Zusammenfassung
Die Rationale für dosiseskalierte Therapien bei soliden Tumoren begründet sich in der Annahme, daß eine Beziehung besteht zwischen der verabfolgten Dosis und dem Ausmaß der Tumorzellzerstörung und daß es daher möglich sein muß, eine Tumorzellpopulation durch entsprechende Erhöhung der Zytostatikadosierungen komplett zu zerstören. Nach Schätzungen von Frei et al. (1989) liegt die Tumorzellzahl bei einem Patienten mit klinisch evidenter, metastasierter Erkrankung bei ca. 1011 Zellen; ca. 1–0,1%, also 108–107 Zellen sind Tumorstammzellen. Unter der Annahme, daß eine konventionelle Chemotherapie in einer hypothetischen Situation in der Lage ist, eine gute partielle oder kurzanhaltende komplette Remission zu induzieren — entsprechend einer Tumorzellreduktion von ca. 1–2 log -, ist im idealen Fall eine Dosiseskalation um den Faktor 5–8 notwendig, um kurativ sein zu können. Diese Annahme hat allerdings nur Gültigkeit, wenn man davon ausgeht, daß für die verwendeten Substanzen eine log-lineare Dosis-Wirkungs-Beziehung über mehrere Zehnerpotenzen der Tumorzellreduktion vorliegt. Viele Substanzen, v. a. die Antimetaboliten und die Vincaalkaloide, weisen in experimentellen Systemen ein Plateau nach 1–2 log Tumorzellzerstörung auf und scheinen schon aufgrund dieser Charakteristika nicht besonders geeignet für Hochdosistherapien zu sein.
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Harstrick, A. et al. (1996). Neue Entwicklungen in der Tumortherapie. In: Schmoll, HJ., Höffken, K., Possinger, K. (eds) Kompendium Internistische Onkologie. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-79214-4_19
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