Influence of Adriamycin on Growth Kinetics of Lewis Lung Carcinoma and Its Lung Metastases

Abstract

Using a Gompertzian pharmacodynamic model, we have studied the changes induced by graded doses of adriamycin (AM) on the growth of intramuscular Lewis lung carcinoma (3LL) and its lung metastases in C57B1/6 mice. An interpretation of the drug’s effects on free growth of the tumor cells is given in the Appendix. Unlike other tumors (1–6), in which AM treatment induces no long-term change in growth parameters, in the 3LL model after an initial phase of inhibited growth following treatment with AM, the theoretically attainable plateau value is lowered. This is dose dependent for the primary tumor and even more so for metastases. In order to investigate whether the drug effect was irreversible or whether the host’s weakened condition was a factor in the altered growth conditions, the tumor and its metastases were removed from AM-treated mice and transplanted in healthy animals in which its growth was then observed over time. For transplants of the primary intramuscular tumor no differences could be seen between treated and nontreated mice, but for the metastases the growth was markedly slowed. However, after a ‘lag’ period, the tumors arising from metastases returned to a growth pattern whose kinetic parameters, analyzed statistically, were not different from controls.

Cytostatic activity of eupatoriopicrin in fibrosarcoma bearing mice

“…From the literature, we know that doxorubicin 0.2mg/mouse hardly affected the growth rate of the solidly growing Lewis Lung tumour (Madonna et al, 1983). Cyclophosphamide 4 mg/mouse inhibited Lewis Lung tumour growth significantly (Steel and Adams, 1975).…”