RESPONSE OF THE DUNNING R3327H PROSTATIC ADENOCARCINOMA TO RADIATION AND VARIOUS CHEMOTHERAPEUTIC DRUGS

Abstract

Dunning [rat] R3327H prostatic adenocarcinoma was bilaterally transplanted in the flanks of animals at the Papanicolaou Institute in Miami [Florida, USA]; the animals were received at the Cross Cancer Institute (Edmonton, Alberta, Canada) each month. The animal flanks were palpated weekly, when tumor volumes reached a size of .apprx. 300 mm3 the animals were randomized into treatment groups for the assessment of various therapies. Tumor volumes were determined each week before and after various treatments; tumor growth was compared to that in untreated controls. Ionizing radiation at relatively small single doses completely inhibits tumor growth for a period of up to 6 mo. Some interesting characteristics of this radiation-induced growth arrest are that tumors do not die and shrink away as with some other tumor models but remain static in size and show histologic evidence of viable tumor cells. The hypoxic cell radiosensitizer misonidazole potentiates radiation response in this tumor model. Cisplatin, vincristine, etoposide and estramustine phosphate administered in drug doses approaching their toxic limits have a partial effect on tumor growth.