129 results on '"Paiss T"'
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2. Prospektive Evaluierung der Prostatakarzinomfrüherkennung bei Männern mit familiärer Disposition
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Paiss, T., Herkommer, K., Kahn, D., Gschwend, J. E., Küfer, R., Maier, C., Vogel, W., Högel, J., and Hautmann, R. E.
- Published
- 2006
- Full Text
- View/download PDF
3. Ist das Vorsorgeverhalten bei Männern mit familiärer Prädisposition für ein Prostatakarzinom vorhersehbar?*
- Author
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Paiss, T., Kahn, D., Küfer, R., Maier, C., Vogel, W., Gschwend, J. E., Hautmann, R. E., and Herkommer, K.
- Published
- 2005
- Full Text
- View/download PDF
4. Familiäres versus sporadisches Prostatakarzinom in der deutschen Population: Klinische und pathologische Charakteristika bei Patienten nach radikaler Prostatektomie
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Paiss, T., Bock, B., Gschwend, J. E., Heinz, H., Vogel, W., Kron, M., Hautmann, R. E., and Herkommer, K.
- Published
- 2003
- Full Text
- View/download PDF
5. Prostatakarzinomvorsorge bei Männern mit familiärer Disposition
- Author
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Paiss, T., Gschwend, J. E., Maier, C., Eisele, M., Vogel, W., Hautmann, R. E., and Herkommer, K.
- Published
- 2002
- Full Text
- View/download PDF
6. Das familiäre Prostatakarzinom in Deutschland
- Author
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Paiss, T., Herkommer, K., Chab, A., Häussler, J., Vogel, W., Gschwend, J. E., and Hautmann, R. E.
- Published
- 2002
- Full Text
- View/download PDF
7. Genetische Disposition zum Prostatakarzinom
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Häußler, J., Bochum, S., Rösch, K., Paiss, T., and Vogel, W.
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- 2000
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8. Vitamin D receptor polymorphisms as markers in prostate cancer
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Correa-Cerro, L., Berthon, P., Häussler, J., Bochum, S., Drelon, E., Mangin, P., Fournier, G., Paiss, T., Cussenot, O., and Vogel, W.
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- 1999
- Full Text
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9. Real-world outcomes with abiraterone in metastatic castration-resistant prostate cancer: The Prostate Cancer Registry
- Author
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Bjartell, A.S., primary, Lumen, N., additional, Maroto, P., additional, Paiss, T., additional, Gomez Veiga, F., additional, Birtle, A., additional, Kramer, G., additional, Kalinka, E., additional, Spaëth, D., additional, Feyeraband, S., additional, Matveev, V., additional, Lefresne, F., additional, Lukac, M., additional, Wapenaar, R., additional, Costa, L., additional, and Chowdhury, S., additional
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- 2019
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10. Klippel-Trenaunay-Syndrom: Eine seltene Ursache für rezidivierende Makrohämaturie – kasuistische Falldarstellung
- Author
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Rinnab, L., Paiss, T., and Küfer, R.
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- 2006
- Full Text
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11. The ileal neobladder — updated experience with 306 patients
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Flohr, P., Hefty, R., Paiss, T., and Hautmann, R.
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- 1996
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12. Association between the Clinical Presentation and Epidemiological Features of Familial Prostate Cancer in Patients Selected for Radical Prostatectomy
- Author
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Paiss, T., Herkommer, K., Bock, B., Heinz, H., Vogel, W., Kron, Martina, Kuefer, R., Hautmann, R.E., and Gschwend, J.E.
- Published
- 2003
- Full Text
- View/download PDF
13. High-dose pelvic irradiation followed by ileal neobladder urinary diversion: complications and long-term results
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GSCHWEND, J. E., MAY, F., PAISS, T., GOTTFRIED, H. W., and HAUTMANN, R. E.
- Published
- 1996
14. Results from a prospective observational study of men with premature ejaculation treated with dapoxetine or alternative care: The PAUSE study
- Author
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Mirone V, ARCANIOLO, Davide, Rivas D, Bull S, Aquilina JW, Verze P, PAUSE study team Berchart G, Hass M, Ludvik G, Aalto J, Hendolin N, Lukkarinen O, Multanen M, Nurmenniemi V, Piha J, Aheimer C, Alebrahim Dehkordy A, Andreessen R, Aust C, Baer P, Bath V, Baumgrass H, Beck C, Beecken WD, Behre H, Beitzinger M, Belusa A, Bermes UR, Berning T, Bieringer La Roche D, Blasko S, Boehmer S, Borchardt A, Boerner T, Brands F, Braun PM, Braun R, Breu D, Briken P, Brueske T, Bueker R, Buse A, Carius A, Christoph F, Cuno M, Dats E, Degen N, Denil J, Dietrichs K, Domnitz R, Dorn B, Dubiel J, Eckert R, Ehrenberg W, Eichler S, El Khadra S, Engl T, Esser O, Faragallah EA, Farahmandi R, Finke G, Fleig P, Fruehauf E, Gerhardt U, Girke CG, Glauche J, Gleissner J, Gnann R, Gralla O, Grandin A, Grewe W, Gronau E, Gruber S, Grunert S, Guelbeyaz M, Guelden H, Haendel D, Haefele J, Haghighat M, Hahne D, Haschemi Schirazi R, Hecker D, Herzig J, Hettmmer R, Hitschfeld K, Hofmann J, Hohmuth H, Hoelker D, Huebner A, Hudemann B, Hung Wehmann D, Huenninghaus K, Hueter K, Igde H, Jaeger T, Javadi P, John G, Ju M, Kaisser G, Kamann L, Kastein A, Kaup F, Kellner T, Kempe T, Kempter F, Kennerknecht M, Kirschner P, Koenig M, Konert J, Kowalik S, Krieger JU, Kruppa GL, Kube U, Kuehn F, Kuefer R, Kurt T, Kwela M, Laag R, Langen L, Lehmann J, Linder C, Loeber T, Lock UC, Loebenau M, Luberg Sievers G, Luebbe R, Lutz K, Maier S, Maletz C, Mertins B, Meschede E, Meschi MR, Miersch WD, Misera A, Muehlich S, Mueller HW, Mueller D, Muench HC, Nawka P, Othman K, Paiss T, Peter K, Peters T, Petras T, Petrischenko B, Pfund A, Plate H, Ploss HJ, Pohrt U, Pooyeh S, Potempa AJ, Pusinelli WD, Rausch U, Reinhardt F, Rengel U, Rietheimer W, Rinnab L, Rohrmann K, Romahn E, Romitan Baum R, Roessler T, Rudolph R, Rueffer J, Rug M, Rueth J, Ruettgers E, Santiago RB, Schaefer A, Schaefer T, Schaetzle P, Scheunpflug K, Schlicht J, Schmidt P, Schneider J, Schnitzler M, Schonfelder R, Schreier H, Schroeder A, Schulz FM, Schulze M, Schumann M, Seidler A, Seseke S, Siebel Eggeling G, Siebels M, Sinner B, Sippel F, Soballa M, Sommer F, Spielhaupter A, Steffen H, Steinacker M, Stiersdorfer A, Stoehr C, Sturm S, Surrey HW, Swoboda A, Szymula S, Telle J, Uththoff H, Vierneisel C, Vilmar W, Wagner M, Walhoefer F, Warnack W, Weiss J, Weizert P, Wicht A, Wieland J, Willgerodt J, Wilski B, Wilson E, Wipfler G, Wohn HG, Wolf J, Zoehrlaut B, Zuerner T, Angeletti G, Avolio A, Baldassarre R, Balercia G, Balloni F, Barba G, Bartoletti R, Basile Fasolo C, Bassi PF, Beatrici V, Bertozzi MA, Bocciardi AM, Bondavalli C, Bonini F, Bonsanto M, Branchi A, Briganti A, Calabrese M, Calafiore R, Calogero AE, Cantelmo P, Caraceni E, Carbone A, Cardella A, Carini M, Carmignani L, Carmignani G, Carrino M, Caviglia C, Cecchi M, Ceruti C, Chiovato L, Cicalese V, Colpi G, Corinti M, Cormio L, Cova G, Cozzupoli P, Ottavio G, Damiano R, De Ceglie G, De Grande G, De Lisa A, DE SIO, Marco, De Stefani S, Dehò F, Delsignore A, Di Filippo A, Di Lena S, Di Trapani D, Diambrini M, Drei GN, Fabbri A, Fasolis G, Ferone D, Ferrari G, Foresta C, Francavilla S, Gadda F, Galantini A, Galì A, Gentile V, Giammusso B, Giannubilo W, Granata A, Grasso M, Iafrate M, Ilacqua N, Isidori A, Italiano E, Jallous HA, Jannini E, La Pera G, Laganà F, Lauretti S, Leonardi R, Liguori G, Loiero G, Lombardi G, Lombardo F, Lusenti C, Maffucci A, Maggi M, Maio G, Mammana G, Manieri C, Marzotto Caotorta M, Mastroeni F, Mazzilli F, Mazzone L, Minervini M, Mirone VG, Montorsi F, Morelli G, Morrone G, Nicita G, Nicola M, Palmiotto F, Paradiso M, Paulis G, Pavone C, Pescatori ES, Petterle V, Piazza N, Pittaluga P, Piubello G, Polito M, Ponchietti R, Porena M, Rago R, Risi O, Roggia A, Salzano L, Sanseverino R, SASSO, Ferdinando Carlo, Savoca G, Scarano P, Schips L, Serao A, Sforza A, Sidari V, Silvani M, Sinisi A, Sorrentino F, Spera E, Strada G, Tenaglia R, Terrone C, Titta M, Tracia A, Turchi P, Ughi G, Vecchio D, Veneziano IA, Vicini P, Vita A, Vitti P, Volpi R, Zago T, Zenico T, Zito AR, Apolinario M, Carvalho AP, Corte Real J, Matos Cabeca J, Mendes Leal A, Monteiro Pereira N, Palma dos Reis J, Patricio A, Prisco R, Rocha Mendes J, Santos A, Vieira R, Abad Gairín C, Abascal García JM, Adot Zurbano JM, Álvarez de la Red PL, Al Wattar W, Antón Saiz C, Aranda Doncel N, Arrosagaray PM, Arteaga Serrano F, Barberán Soriano J, Bataller Perello V, Beltrán Persiva J, Benejam Gual J, Blanco Díez A, Blasco Casares FJ, Blasco Villalonga M, Blázquez Izquierdo J, Boladeras Sabater J, Borrás JJ, Bouchi Bakrim AR, Bucar Terrades S, Burgués Gasión JP, Busto Castañón L, Caballero JM, Cabello Santamaría F, Cabreja López E, Carrasco Aznar JC, Casasola Chamorro J, Castellanos González L, Cimadevila García A, Closas Capdevila M, Concepción Masip T, Conde C, Conde Santos G, Cortada i. Robert J, Cos Calvet JM, Crespi Martínez F, Cruz N, De la Rosa Khermann M, Delgado Martín JA, Devesa Mújica M, Doganis Peppas C, Domínguez Freire F, Donderis Guastavino C, Duarte Vázquez JJ, El Khoury Yacob R, Escobal Tamayo V, Farré Martí JM, Fernández Fernández A, Fernández Lozano A, Fernández Viñas JA, Fiter Gómez L, Fleitas Asencio E, Frago Valls SM, Galiana Álvarez A, García Bayo I, García Contreras J, García Cruz E, García de Jalón Martín A, García Giralda L, García Marco MA, García Navas R, García Reboll L, Garrido Insúa S, Giner Santamaría C, Gómez Berjón F, Gómez Gil E, Gómez Lanza E, Gómez Pérez L, Gómez Rodríguez A, González Sala JL, González Sala MJ, Gonzalvo Ybarra A, Guerrero Martínez V, Gutiérrez González MA, Gutierrez Mínguez E, Hidalgo Arroyo J, Hmeidan M, Idígora i. Planas X, Jara Rascón J, Jiménez Verdejo J, Lledó García E, Lliteras Arañi M, López Almansa M, López Palacios MÁ, López Tello J, Lorenzo Gómez MF, Luque Gálvez P, Luque López AJ, Mallafré Sala JM, Martí Cebrián JM, Martín Clos J, Martín Huescar A, Martín Morales A, Martín Rodríguez A, Martínez Rodríguez R, Martínez Salamanca JI, Mascarós Balaguer E, Mejide Manresa R, Molero Rodríguez F, Molina Carranza A, Moncada Iribarren I, Montagud Moncho JB, Montesino Semper M, Mosteiro Ponce JA, Mouaffak Tatari N, Navarro Gil JM, Novás Castro S, Ortiz del Corral ML, Ortiz Gamiz A, Osca García JM, Padilla León M, Palomino García A, Pascual Mateo C, Peinado Ibarra F, Pérez Mestre M, Portillo Martín JA, Poyato Galán JM, Prats de Puig J, Prieto Castro R, Puigvert Martínez A, Quintana de la Rosa JL, Ramada Benlloch FJ, Reyes Martínez F, Rigabert M, Ríos Espuny AF, Robles Iniesta A, Rodrigo Aliaga M, Rodríguez Alba JL, Rodríguez Bethencourt F, Rodríguez Jiménez FJ, Rodríguez Leal DA, Rodríguez Rubio F, Rodríguez Tolrá J, Rodríguez Vallejo JM, Romero Otero J, Roselló Barbará M, Rubio Briones J, Ruíz Moriana O, Sampol Company J, San Martín Blanco C, Sánchez Encinas M, Sánchez Sánchez F, Sancho Serrano C, Santandreu Puifros J, Santisteban González M, Santos Ascarza Tabares JL, Sanz Lahoz I, Sapiña Ortola F, Sarquella Geli J, Segarra Tomás J, Soler Fernández J, Tato Rodríguez J, Tesedo Cubedo J, Traid Sender V, Valbuena Álvarez R, Valverde Rubio JM, Varela Salgado M, Vargas Rugeles M, Vilches Cocovi E, Virto Bajo FJ, Andius P, Anker Hansen O, Arver S, Bosson P, Brattberg A, Grenabo L, Hanning J, Hassler L, Paradis AÅ, Wang E., Mirone, Vincenzo, Arcaniolo, Davide, David, Riva, Scott, Bull, Joseph W., Aquilina, Verze, Paolo, Mirone, V, Arcaniolo, D, Rivas, D, Bull, S, Aquilina, JW, Verze, P, Pavone, C, Aquilina, Jw, PAUSE study team Berchart, G, Hass, M, Ludvik, G, Aalto, J, Hendolin, N, Lukkarinen, O, Multanen, M, Nurmenniemi, V, Piha, J, Aheimer, C, Alebrahim Dehkordy, A, Andreessen, R, Aust, C, Baer, P, Bath, V, Baumgrass, H, Beck, C, Beecken, Wd, Behre, H, Beitzinger, M, Belusa, A, Bermes, Ur, Berning, T, Bieringer La Roche, D, Blasko, S, Boehmer, S, Borchardt, A, Boerner, T, Brands, F, Braun, Pm, Braun, R, Breu, D, Briken, P, Brueske, T, Bueker, R, Buse, A, Carius, A, Christoph, F, Cuno, M, Dats, E, Degen, N, Denil, J, Dietrichs, K, Domnitz, R, Dorn, B, Dubiel, J, Eckert, R, Ehrenberg, W, Eichler, S, El Khadra, S, Engl, T, Esser, O, Faragallah, Ea, Farahmandi, R, Finke, G, Fleig, P, Fruehauf, E, Gerhardt, U, Girke, Cg, Glauche, J, Gleissner, J, Gnann, R, Gralla, O, Grandin, A, Grewe, W, Gronau, E, Gruber, S, Grunert, S, Guelbeyaz, M, Guelden, H, Haendel, D, Haefele, J, Haghighat, M, Hahne, D, Haschemi Schirazi, R, Hecker, D, Herzig, J, Hettmmer, R, Hitschfeld, K, Hofmann, J, Hohmuth, H, Hoelker, D, Huebner, A, Hudemann, B, Hung Wehmann, D, Huenninghaus, K, Hueter, K, Igde, H, Jaeger, T, Javadi, P, John, G, Ju, M, Kaisser, G, Kamann, L, Kastein, A, Kaup, F, Kellner, T, Kempe, T, Kempter, F, Kennerknecht, M, Kirschner, P, Koenig, M, Konert, J, Kowalik, S, Krieger, Ju, Kruppa, Gl, Kube, U, Kuehn, F, Kuefer, R, Kurt, T, Kwela, M, Laag, R, Langen, L, Lehmann, J, Linder, C, Loeber, T, Lock, Uc, Loebenau, M, Luberg Sievers, G, Luebbe, R, Lutz, K, Maier, S, Maletz, C, Mertins, B, Meschede, E, Meschi, Mr, Miersch, Wd, Misera, A, Muehlich, S, Mueller, Hw, Mueller, D, Muench, Hc, Nawka, P, Othman, K, Paiss, T, Peter, K, Peters, T, Petras, T, Petrischenko, B, Pfund, A, Plate, H, Ploss, Hj, Pohrt, U, Pooyeh, S, Potempa, Aj, Pusinelli, Wd, Rausch, U, Reinhardt, F, Rengel, U, Rietheimer, W, Rinnab, L, Rohrmann, K, Romahn, E, Romitan Baum, R, Roessler, T, Rudolph, R, Rueffer, J, Rug, M, Rueth, J, Ruettgers, E, Santiago, Rb, Schaefer, A, Schaefer, T, Schaetzle, P, Scheunpflug, K, Schlicht, J, Schmidt, P, Schneider, J, Schnitzler, M, Schonfelder, R, Schreier, H, Schroeder, A, Schulz, Fm, Schulze, M, Schumann, M, Seidler, A, Seseke, S, Siebel Eggeling, G, Siebels, M, Sinner, B, Sippel, F, Soballa, M, Sommer, F, Spielhaupter, A, Steffen, H, Steinacker, M, Stiersdorfer, A, Stoehr, C, Sturm, S, Surrey, Hw, Swoboda, A, Szymula, S, Telle, J, Uththoff, H, Vierneisel, C, Vilmar, W, Wagner, M, Walhoefer, F, Warnack, W, Weiss, J, Weizert, P, Wicht, A, Wieland, J, Willgerodt, J, Wilski, B, Wilson, E, Wipfler, G, Wohn, Hg, Wolf, J, Zoehrlaut, B, Zuerner, T, Angeletti, G, Avolio, A, Baldassarre, R, Balercia, G, Balloni, F, Barba, G, Bartoletti, R, Basile Fasolo, C, Bassi, Pf, Beatrici, V, Bertozzi, Ma, Bocciardi, Am, Bondavalli, C, Bonini, F, Bonsanto, M, Branchi, A, Briganti, A, Calabrese, M, Calafiore, R, Calogero, Ae, Cantelmo, P, Caraceni, E, Carbone, A, Cardella, A, Carini, M, Carmignani, L, Carmignani, G, Carrino, M, Caviglia, C, Cecchi, M, Ceruti, C, Chiovato, L, Cicalese, V, Colpi, G, Corinti, M, Cormio, L, Cova, G, Cozzupoli, P, Ottavio, G, Damiano, R, De Ceglie, G, De Grande, G, De Lisa, A, DE SIO, Marco, De Stefani, S, Dehò, F, Delsignore, A, Di Filippo, A, Di Lena, S, Di Trapani, D, Diambrini, M, Drei, Gn, Fabbri, A, Fasolis, G, Ferone, D, Ferrari, G, Foresta, C, Francavilla, S, Gadda, F, Galantini, A, Galì, A, Gentile, V, Giammusso, B, Giannubilo, W, Granata, A, Grasso, M, Iafrate, M, Ilacqua, N, Isidori, A, Italiano, E, Jallous, Ha, Jannini, E, La Pera, G, Laganà, F, Lauretti, S, Leonardi, R, Liguori, G, Loiero, G, Lombardi, G, Lombardo, F, Lusenti, C, Maffucci, A, Maggi, M, Maio, G, Mammana, G, Manieri, C, Marzotto Caotorta, M, Mastroeni, F, Mazzilli, F, Mazzone, L, Minervini, M, Mirone, Vg, Montorsi, F, Morelli, G, Morrone, G, Nicita, G, Nicola, M, Palmiotto, F, Paradiso, M, Paulis, G, Pescatori, E, Petterle, V, Piazza, N, Pittaluga, P, Piubello, G, Polito, M, Ponchietti, R, Porena, M, Rago, R, Risi, O, Roggia, A, Salzano, L, Sanseverino, R, Sasso, Ferdinando Carlo, Savoca, G, Scarano, P, Schips, L, Serao, A, Sforza, A, Sidari, V, Silvani, M, Sinisi, A, Sorrentino, F, Spera, E, Strada, G, Tenaglia, R, Terrone, C, Titta, M, Tracia, A, Turchi, P, Ughi, G, Vecchio, D, Veneziano, Ia, Vicini, P, Vita, A, Vitti, P, Volpi, R, Zago, T, Zenico, T, Zito, Ar, Apolinario, M, Carvalho, Ap, Corte Real, J, Matos Cabeca, J, Mendes Leal, A, Monteiro Pereira, N, Palma dos Reis, J, Patricio, A, Prisco, R, Rocha Mendes, J, Santos, A, Vieira, R, Abad Gairín, C, Abascal García, Jm, Adot Zurbano, Jm, Álvarez de la Red, Pl, Al Wattar, W, Antón Saiz, C, Aranda Doncel, N, Arrosagaray, Pm, Arteaga Serrano, F, Barberán Soriano, J, Bataller Perello, V, Beltrán Persiva, J, Benejam Gual, J, Blanco Díez, A, Blasco Casares, Fj, Blasco Villalonga, M, Blázquez Izquierdo, J, Boladeras Sabater, J, Borrás, Jj, Bouchi Bakrim, Ar, Bucar Terrades, S, Burgués Gasión, Jp, Busto Castañón, L, Caballero, Jm, Cabello Santamaría, F, Cabreja López, E, Carrasco Aznar, Jc, Casasola Chamorro, J, Castellanos González, L, Cimadevila García, A, Closas Capdevila, M, Concepción Masip, T, Conde, C, Conde Santos, G, Cortada i., Robert J, Cos Calvet, Jm, Crespi Martínez, F, Cruz, N, De la Rosa Khermann, M, Delgado Martín, Ja, Devesa Mújica, M, Doganis Peppas, C, Domínguez Freire, F, Donderis Guastavino, C, Duarte Vázquez, Jj, El Khoury Yacob, R, Escobal Tamayo, V, Farré Martí, Jm, Fernández Fernández, A, Fernández Lozano, A, Fernández Viñas, Ja, Fiter Gómez, L, Fleitas Asencio, E, Frago Valls, Sm, Galiana Álvarez, A, García Bayo, I, García Contreras, J, García Cruz, E, García de Jalón Martín, A, García Giralda, L, García Marco, Ma, García Navas, R, García Reboll, L, Garrido Insúa, S, Giner Santamaría, C, Gómez Berjón, F, Gómez Gil, E, Gómez Lanza, E, Gómez Pérez, L, Gómez Rodríguez, A, González Sala, Jl, González Sala, Mj, Gonzalvo Ybarra, A, Guerrero Martínez, V, Gutiérrez González, Ma, Gutierrez Mínguez, E, Hidalgo Arroyo, J, Hmeidan, M, Idígora i., Planas X, Jara Rascón, J, Jiménez Verdejo, J, Lledó García, E, Lliteras Arañi, M, López Almansa, M, López Palacios, Má, López Tello, J, Lorenzo Gómez, Mf, Luque Gálvez, P, Luque López, Aj, Mallafré Sala, Jm, Martí Cebrián, Jm, Martín Clos, J, Martín Huescar, A, Martín Morales, A, Martín Rodríguez, A, Martínez Rodríguez, R, Martínez Salamanca, Ji, Mascarós Balaguer, E, Mejide Manresa, R, Molero Rodríguez, F, Molina Carranza, A, Moncada Iribarren, I, Montagud Moncho, Jb, Montesino Semper, M, Mosteiro Ponce, Ja, Mouaffak Tatari, N, Navarro Gil, Jm, Novás Castro, S, Ortiz del Corral, Ml, Ortiz Gamiz, A, Osca García, Jm, Padilla León, M, Palomino García, A, Pascual Mateo, C, Peinado Ibarra, F, Pérez Mestre, M, Portillo Martín, Ja, Poyato Galán, Jm, Prats de Puig, J, Prieto Castro, R, Puigvert Martínez, A, Quintana de la Rosa, Jl, Ramada Benlloch, Fj, Reyes Martínez, F, Rigabert, M, Ríos Espuny, Af, Robles Iniesta, A, Rodrigo Aliaga, M, Rodríguez Alba, Jl, Rodríguez Bethencourt, F, Rodríguez Jiménez, Fj, Rodríguez Leal, Da, Rodríguez Rubio, F, Rodríguez Tolrá, J, Rodríguez Vallejo, Jm, Romero Otero, J, Roselló Barbará, M, Rubio Briones, J, Ruíz Moriana, O, Sampol Company, J, San Martín Blanco, C, Sánchez Encinas, M, Sánchez Sánchez, F, Sancho Serrano, C, Santandreu Puifros, J, Santisteban González, M, Santos Ascarza Tabares, Jl, Sanz Lahoz, I, Sapiña Ortola, F, Sarquella Geli, J, Segarra Tomás, J, Soler Fernández, J, Tato Rodríguez, J, Tesedo Cubedo, J, Traid Sender, V, Valbuena Álvarez, R, Valverde Rubio, Jm, Varela Salgado, M, Vargas Rugeles, M, Vilches Cocovi, E, Virto Bajo, Fj, Andius, P, Anker Hansen, O, Arver, S, Bosson, P, Brattberg, A, Grenabo, L, Hanning, J, Hassler, L, Paradis, Aå, and Wang, E.
- Subjects
Adult ,Complementary Therapies ,Male ,medicine.medical_specialty ,Benzylamines ,Adolescent ,Nausea ,Urology ,Naphthalenes ,Dapoxetine Safety Cardiovascular events Syncope ,Syncope ,Cardiovascular events ,Young Adult ,Internal medicine ,Premature ejaculation ,medicine ,80 and over ,Dapoxetine ,Safety ,Aged ,Aged, 80 and over ,Humans ,Middle Aged ,Premature Ejaculation ,Prospective Studies ,Serotonin Uptake Inhibitors ,Adverse effect ,Prospective cohort study ,Sertraline ,business.industry ,Settore MED/24 - UROLOGIA ,Incidence (epidemiology) ,syncope ,Anesthesia ,Observational study ,medicine.symptom ,business ,Selective Serotonin Reuptake Inhibitors ,medicine.drug ,Cardiovascular events, Dapoxetine, Safety, Syncope - Abstract
Background Dapoxetine hydrochloride is a selective serotonin reuptake inhibitor and the first drug approved for the on-demand treatment of premature ejaculation (PE). Its safety was established in a thorough clinical development program. Objective To characterize the safety profile of dapoxetine in PE treatment and to report the incidence, severity, and type of adverse events. Design, setting, and participants We conducted a 12-wk, open-label, observational study with a 4-wk, postobservational contact. A total of 10 028 patients were enrolled, with 6712 patients (67.6%) treated with dapoxetine 30–60mg (group A)and 3316 (32.4%) treated with alternative care/nondapoxetine (group B). Interventions Treatment with dapoxetine or alternative care/nondapoxetine. Outcome measurements and statistical analysis Treatment-emergent adverse events (TEAEs) and concomitant therapy use during the 12-wk observational and the postobservational period were reported. Results and limitations The mean age for all patients was 40.5 yr. In group A, 93.0% of the patients were initially prescribed dapoxetine 30mg. Treatment options for group B patients included clomipramine, paroxetine, fluoxetine, sertraline, topical drugs, condoms, and behavioral counseling. Both treatment regimens were well tolerated. TEAEs were reported by 12.0% and 8.9% of group A and group B, respectively, with the highest incidence observed in patients aged >65 yr for group A (21.4%) and 30–39 yr (9.8%) for group B. The most commonly reported TEAEs were nausea, headache, and vertigo, with a higher incidence in group A (3.1%, 2.6%, and 1.0%, respectively) than in group B (oral drugs: 2.3%, 1.3%, and 0.9%, respectively). There were no cases of syncope in group A and one case in group B. A major limitation is that this was a nonrandomized, open-label, short-term study lacking efficacy data. Conclusions The results of this postmarketing observational study demonstrated that dapoxetine for treatment of PE has a good safety profile and low prevalence of TEAEs. Syncope and major cardiovascular adverse events were not reported. The high level of adherence by healthcare providers to the contraindications, special warnings, and precautions for dapoxetine minimizes the risk for its use in routine clinical practice. The current risk minimization measures for its identified and potential risks are effective.
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- 2014
15. P045 - Real-world outcomes with abiraterone in metastatic castration-resistant prostate cancer: The Prostate Cancer Registry
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Bjartell, A.S., Lumen, N., Maroto, P., Paiss, T., Gomez Veiga, F., Birtle, A., Kramer, G., Kalinka, E., Spaëth, D., Feyeraband, S., Matveev, V., Lefresne, F., Lukac, M., Wapenaar, R., Costa, L., and Chowdhury, S.
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- 2019
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16. The prostate cancer registry: Patient characteristics, treatments and preliminary outcomes from a large observational study of metastatic castration-resistant prostate cancer (mCRPC)
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Chowdhury, S., primary, Birtle, A.J., additional, Bjartell, A., additional, Costa, L.A.M., additional, Feyerabend, S., additional, Galli, L., additional, Kalinka-Warzocha, E., additional, Kramer, G., additional, Rey, J.P. Maroto, additional, Lumen, N., additional, Matveev, V.B., additional, Paiss, T., additional, Spaeth, D., additional, Antoni, L., additional, Klumper, E., additional, Wapenaar, R., additional, and Lee, E., additional
- Published
- 2016
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17. Linkage analysis in a collection of German PCA families reveals a high contribution of HPCX
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Vogel, W., Paiss, T., Herkommer, K., Haeussler, J., and Bochum, S.
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Human genetics -- Research ,Genetic disorders -- Research ,Linkage (Genetics) -- Analysis ,Prostate cancer -- Genetic aspects ,Biological sciences - Published
- 2001
18. The Prostate Cancer Registry: Analysis of Medical Resource Utilisation (Mru) in An International, Prospective, Observational Study of Men with Metastatic Castration-Resistant Prostate Cancer (Mcrpc)
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Chowdhury, S, primary, Birtle, A, additional, Bjartell, A, additional, Costa, L, additional, Feyerabend, S, additional, Galli, L, additional, Lumen, N, additional, Kalinka-Warzocha, E, additional, Maroto, P, additional, Matveev, V, additional, Paiss, T, additional, Spaeth, D, additional, Dearden, L, additional, Klumper, E, additional, Thingstad, T, additional, Wapenaar, R, additional, and Lee, E, additional
- Published
- 2015
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19. 2548 The Prostate Cancer Registry: First results from an international, prospective, observational study of men with metastatic castration-resistant prostate cancer (mCRPC)
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Chowdhury, S., primary, Birtle, A.J., additional, Bjartell, A., additional, Costa, L., additional, Feyerabend, S., additional, Galli, L., additional, Lumen, N., additional, Kalinka-Warzocha, E., additional, Maroto, P., additional, Matveev, V.B., additional, Paiss, T., additional, Spaeth, D., additional, Klumper, E., additional, Thingstad, T., additional, Wapenaar, R., additional, and Lee, E., additional
- Published
- 2015
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20. 746P - The prostate cancer registry: Patient characteristics, treatments and preliminary outcomes from a large observational study of metastatic castration-resistant prostate cancer (mCRPC)
- Author
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Chowdhury, S., Birtle, A.J., Bjartell, A., Costa, L.A.M., Feyerabend, S., Galli, L., Kalinka-Warzocha, E., Kramer, G., Rey, J.P. Maroto, Lumen, N., Matveev, V.B., Paiss, T., Spaeth, D., Antoni, L., Klumper, E., Wapenaar, R., and Lee, E.
- Published
- 2016
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21. [Genetic analysis of familial prostatic cancer: localization of a gene predisposing to prostatic cancer (PCaP) on chromosome 1q 42.2-43]
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Valeri A, Drelon E, Paiss T, Vogel W, de Petriconi R, Hautmann R, Fournier G, Mangin P, Berthon P, and olivier cussenot
- Subjects
Adult ,Aged, 80 and over ,Male ,Genetic Linkage ,Age Factors ,Chromosome Mapping ,Prostatic Neoplasms ,Genetic Counseling ,Middle Aged ,Chromosomes, Human, Pair 1 ,Humans ,Genetic Predisposition to Disease ,Lod Score ,Aged ,Microsatellite Repeats ,Probability - Abstract
To conduct genetic linkage analysis in order to localize predisposition genes for hereditary prostate cancer (CaP), as various epidemiological studies have demonstrated a family aggregation in 15 to 25% of cases, and the development of hereditary forms in 5 to 10% of cases of CaP.A genetic study on 47 French and German families included 122 patients and 72 subjects considered to be healthy after PSA assay. This study was conducted by linkage analysis of 364 microsatellite markers distributed throughout the genome (on average every 10 cM).Parametric and nonparametric linkage analysis identified a locus on chromosome 1q 42.2-43, which could be with a gene predisposing to CaP (called PCaP). The primary site was confirmed by several markers, using 3 different genetic models. The maximum LOD score (probability of linkage between the locus and the disease) on two-point analysis was 2.7 for the D1S2785 marker. Parametric and nonparametric multipoint analysis provided an HLOD score and an NPL score of 2.2 and 3.1, respectively (with P = 0.001). Heterogeneity analysis with calculations of LOD scores by multipoint analysis estimated that up to 50% of hereditary CaPs were related to this locus, with a heterogeneity probability of 157/1. Analysis of a subgroup of 9/47 families characterized by early onset CaP (before the age of 60 years) confirmed the very high probability of localization of a predisposition gene at locus 1q42.2-43 for these families (multipoint LOD score and NPL score of 3.31 and 3.32, respectively; with P = 0.001).The identification of predisposition genes will eventually allow identification within certain families of those subjects who have inherited the genetic abnormality and who therefore present a high risk of CaP. It will then be possible to perform targeted screening of CaP in order to diagnose CaP as early as possible.
- Published
- 1999
22. PCN296 - The Prostate Cancer Registry: Analysis of Medical Resource Utilisation (Mru) in An International, Prospective, Observational Study of Men with Metastatic Castration-Resistant Prostate Cancer (Mcrpc)
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Chowdhury, S, Birtle, A, Bjartell, A, Costa, L, Feyerabend, S, Galli, L, Lumen, N, Kalinka-Warzocha, E, Maroto, P, Matveev, V, Paiss, T, Spaeth, D, Dearden, L, Klumper, E, Thingstad, T, Wapenaar, R, and Lee, E
- Published
- 2015
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23. Gibt es einen Zusammenhang zwischen dem männlichen Alter und der Qualität des Erbguts in humanen Spermien?
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Winkle, T, primary, Köder, S, additional, Rosenbusch, B, additional, Gagsteiger, F, additional, Paiss, T, additional, and Ditzel, N, additional
- Published
- 2008
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24. 35 years: the border between good and bad sperm?
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Winkle, T., primary, Gagsteiger, F., additional, Paiss, T., additional, and Ditzel, N., additional
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- 2007
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25. Möglichkeiten der Spermienisolation mittels MACS- System
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Winkle, T, primary, Paiss, T, additional, Reeka, N, additional, and Ditzel, N, additional
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- 2006
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26. Klippel-Trenaunay-Syndrom
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Rinnab, L., primary, Paiss, T., additional, and Küfer, R., additional
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- 2006
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27. Mutation screening and association study of RNASEL as a prostate cancer susceptibility gene
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Maier, C, primary, Haeusler, J, additional, Herkommer, K, additional, Vesovic, Z, additional, Hoegel, J, additional, Vogel, W, additional, and Paiss, T, additional
- Published
- 2005
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28. Radiosensitivity detected by the micronucleus test is not generally increased in sporadic prostate cancer patients
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Varga, D., primary, Michel, I., additional, Patino-Garcia, B., additional, Paiss, T., additional, Vogel, W., additional, and Maier, C., additional
- Published
- 2005
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29. 390 Is a positive familial history of prostate cancer a prognostically relevant factor?
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Herkommer, K., primary, Gschwend, J., additional, Kron, M., additional, Hautmann, R., additional, and Paiss, T., additional
- Published
- 2004
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30. 387 Prostate cancer screening in persons with a positive family history
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Herkommer, K., primary, Gschwend, J., additional, Kron, M., additional, Hautmann, R., additional, and Paiss, T., additional
- Published
- 2004
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31. Clinical presentation of patients with a stage PT0 in the radical prostatectomy specimens
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Herkommer, K., primary, Volkmer, B., additional, Paiss, T., additional, Gschwend, J., additional, and Hautmann, R., additional
- Published
- 2003
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32. Early onset prostate cancer — Impact of familial history on pathology and clinical course following radical prostatectomy
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Herkommer, K., primary, Gschwend, J., additional, Kron, M., additional, Hautmann, R., additional, and Paiss, T., additional
- Published
- 2003
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33. Does the awareness of a positive family history of prostate cancer have an influence on screening?
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Herkommer, K., primary, Volkmer, B., additional, Paiss, T., additional, Hautmann, R., additional, and Gschwend, J., additional
- Published
- 2003
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34. Prostate cancer and the problem of genotype phenotype correlation
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Vogel, W., primary, Maier, C., additional, and Paiss, T., additional
- Published
- 2001
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35. High-dose pelvic irradiation followed by ileal neobladder urinary diversion: complications and long-term results
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Gschwend, J.E., primary, May, F., additional, Paiss, T., additional, Gottfried, H.W., additional, and Hautmann, R.E., additional
- Published
- 1996
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36. The Ileal Neobladder in Women: 9 Years of Experience with 18 Patients
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Hautmann, R.E., Paiss, T., and de Petriconi, R.
- Abstract
Purpose: We present our surgical and functional experience with orthotopic bladder replacement in women. Materials and Methods: Since 1986, 18 women have undergone lower urinary tract reconstruction with an ileal neobladder. A nerve sparing cystectomy is done, and reservoirs are connected to the proximal urethra or urethrovesical junction. A total of 13 patients was available for complete followup as of March 1995. Results: There were no perioperative deaths and few early complications. The only 2 failures were a neobladder vaginal fistula and these cases, which were converted to a conduit, are excluded from this study. Late complications requiring rehospitalization or reoperation in 2 patients included urethroileal stenosis that had to be dilated without further sequelae and bilateral ureteroileal stenosis that was treated endoscopically. At 3 months postoperatively excellent continence was achieved in 8 patients, while 2 had grade 1 stress incontinence and 3 were hypercontinent. As of March 1995 only 4 patients voided to completion while 9 required intermittent catheterization (continuously in 5 and twice daily for residual urine in 4). We were unable to demonstrate a functional difference of the various resection lines located at the proximal urethra or urethrovesical junction. Conclusions: Urethral support and nerve sparing cystectomy plus the ileal neobladder as a reservoir guarantee excellent continence in all patients. Despite our efforts, we have been unable to demonstrate any advantage of the nerve and urethral support sparing cystectomy technique as far as micturition is concerned. The development of hypercontinence in 70 percent of the patients with time demonstrates that our current understanding of the functional and anatomical basics of the voiding process is too limited to allow bladder replacement with a perfect functional result in all female patients. Our long-term experience, which is different from initial reports, justifies creation of an ileal neobladder in select female patients as long as they accept a 70 percent risk of clean intermittent catheterization in the long term. Overall patient satisfaction, including sexual life, is exceptional. However, disappointment is considerable when clean intermittent catheterization is required after periods of successful voiding per urethram.
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- 1996
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37. THE IMPACT OF CLINICAL FEATURES ON LINKAGE TO PROSTATE CANCER PREDISPOSITION IN GERMAN PROSTATE CANCER FAMILIES
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Herkommer, K., Martin, C., Maier, C., Vogel, W., Hautmann, R.E., Paiss, T., and Hoegel, J.
- Published
- 2006
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38. DIFFERENCES IN KNOWLEDGE OF PROSTATE CANCER AMONG BROTHERS OF MEN WITH PROSTATE CANCER AND CONTROLS
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Herkommer, K., Hohl, K., Gschwend, J.E., Paiss, T., and Kron, M.
- Published
- 2006
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39. PCN296 The Prostate Cancer Registry: Analysis of Medical Resource Utilisation (Mru) in An International, Prospective, Observational Study of Men with Metastatic Castration-Resistant Prostate Cancer (Mcrpc)
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Chowdhury, S, Birtle, A, Bjartell, A, Costa, L, Feyerabend, S, Galli, L, Lumen, N, Kalinka-Warzocha, E, Maroto, P, Matveev, V, Paiss, T, Spaeth, D, Dearden, L, Klumper, E, Thingstad, T, Wapenaar, R, and Lee, E
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40. A Candidate Gene Approach within the Susceptibility Region PCaP on 1q42.2–43 Excludes Deleterious Mutations of the PCTA-1 Gene to be Responsible for Hereditary Prostate Cancer
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Maier, C., Rösch, K., Herkommer, K., Bochum, S., Cancel-Tassin, G., Cussenot, O., Häussler, J., Assum, G., Vogel, W., and Paiss, T.
- Subjects
- *
PROSTATE cancer , *CHROMOSOMES - Abstract
Objective: The Prostate Carcinoma Tumor Antigen-1 (PCTA-1) is located at the prostate cancer susceptibility locus on chromosome 1q42.2–43 (PCaP). In this candidate gene approach, we searched for deleterious mutations within the PCTA-1 gene and its promoter.Materials and Methods: Seventy-seven familial prostate cancer cases from 36 German and French pedigrees were screened for germline mutations in the PCTA-1 gene using enzymatic mutation detection (EMD). Putative missense mutations were genotyped by RPLP and ddNTP primer extension assays in 88 controls to assess allele frequencies and haplotypes.Results: Several sequence variants were found but none of the findings indicated a deleterious mutation. Three affected brothers showed an intronic variation, which may interfere with correct splicing. Four non-conservative SNPs were characterized, coding for the amino acid alterations Y19F, C36R, V56M and S184R. All exchanges were found in controls with common allelic frequencies of at least 28%. Haplotype definition including six SNPs within the PCTA-1 gene revealed a complete linkage disequilibrium. Low haplotype diversity leads to a predominance of only two peptide variants of the PCTA-1 protein, coded by 95% of all chromosomes.Conclusions: PCTA-1 is not a classical high risk gene with deleterious mutations predisposing to hereditary prostate cancer. Its contribution to prostate cancer susceptibility as a low risk factor in sporadic disease has to be assessed in larger samples by association studies. [ABSTRACT FROM AUTHOR]
- Published
- 2002
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41. Real-World Safety and Efficacy Outcomes with Abiraterone Acetate Plus Prednisone or Prednisolone as the First- or Second-Line Treatment for Metastatic Castration-Resistant Prostate Cancer: Data from the Prostate Cancer Registry.
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Bjartell A, Lumen N, Maroto P, Paiss T, Gomez-Veiga F, Birtle A, Kramer G, Kalinka E, Spaëth D, Feyerabend S, Matveev V, Lefresne F, Lukac M, Wapenaar R, Costa L, and Chowdhury S
- Subjects
- Abiraterone Acetate pharmacology, Aged, Humans, Male, Prednisone pharmacology, Registries, Abiraterone Acetate therapeutic use, Prednisone therapeutic use, Prostatic Neoplasms, Castration-Resistant drug therapy
- Abstract
Background: Despite standard-of-care androgen-deprivation therapy and an increasing number of treatment options, the mortality rate for prostate cancer remains high. Progress to metastatic castration-resistant prostate cancer (mCRPC) necessitates additional treatments. Abiraterone acetate plus prednisone or prednisolone (AAP) prolongs survival in chemotherapy-naive and docetaxel-experienced patients., Objective: To evaluate the real-world safety and efficacy of AAP as first-line and second-line [post-docetaxel only (AAP-PD)] treatment in patients with mCRPC., Patients and Methods: The Prostate Cancer Registry (PCR) was a prospective, international, observational study of patients with mCRPC in routine clinical practice. Men aged ≥ 18 years with confirmed mCRPC were included. Baseline characteristics, safety (treatment-emergent adverse events, treatment-emergent severe adverse events), and efficacy [progression-free survival (PFS) and overall survival (OS)] were analyzed., Results: At baseline, patients who received first-line AAP (n = 754) were generally older than patients who received AAP-PD (n = 354); median age was 76 years and 70 years, respectively. However, the rate of visceral metastasis was higher in the AAP-PD cohort than in the AAP cohort (17.7% vs. 9.6%, respectively). Demographics and disease characteristics of patients with baseline cardiovascular disease were similar to those of the overall registry population. Efficacy outcomes were similar for all patients, regardless of the line of AAP therapy. For first-line AAP and AAP-PD, respectively, the median PFS was 8.9 and 5.8 months for all patients and 9.1 and 6.0 months for patients with cardiovascular comorbidities; median OS was 27.1 and 23.4 months for all patients, and 27.4 and 23.1 months for patients with cardiovascular comorbidities. There were no unexpected adverse events in any patient subgroup., Conclusions: These real-world data complement the findings from randomized controlled trials, indicating that first- and second-line AAP is well tolerated and effective in patients with mCRPC, including those with underlying CV comorbidities., Trial Registration Number: NCT02236637, registered 8 September 2014.
- Published
- 2021
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42. Real-World Outcomes in First-Line Treatment of Metastatic Castration-Resistant Prostate Cancer: The Prostate Cancer Registry.
- Author
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Chowdhury S, Bjartell A, Lumen N, Maroto P, Paiss T, Gomez-Veiga F, Birtle A, Kramer G, Kalinka E, Spaëth D, Feyerabend S, Matveev V, Lefresne F, Lukac M, Wapenaar R, and Costa L
- Subjects
- Adult, Aged, Aged, 80 and over, Humans, Male, Middle Aged, Neoplasm Metastasis, Prospective Studies, Prostatic Neoplasms, Castration-Resistant mortality, Registries, Survival Rate, Treatment Outcome, Prostatic Neoplasms, Castration-Resistant drug therapy
- Abstract
Background: Metastatic prostate cancer has a 30% 5-year survival rate despite recent therapeutic advances. There is a need to improve the clinical understanding and treatment of this disease, particularly in the real-world setting and among patients who are under-represented in clinical trials., Objective: We aimed to evaluate the characteristics and clinical outcomes of patients who received their first treatment for metastatic castration-resistant prostate cancer (mCRPC) in routine clinical practice, independent of treatment used, including subgroups with baseline cardiac disease, diabetes mellitus, or visceral metastases., Patients and Methods: Prospective, noninterventional analysis of patient record data in the multicenter Prostate Cancer Registry (PCR) of men with mCRPC. The data were collected in 16 countries with the aim of recruiting more than 3000 patients between 2013 and 2016. The study end date was 9 July 2018. Data evaluated included baseline characteristics, treatment exposure, and efficacy outcomes [overall survival (OS) and time to progression (TTP)] of patients treated with abiraterone acetate plus prednisone or prednisolone (collectively, "abiraterone"), enzalutamide, or docetaxel. Descriptive outcomes are reported from the overall patient population and subgroups of patients with baseline cardiovascular disease, diabetes mellitus, or visceral metastases. The treatment effects for time to progression were compared for the overall patient population., Results: The study enrollment period lasted 2.5 years, and each patient was followed for a maximum of 3 years. A total of 1874 patients in the PCR had not received previous mCRPC treatment at baseline, although they had received androgen-deprivation therapy. Prevalent co-morbidities included cardiovascular disease in 65.4% and diabetes mellitus in 17.4% of patients. Baseline characteristics suggested that patients with more advanced disease received docetaxel treatment. In the overall patient population, the median time to progression with abiraterone, enzalutamide, and docetaxel as first-line mCRPC therapy was 9.6, 10.3, and 7.6 months, respectively, and median OS was 27.1, 27.1, and 27.9 months, respectively. Outcomes in the subgroups of patients with cardiovascular disease or diabetes mellitus were similar to those of the whole population in the analysis. As expected, patients with visceral metastases had shorter TTP and OS than patients in the overall population., Conclusions: This analysis shows, for the first time, the effectiveness in parallel of first-line abiraterone, enzalutamide, and docetaxel in mCRPC, including in patients with co-morbidities such as cardiovascular disease or diabetes mellitus or in patients with visceral metastases. These real-world findings from the PCR provide meaningful information to help manage mCRPC, particularly in patients under-represented in clinical studies., Trial Registration: ClinicalTrials.gov identifier NCT02236637; registered September 2014.
- Published
- 2020
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43. Genome-wide linkage analysis of 1,233 prostate cancer pedigrees from the International Consortium for Prostate Cancer Genetics using novel sumLINK and sumLOD analyses.
- Author
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Christensen GB, Baffoe-Bonnie AB, George A, Powell I, Bailey-Wilson JE, Carpten JD, Giles GG, Hopper JL, Severi G, English DR, Foulkes WD, Maehle L, Moller P, Eeles R, Easton D, Badzioch MD, Whittemore AS, Oakley-Girvan I, Hsieh CL, Dimitrov L, Xu J, Stanford JL, Johanneson B, Deutsch K, McIntosh L, Ostrander EA, Wiley KE, Isaacs SD, Walsh PC, Isaacs WB, Thibodeau SN, McDonnell SK, Hebbring S, Schaid DJ, Lange EM, Cooney KA, Tammela TL, Schleutker J, Paiss T, Maier C, Grönberg H, Wiklund F, Emanuelsson M, Farnham JM, Cannon-Albright LA, and Camp NJ
- Subjects
- Chromosome Mapping, Chromosomes, Human, Pair 22 genetics, Genetic Predisposition to Disease, Genome, Human, Genome-Wide Association Study, Genotype, Humans, Male, Genetic Linkage, Pedigree, Prostatic Neoplasms genetics
- Abstract
Background: Prostate cancer (PC) is generally believed to have a strong inherited component, but the search for susceptibility genes has been hindered by the effects of genetic heterogeneity. The recently developed sumLINK and sumLOD statistics are powerful tools for linkage analysis in the presence of heterogeneity., Methods: We performed a secondary analysis of 1,233 PC pedigrees from the International Consortium for Prostate Cancer Genetics (ICPCG) using two novel statistics, the sumLINK and sumLOD. For both statistics, dominant and recessive genetic models were considered. False discovery rate (FDR) analysis was conducted to assess the effects of multiple testing., Results: Our analysis identified significant linkage evidence at chromosome 22q12, confirming previous findings by the initial conventional analyses of the same ICPCG data. Twelve other regions were identified with genome-wide suggestive evidence for linkage. Seven regions (1q23, 5q11, 5q35, 6p21, 8q12, 11q13, 20p11-q11) are near loci previously identified in the initial ICPCG pooled data analysis or the subset of aggressive PC pedigrees. Three other regions (1p12, 8p23, 19q13) confirm loci reported by others, and two (2p24, 6q27) are novel susceptibility loci. FDR testing indicates that over 70% of these results are likely true positive findings. Statistical recombinant mapping narrowed regions to an average of 9 cM., Conclusions: Our results represent genomic regions with the greatest consistency of positive linkage evidence across a very large collection of high-risk PC pedigrees using new statistical tests that deal powerfully with heterogeneity. These regions are excellent candidates for further study to identify PC predisposition genes.
- Published
- 2010
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44. Genome-wide linkage analysis of TMPRSS2-ERG fusion in familial prostate cancer.
- Author
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Hofer MD, Kuefer R, Maier C, Herkommer K, Perner S, Demichelis F, Paiss T, Vogel W, Rubin MA, and Hoegel J
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- Aged, Chromosomes, Human, Pair 21, Cohort Studies, Genetic Linkage, Genetic Predisposition to Disease, Genome, Human, Humans, In Situ Hybridization, Fluorescence, Male, Middle Aged, Neoplasm Staging, Prostatic Neoplasms pathology, Oncogene Proteins, Fusion genetics, Prostatic Neoplasms genetics
- Abstract
Fusion of the 5'-untranslated region of androgen-regulated TMPRSS2 promoter with ETS transcription factor family members is found frequently in prostate cancers, and recent work suggests that the most common TMPRSS2-ERG fusion is associated with an aggressive clinical phenotype compared with fusion-negative prostate cancer. Thus far, analysis of the fusion has been limited to sporadic cases of prostate cancer. In the current study, we explore for an enrichment of TMPRSS2-ERG fusion in familial prostate cancer. TMPRSS2-ERG fusion was identified using a break-apart fluorescence in situ hybridization assay on tissue microarrays. Presence of TMPRSS2-ERG fusion was associated with higher Gleason scores (P = 0.027). Of 75 patients with established history of prostate cancer, we detected the TMPRSS2-ERG fusion in 44 (59%) patients. Almost three quarters (73%) of fusion-positive patients accumulated within 16 specific families whereas only 27% were single fusion-positive cases within one family. Based on reported prevalence rates, we calculated a sibling recurrence risk ratio of up to 18.9. A subset (63%) of families with uniformly TMPRSS2-ERG-positive prostate cancer underwent a genome-wide linkage scan at 500 markers. This revealed several loci located on chromosomes #9, #18, and X that were suggestive of linkage to the TMPRSS2-ERG fusion-positive prostate cancer phenotype with linkage-of-disease scores up to 2.16 and nonparametric linkage scores up to 2.77. This suggests the presence of an inherited susceptibility to developing the TMPRSS2-ERG fusion. Given the association of TMPRSS2-ERG fusion and aggressive prostate cancer, close surveillance of relatives of patients with established fusion-positive prostate cancer or a family history of prostate cancer in general would be warranted.
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- 2009
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45. The correlation between male age, sperm quality and sperm DNA fragmentation in 320 men attending a fertility center.
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Winkle T, Rosenbusch B, Gagsteiger F, Paiss T, and Zoller N
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- Adult, Aging pathology, Ambulatory Care Facilities, DNA physiology, Flow Cytometry, Humans, Infertility, Male pathology, Male, Middle Aged, Semen cytology, Sperm Count, Sperm Motility, Spermatozoa pathology, Aging genetics, DNA Fragmentation, Infertility, Male genetics, Infertility, Male physiopathology, Spermatozoa physiology
- Abstract
Purpose: To investigate the effects of male aging on sperm quality and sperm DNA fragmentation., Methods: The ejaculates of 320 unselected men attending a fertility clinic and, as a control, 84 normozoospermic men without any history of ART were analyzed according to WHO guidelines. Sperm DNA fragmentation was measured by flow cytometry after staining with propidiumiodide., Results: The patients were divided into four groups: <30 years, 30-35 years, 36-39 years and >or=40 years. Sperm motility decreased with increasing age whereas sperm concentration, morphology, and DNA fragmentation fluctuated throughout the four groups both among patients and among controls. However, we could not detect any significant correlation between male age and conventional semen parameters or sperm DNA fragmentation, respectively, neither in the patients' group nor among the controls. This also applies to a classification of patients and controls into only two age groups with a cut-off point at 35 years., Conclusions: Our findings suggest that neither the routinely assessed semen parameters nor the amount of spermatozoa with fragmented DNA are affected by male age.
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- 2009
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46. Expression changes of CAV1 and EZH2, located on 7q31 approximately q36, are rarely related to genomic alterations in primary prostate carcinoma.
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Bachmann N, Haeusler J, Luedeke M, Kuefer R, Perner S, Assum G, Paiss T, Hoegel J, Vogel W, and Maier C
- Subjects
- CpG Islands, DNA Methylation, DNA Primers, Enhancer of Zeste Homolog 2 Protein, Gene Dosage, Humans, In Situ Hybridization, Fluorescence, Male, Middle Aged, Polycomb Repressive Complex 2, Prostatic Neoplasms pathology, RNA, Messenger genetics, RNA, Messenger metabolism, Reverse Transcriptase Polymerase Chain Reaction, Caveolin 1 genetics, Chromosomes, Human, Pair 7 genetics, DNA-Binding Proteins genetics, Gene Expression Regulation, Neoplastic, Prostatic Neoplasms genetics, Transcription Factors genetics
- Abstract
The chromosomal region 7q was repeatedly found to be rearranged in prostate carcinoma. It harbors several well described candidate tumor suppressor and oncogenes. We addressed two genes with opposite roles in cancer; CAV1, a putative tumor suppressor gene at 7q31, and EZH2 at 7q36, which is believed to promote tumor progression. Our primary aim was to assess their expression changes in primary tumors, and then to elucidate the underlying mechanism, assuming that genomic alterations of either locus could affect the other gene as well. In 35 prostate tumor samples, compared with adjacent tissues, CAV1 was overall downregulated (P < 10(-06)), whereas EZH2 was significantly overexpressed (P < 10(-06)). The observed dysregulations were coincident in nearly 70% of the cases. Copy number changes occurred in few tumors. Loss of CAV1 DNA was only marginally associated with reduced expression (P = 0.07), however, and genomic amplification of EZH2 could not explain its upregulation. Through bisulfite sequencing of four tumor samples, CpG-hypermethylation was verified as an alternative mechanism for CAV1 silencing, as reported previously. Moreover, it could also be involved in the reactivation of EZH2.
- Published
- 2008
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47. Compelling evidence for a prostate cancer gene at 22q12.3 by the International Consortium for Prostate Cancer Genetics.
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Camp NJ, Cannon-Albright LA, Farnham JM, Baffoe-Bonnie AB, George A, Powell I, Bailey-Wilson JE, Carpten JD, Giles GG, Hopper JL, Severi G, English DR, Foulkes WD, Maehle L, Moller P, Eeles R, Easton D, Badzioch MD, Whittemore AS, Oakley-Girvan I, Hsieh CL, Dimitrov L, Xu J, Stanford JL, Johanneson B, Deutsch K, McIntosh L, Ostrander EA, Wiley KE, Isaacs SD, Walsh PC, Thibodeau SN, McDonnell SK, Hebbring S, Schaid DJ, Lange EM, Cooney KA, Tammela TL, Schleutker J, Paiss T, Maier C, Grönberg H, Wiklund F, Emanuelsson M, and Isaacs WB
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- Humans, International Cooperation, Lod Score, Male, Chromosomes, Human, Pair 22 genetics, Genetic Predisposition to Disease, Prostatic Neoplasms genetics, Societies, Medical
- Abstract
Previously, an analysis of 14 extended, high-risk Utah pedigrees localized in the chromosome 22q linkage region to 3.2 Mb at 22q12.3-13.1 (flanked on each side by three recombinants) contained 31 annotated genes. In this large, multi-centered, collaborative study, we performed statistical recombinant mapping in 54 pedigrees selected to be informative for recombinant mapping from nine member groups of the International Consortium for Prostate Cancer Genetics (ICPCG). These 54 pedigrees included the 14 extended pedigrees from Utah and 40 pedigrees from eight other ICPCG member groups. The additional 40 pedigrees were selected from a total pool of 1213 such that each pedigree was required to contain both at least four prostate cancer (PRCA) cases and exhibit evidence for linkage to the chromosome 22q region. The recombinant events in these 40 independent pedigrees confirmed the previously proposed region. Further, when all 54 pedigrees were considered, the three-recombinant consensus region was narrowed down by more than a megabase to 2.2 Mb at chromosome 22q12.3 flanked by D22S281 and D22S683. This narrower region eliminated 20 annotated genes from that previously proposed, leaving only 11 genes. This region at 22q12.3 is the most consistently identified and smallest linkage region for PRCA. This collaborative study by the ICPCG illustrates the value of consortium efforts and the continued utility of linkage analysis using informative pedigrees to localize genes for complex diseases.
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- 2007
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48. Pooled genome linkage scan of aggressive prostate cancer: results from the International Consortium for Prostate Cancer Genetics.
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Schaid DJ, McDonnell SK, Zarfas KE, Cunningham JM, Hebbring S, Thibodeau SN, Eeles RA, Easton DF, Foulkes WD, Simard J, Giles GG, Hopper JL, Mahle L, Moller P, Badzioch M, Bishop DT, Evans C, Edwards S, Meitz J, Bullock S, Hope Q, Guy M, Hsieh CL, Halpern J, Balise RR, Oakley-Girvan I, Whittemore AS, Xu J, Dimitrov L, Chang BL, Adams TS, Turner AR, Meyers DA, Friedrichsen DM, Deutsch K, Kolb S, Janer M, Hood L, Ostrander EA, Stanford JL, Ewing CM, Gielzak M, Isaacs SD, Walsh PC, Wiley KE, Isaacs WB, Lange EM, Ho LA, Beebe-Dimmer JL, Wood DP, Cooney KA, Seminara D, Ikonen T, Baffoe-Bonnie A, Fredriksson H, Matikainen MP, Tammela TL, Bailey-Wilson J, Schleutker J, Maier C, Herkommer K, Hoegel JJ, Vogel W, Paiss T, Wiklund F, Emanuelsson M, Stenman E, Jonsson BA, Grönberg H, Camp NJ, Farnham J, Cannon-Albright LA, Catalona WJ, Suarez BK, and Roehl KA
- Subjects
- Black or African American genetics, Aged, Chromosome Mapping, Family Health, Female, Genetic Heterogeneity, Genetic Predisposition to Disease ethnology, Genotype, Humans, International Cooperation, Lod Score, Male, Microsatellite Repeats, Middle Aged, Pedigree, Prostatic Neoplasms ethnology, White People genetics, Genetic Linkage, Genome, Human, Prostatic Neoplasms genetics
- Abstract
While it is widely appreciated that prostate cancers vary substantially in their propensity to progress to a life-threatening stage, the molecular events responsible for this progression have not been identified. Understanding these molecular mechanisms could provide important prognostic information relevant to more effective clinical management of this heterogeneous cancer. Hence, through genetic linkage analyses, we examined the hypothesis that the tendency to develop aggressive prostate cancer may have an important genetic component. Starting with 1,233 familial prostate cancer families with genome scan data available from the International Consortium for Prostate Cancer Genetics, we selected those that had at least three members with the phenotype of clinically aggressive prostate cancer, as defined by either high tumor grade and/or stage, resulting in 166 pedigrees (13%). Genome-wide linkage data were then pooled to perform a combined linkage analysis for these families. Linkage signals reaching a suggestive level of significance were found on chromosomes 6p22.3 (LOD = 3.0), 11q14.1-14.3 (LOD = 2.4), and 20p11.21-q11.21 (LOD = 2.5). For chromosome 11, stronger evidence of linkage (LOD = 3.3) was observed among pedigrees with an average at diagnosis of 65 years or younger. Other chromosomes that showed evidence for heterogeneity in linkage across strata were chromosome 7, with the strongest linkage signal among pedigrees without male-to-male disease transmission (7q21.11, LOD = 4.1), and chromosome 21, with the strongest linkage signal among pedigrees that had African American ancestry (21q22.13-22.3; LOD = 3.2). Our findings suggest several regions that may contain genes which, when mutated, predispose men to develop a more aggressive prostate cancer phenotype. This provides a basis for attempts to identify these genes, with potential clinical utility for men with aggressive prostate cancer and their relatives.
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- 2006
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49. Role of the Nijmegen breakage syndrome 1 gene in familial and sporadic prostate cancer.
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Hebbring SJ, Fredriksson H, White KA, Maier C, Ewing C, McDonnell SK, Jacobsen SJ, Cerhan J, Schaid DJ, Ikonen T, Autio V, Tammela TL, Herkommer K, Paiss T, Vogel W, Gielzak M, Sauvageot J, Schleutker J, Cooney KA, Isaacs W, and Thibodeau SN
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- Aged, Aged, 80 and over, Case-Control Studies, Genetic Predisposition to Disease, Genotype, Humans, Logistic Models, Male, Middle Aged, Mutation, Nijmegen Breakage Syndrome epidemiology, Prostatic Neoplasms epidemiology, Risk Factors, Cell Cycle Proteins genetics, Nijmegen Breakage Syndrome genetics, Nuclear Proteins genetics, Prostatic Neoplasms genetics
- Abstract
The Nijmegen breakage syndrome 1 (NBS1) gene, which participates in DNA double strand break repair, has been postulated to be a susceptibility factor for a number of cancers, including prostate cancer. Numerous mutations have been identified in NBS1, including the founder mutation 657del5. In this study, a number of analyses were done to determine whether mutations in NBS1 are associated with an increased risk for prostate cancer. The frequency of the 657del5 mutation in both familial prostate cancer cases (1,819 affected men among 909 families) and sporadic prostate cancer cases (1,218 affected men) collected from five centers participating in the International Consortium for Prostate Cancer Genetics were compared with that found in 697 normal controls. Seven individuals were identified to carry the mutation among the 3,037 cases screened: four in the familial group (three from one family and one from another) and three in the sporadic cases. The carrier frequency was 0.22% (2 of 909) for the probands and 0.25% (3 of 1,218) for the sporadic cases of prostate cancer. The 657del5 mutation was not detected in either the 293 unaffected members of the prostate cancer families or in the 697 control samples tested. The entire NBS1 gene was also sequenced in 20 of the youngest affected individuals from the Finnish group of familial cases to identify the presence of possible mutations in this high-risk group. One rare (D95N) and one common (E185Q) missense alteration was identified. More detailed analyses of the E185Q polymorphism, along with a third rare variant (R215W), failed to show an association with prostate cancer. Because the 657del5 mutation was absent from the control population, we are unable to determine if this alteration predisposes to prostate cancer. However, our data does suggest that mutations within NBS1, and in particular, 657del5, do not significantly contribute to the overall prostate cancer burden within our patient samples.
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- 2006
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50. Germline mutations of the MSR1 gene in prostate cancer families from Germany.
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Maier C, Vesovic Z, Bachmann N, Herkommer K, Braun AK, Surowy HM, Assum G, Paiss T, and Vogel W
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- Aged, Aged, 80 and over, Alleles, DNA Mutational Analysis, Exons genetics, Gene Expression Regulation, Neoplastic, Germany, Humans, Introns genetics, Male, Middle Aged, Neoplasm Proteins genetics, Pedigree, RNA Splice Sites genetics, RNA, Messenger genetics, RNA, Messenger metabolism, Scavenger Receptors, Class A metabolism, Germ-Line Mutation genetics, Prostatic Neoplasms ethnology, Prostatic Neoplasms genetics, Scavenger Receptors, Class A genetics
- Abstract
The MSR1 gene at 8p22 has been suggested as a candidate gene for hereditary prostate cancer because germline variants have been found to be associated with the disease. Aside from a single nonsense mutation (R293X) that was found repeatedly at low frequencies in several samples, little evidence has been gained by follow-up studies to confirm the gene's relevance for prostate cancer. Prompted by reasonable support for a linkage to 8p22, we sought to determine the mutation spectrum of MSR1 in our family sample. Screening of 139 probands (representing 139 prostate cancer families) revealed 15 novel and a total of 20 sequence variants within the 10 coding exons and their intronic proximities. Aside from the known mutation c.877C>T (R293X) present in two of our families, we identified a second nonsense allele (c.251C>G; S84X) and a splice-site mutation (c.818-1G>A) that results in mRNA instability (each in a single pedigree). The novel missense alleles were c.703C>T (H235Y), c.856C>T (P286S), c.905C>T (P302L), c.1193C>G (A398G), and c.1289A>G (K430R). Of the eight variants that affect the encoded protein (splice site, nonsense, and missense), only R293X as well as the polymorphism c.823C>G (P275A) were additionally present at remarkable frequencies in further samples of sporadic prostate cancer and controls. Of note, carriers of R293X were equally frequent in 367 sporadic prostate cancer cases (1.9%) and in 197 controls (2.0%). To our knowledge, our study is the first to demonstrate further loss of function variants of MSR1 apart from R293X. Nevertheless, the low frequencies of deleterious alleles, in addition to an apparently moderate penetrance, does not support MSR1 as a major susceptibility gene in this family sample., (2005 Wiley-Liss, Inc.)
- Published
- 2006
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