Zusammenfassung
Das Prostatakarzinom stellt in zunehmendem Maße ein medizinisches Problem dar: Es ist der gegenwärtig am häufigsten diagnostizierte Krebs bei der westlichen männlichen Bevölkerung und die zweithäufigste Krebstodesursache bei Männern (Boring et al. 1991) Trotz der wachsenden Patientenanzahl mit klinisch manifester Erkrankung ist über die Mechanismen, die am Beginn und der Progredienz des Prostatakrebses beteiligt sind, nur wenig bekannt. Es scheint jedoch klar zu sein, daß die Prostatakarzinogenese ein aus zahlreichen Schritten bestehender Prozeß ist, der zuerst zu histologischen Prostatakarzinomen führt, und sich nach dem Stattfinden zusätzlicher maligner Ereignisse zur klinischen Krankheit entwickelt (Carter et al. 1990). Während der Phänotyp des Tumors vom benignen zum malignen und möglicherweise metastatischen Zustand wechselt, treten gehäuft genetische Veränderungen, sowohl in qualitativer als auch quantitativer Hinsicht, auf (Nicolson 1991). Die Targetzelle entwickelt dadurch oftmals die Fähigkeit zur Umgehung von Kontrollen, was zu unbegrenzter Proliferationsbereitschaft führt. Die erhöhte Proliferationsfähigkeit hat 2 wichtige Konsequenzen. Erstens ist infolge der Tatsache, daß die am stärksten gentoxischen Agenzien die Gene in Zykluszellen schädigen, die Gefahr größer, daß Genschäden erworben werden. Die erhöhte Proliferationsfähigkeit ist darüber hinaus für das Auswachsen der malignen Zellpopulation erforderlich.
Übersetzung aus dem Engl, von Belinde Junkers.
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Bussemakers, M.J.G., Debruyne, F.M.J., Schalken, J.A. (1993). Genetische Schritte in Zusammenhang mit der Entstehung des Prostatakarzinoms. In: Rübben, H., Goepel, M., Schmitz-Dräger, B.J. (eds) Immuntherapie in der Uroonkologie. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77830-8_16
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