Lysis Syndrome etiology, United States epidemiology, Antineoplastic Agents therapeutic use, Flavonoids therapeutic use, Leukemia, Lymphocytic, Chronic, B-Cell drug therapy, Models, Biological, Piperidines therapeutic use, Tumor Lysis Syndrome epidemiology
- Abstract
Purpose: Flavopiridol, the first clinically evaluated cyclin-dependent kinase inhibitor, shows activity in patients with refractory chronic lymphocytic leukemia, but prevalent and unpredictable tumor lysis syndrome (TLS) presents a major barrier to its broad clinical use. The purpose of this study was to investigate the relationships between pretreatment risk factors, drug pharmacokinetics, and TLS., Experimental Design: A population pharmacokinetic/pharmacodynamic model linking drug exposure and TLS was developed. Plasma data of flavopiridol and its glucuronide metabolite (flavo-G) were obtained from 111 patients treated in early-phase trials with frequent sampling following initial and/or escalated doses. TLS grading was modeled with logistic regression as a pharmacodynamic endpoint. Demographics, baseline disease status, and blood chemistry variables were evaluated as covariates., Results: Gender was the most significant pharmacokinetic covariate, with females displaying higher flavo-G exposure than males. Glucuronide metabolite exposure was predictive of TLS occurrence, and bulky lymphadenopathy was identified as a significant covariate on TLS probability. The estimated probability of TLS occurrence in patients with baseline bulky lymphadenopathy less than 10 cm or 10 cm or more during the first 2 treatments was 0.111 (SE% 13.0%) and 0.265 (SE% 17.9%), respectively, when flavo-G area under the plasma concentration versus time curve was at its median value in whole-patient group., Conclusions: This is the first population pharmacokinetic/pharmacodynamic model of TLS. Further work is needed to explore potential mechanisms and to determine whether the associations between TLS, gender, and glucuronide metabolites are relevant in patients with chronic lymphocytic leukemia treated with other cyclin-dependent kinase inhibitors., (©2012 AACR.)
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- 2013
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48. Somatic INK4a-ARF locus mutations: a significant mechanism of gene inactivation in squamous cell carcinomas of the head and neck.
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Poi MJ, Yen T, Li J, Song H, Lang JC, Schuller DE, Pearl DK, Casto BC, Tsai MD, and Weghorst CM
- Subjects
- Base Sequence, DNA Primers, Humans, Mutagenesis, Site-Directed, Nuclear Magnetic Resonance, Biomolecular, Polymerase Chain Reaction, Polymorphism, Single-Stranded Conformational, Carcinoma, Squamous Cell genetics, Cyclin-Dependent Kinase Inhibitor p16 genetics, Head and Neck Neoplasms genetics, Helminth Proteins genetics, Muscle Proteins genetics, Mutation
- Abstract
The INK4a-ARF locus is located on human chromosome 9p21 and is known to encode two functionally distinct tumor-suppressor genes. The p16(INK4a) (p16) tumor-suppressor gene product is a negative regulator of cyclin-dependent kinases 4 and 6, which in turn positively regulate progression of mammalian cells through the cell cycle. The p14(ARF) tumor-suppressor gene product specifically interacts with human double minute 2, leading to the subsequent stabilization of p53 and G(1) arrest. Previous investigations analyzing the p16 gene in squamous cell carcinomas of the head and neck (SCCHNs) have suggested the predominate inactivating events to be homozygous gene deletions and hypermethylation of the p16 promoter. Somatic mutational inactivation of p16 has been reported to be low (0-10%, with a combined incidence of 25 of 279, or 9%) and to play only a minor role in the development of SCCHN. The present study examined whether this particular mechanism of INK4a/ARF inactivation, specifically somatic mutation, has been underestimated in SCCHN by determining the mutational status of the p16 and p14(ARF) genes in 100 primary SCCHNs with the use of polymerase chain reaction technology and a highly sensitive, nonradioactive modification of single-stranded conformational polymorphism (SSCP) analysis termed "cold" SSCP. Exons 1alpha, 1beta, and 2 of INK4a/ARF were amplified using intron-based primers or a combination of intron- and exon-based primers. A total of 27 SCCHNs (27%) exhibited sequence alterations in this locus, 22 (22%) of which were somatic sequence alterations and five (5%) of which were a single polymorphism in codon 148. Of the 22 somatic alterations, 20 (91%) directly or indirectly involved exon 2, and two (9%) were located within exon 1alpha. No mutations were found in exon 1beta. All 22 somatic mutations would be expected to yield altered p16 proteins, but only 15 of them should affect p14(ARF) proteins. Specific somatic alterations included microdeletions or insertions (nine of 22, 41%), a microrearrangement (one of 22, 5%), and single nucleotide substitutions (12 of 22, 56%). In addition, we analyzed the functional characteristics of seven unique mutant p16 proteins identified in this study by assessing their ability to inhibit cyclin-dependent kinase 4 activity. Six of the seven mutant proteins tested exhibited reduced function compared with wild-type p16, ranging from minor decreases of function (twofold to eightfold) in four samples to total loss of function (29- to 38-fold decrease) in two other samples. Overall, somatic mutation of the INK4a/ARF tumor suppressor locus, resulting in functionally deficient p16 and possibly p14(ARF) proteins, seems to be a prevalent event in the development of SCCHN. Mol. Carcinog. 30:26-36, 2001., (Copyright 2001 Wiley-Liss, Inc.)
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- 2001
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49. Structural basis of the anionic interface preference and kcat* activation of pancreatic phospholipase A2.
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Yu BZ, Poi MJ, Ramagopal UA, Jain R, Ramakumar S, Berg OG, Tsai MD, Sekar K, and Jain MK
- Subjects
- Amino Acid Substitution genetics, Animals, Anions, Binding Sites genetics, Catalysis, Cations, Cattle, Crystallography, X-Ray, Dimyristoylphosphatidylcholine chemistry, Dimyristoylphosphatidylcholine metabolism, Enzyme Activation genetics, Horses, Hydrolysis, Kinetics, Lysine genetics, Models, Chemical, Mutagenesis, Site-Directed, Phosphatidylcholines chemistry, Phosphatidylcholines metabolism, Phospholipases A genetics, Phospholipases A2, Sheep, Spectrometry, Fluorescence, Spectrophotometry, Ultraviolet, Substrate Specificity genetics, Swine, Phospholipases A chemistry, Phospholipases A metabolism
- Abstract
Pancreatic phospholipase A(2) (PLA2) shows a strong preference for the binding to the anionic interface and a consequent allosteric activation. In this paper, we show that virtually all the preference is mediated through 3 (Lys-53, -56, and -120) of the 12 cationic residues of bovine pancreatic PLA2. The lysine-to-methionine substitution enhances the binding of the enzyme to the zwitterionic interface, and for the K53,56,120M triple mutant at the zwitterionic interface is comparable to that for the wild type (WT) at the anionic interface. In the isomorphous crystal structure, the backbone folding of K53,56M K120,121A and WT are virtually identical, yet a significant change in the side chains of certain residues, away from the site of substitution, mostly at the putative contact site with the interface (i-face), is discernible. Such reciprocity, also supported by the spectroscopic results for the free and bound forms of the enzyme, is expected because a distal structural change that perturbs the interfacial binding could also affect the i-face. The results show that lysine-to-methionine substitution induces a structural change that promotes the binding of PLA2 to the interface as well as the substrate binding to the enzyme at the interface. The kinetic results are consistent with a model in which the interfacial Michaelis complex exists in two forms, and the complex that undergoes the chemical step is formed by the charge compensation of Lys-53 and -56. Analysis of the incremental changes in the kinetic parameters shows that the charge compensation of Lys-53 and -56 contributes to the activation and that of Lys-120 contributes only to the structural change that promotes the stability of the Michaelis complex at the interface. The charge compensation effects on these three residues also account for the differences in the anionic interface preference of the evolutionarily divergent secreted PLA2.
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- 2000
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50. Tumor suppressor INK4: quantitative structure-function analyses of p18INK4C as an inhibitor of cyclin-dependent kinase 4.
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Li J, Poi MJ, Qin D, Selby TL, Byeon IJ, and Tsai MD
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- Amino Acid Sequence, Carrier Proteins genetics, Carrier Proteins metabolism, Crystallography, X-Ray, Cyclin-Dependent Kinase 4, Cyclin-Dependent Kinase 6, Cyclin-Dependent Kinase Inhibitor p18, Cyclin-Dependent Kinases chemistry, Cyclin-Dependent Kinases metabolism, Enzyme Inhibitors metabolism, Genes, Tumor Suppressor, Helix-Turn-Helix Motifs, Humans, Models, Molecular, Molecular Sequence Data, Mutagenesis, Site-Directed, Nuclear Magnetic Resonance, Biomolecular, Protein Conformation, Protein Serine-Threonine Kinases antagonists & inhibitors, Protein Serine-Threonine Kinases chemistry, Protein Serine-Threonine Kinases metabolism, Recombinant Proteins chemical synthesis, Recombinant Proteins metabolism, Sequence Deletion, Structure-Activity Relationship, Carrier Proteins chemistry, Carrier Proteins physiology, Cell Cycle Proteins, Cyclin-Dependent Kinases antagonists & inhibitors, Enzyme Inhibitors chemistry, Proto-Oncogene Proteins, Tumor Suppressor Proteins
- Abstract
We report the first detailed structure-function analyses of p18INK4C (p18), which is a homologue of the important tumor suppressor p16INK4A (p16). Twenty-four mutants were designed rationally. The global conformations of the mutants were characterized by NMR, while the function was assayed by inhibition of cyclin-dependent kinase 4 (CDK4). Most of these mutants have unperturbed global structures, thus the changes in their inhibitory abilities can be attributed to the mutated residues. The important results are summarized as follows: (a) some residues at loops 1 and 2, but not 3, are important for the inhibitory function of p18, similar to the results for p16; (b) two residues at the first helix-turn-helix motif and two at the third are important for inhibition; (c) while the results generally agree with the prediction based on the crystal structures of p16-CDK6 and p19-CDK6 binary complexes, there are significant differences in a few residues, suggesting that the interactions in the binary complexes may not accurately represent the interactions in the ternary complexes (in the presence of cyclin D2); (d) most importantly, the extra loop of p18 appears to contribute to the function of p18, even though the crystal structure of the p19INK4D-CDK6 complex indicates no interactions involving this loop; (e) detailed analyses of the crystal structures and the functional results suggest that there are notable differences in the interactions between different members of the INK4 family and CDKs.
- Published
- 2000
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