Measurement of the hypoxic fraction in the same tumor system by different assay techniques often gives incompatible results. The hypoxic fraction of the BA1112 sarcoma has been measured by three assay techniques: tumor control and growth delay assays in which the tumors remain in situ after irradiation, and paired survival curve assays in which the tumors are excised after irradiation. The assays were done with and without anesthesia on tumors growing in two different subcutaneous sites. Anesthesia of the hosts produced a statistically significant decrease in the calculated hypoxic fraction in a tumor control assay, but not in a paired survival assay. The excision assays gave consistently higher hypoxic fraction estimates than either the tumor control or growth delay assays. Some of the factors which could produce higher hypoxic fractions in excision assays than in in situ assays are discussed. Interpretation of the results was complicated by disagreements between the growth delay and tumor control assays, and by disparities between replicate determinations. The discrepancies among assays are caused almost entirely by variations in the response of the artificially hypoxic tumors, rather than variations in the response of aerobic tumors. These results indicate that assumptions commonly made when measuring hypoxic fractions may not be valid.
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Dose response curves were established for local control of the rat rhabdomyosarcoma BA1112 for radiation alone and for radiation following a cytoreductive operation. Removal of one-half of the tumor prior to irradiation did not significantly alter the dose of radiation necessary to cure 50 per cent of the tumors. This experimental result confirms the theoretic predictions and suggests that, to be useful in combination with radiation, surgical treatment must remove in excess of 90 per cent of the tumor.
The rat rhabdomyosarcoma BA1112 has a number of features which make it a useful model for the study of tumour response to radiation therapy. It is a transplantable tumour, isologous to an inbred line of WAG/Rij rats and it elicits no demonstrable host immune response. The tumour grows locally at the implantation site and rarely metastasizes. It is known to contain hypoxic cells which reoxygenate during a prolonged course of fractionated radiation therapy. The growth and radiation response characteristics of the tumour have remained stable for over 15 years. A newly developed in vitro assay for tumour cell clonogenicity greatly facilitates the measurement of radiation dose-response curves and the monitoring of cell response following in vivo treatment. The in vivo response of the tumour to fractionated radiation therapy is analysed in terms of cellular response, reoxygenation and cell proliferation.
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