Response of the Dunning R3327H prostatic adenocarcinoma to radiation and various chemotherapeutic drugs.
Dunning R3327H prostatic adenocarcinoma was bilaterally transplanted in the flanks of animals at the Papanicolaou Institute in Miami, and the animals were received at the Cross Cancer Institute (Edmonton, Alberta, Canada) each month. The animal flanks were palpated weekly, and when tumor volumes reached a size of approximately 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, and 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 months. 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.
D000230:Adenocarcinoma / Q000532:radiotherapy / Q000628:therapy*; D000818:Animals; D002945:Cisplatin / Q000627:therapeutic use; D004961:Estramustine / Q000627:therapeutic use; D005047:Etoposide / Q000627:therapeutic use; D005260:Female; D008297:Male; D009368:Neoplasm Transplantation; D011471:Prostatic Neoplasms / Q000532:radiotherapy / Q000628:therapy*; D051381:Rats; D014750:Vincristine / Q000627:therapeutic use
D004961:Estramustine; D014750:Vincristine; D005047:Etoposide; D002945:Cisplatin