Hypoxia in Du-145 Prostate Cancer Xenografts After Estramustine Phosphate and Radiotherapy
Methods and Materials: Nude mice with DU 145 human prostate cancer cell tumours were divided into four groups: group ER was treated with EMP 0.2 mg/d and external irradiation 3 × 6 Gy; group E received EMP, group R irradiation only; and group O no treatment. The degree of hypoxia in the tumours before and after treatment was measured using 18F-labelled fluoromisonidazole ([18F]FMISO) as a marker. The testis served as a control organ. Histological samples were studied for necrosis and proliferation (DAPI-stain for mitoses and Ki-67).
Results: The tumours showed more [18F]FMISO uptake, indicating more hypoxia, than the testes in all four groups. EMP did not improve tumour oxygenation but enhanced the ability of radiotherapy to cause tumour necrosis.
Conclusions: The angiogenic effect of EMP, if present, is not crucial in the mechanism of radiosensitation.
Keywords: BT4C; DAPI-stain for mitoses and Ki-67; DNA; DU-145; Dunnett's method; Dunning R 3327; Estramustine; Estramustine Phosphate; G2/M-phase; Immunohistochemistry; Monoclonal antibody PP-67; Nitroimidazoles; Prostate Cancer Xenografts; R3327; Rat glioma model; SAS/STAT® software; analysis of variance (ANOVA); angiogenesis; carcinomas; central hypoxia; central necrosis; chemotherapy; deoxyribonucleic acid; fluorescein isothiocyanate (FITC)-coupled goat; fluorine-18 labelled fluoromisonidazole; fluoromisonidazole; hormone-independent prostate cancer; human prostate cancer; hypoxia; hypoxia-specific factor; malignant tumours; necrosis; neovascularisation; neurological malignancies; polymethylmethacrylate; positron emission tomography (PET) technology; prostate carcinoma model; radiosensitation; radiotherapy; tumour necrosis; vascular endothelial growth factor
Document Type: Research Article
Publication date: October 1, 2010
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