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THE ABILITY of a series of human lung carcinoma xenografts to predict clinical response to cytotoxic drugs was demonstrated by Shorthouse et al. (1980) when tumour biopsy samples from patients with lung cancer were established as xenografts in immune-suppressed mice and the drug combinations used to treat the patients were also administered to the xenograftbearing mice. Tumour-growth delay in the xenografts correlated closely with the clinical tumour response in the patients. That study suggested that these lung tumour xenografts might be useful in comparing the efficacy of new drug analogues with the parent drugs. Vindesine is a new Vinca alkaloid, derived from vinblastine and closely related to vincristine. Phase II clinical trials suggest that vindesine has activity against small-cell and adenocarcinoma of the lung (Natale et al., 1980; Mattson et al., 1980). Its clinical efficacy has not been compared with that of vincristine, however. The anti-tumour effect of vindesine was therefore compared with vincristine in 4 lungcarcinoma xenografts. Female CBA/lac mice were immunesuppressed by neonatal thymectomy, followed 2-4 weeks later by 9 Gy whole-body irradiation (Steel et al., 1978). The 4 xenograft lines used in these experiments were in early passage (6-12) and had originally been established from human material obtained at biopsy: small-cell xenograft I from a peural metastasis and the other 3 from skin metastases. For each xenograft line, tumour fragments were bilaterally implanted s.c. into the flanks of 8-10-weekold mice, prepared as described above. When the tumours had reached a volume of 0 3-0'5 cm3 they were ranked according to their volume, calculated by the formula TLD2/6, where L is the longest diameter and D is the diameter at right angles to it (Cobb & Mitchley, 1974) and allocated to treatment or control groups. Each group contained about 12 tumours of similar volume to those in the other groups. Histology and chromosome analysis, performed on each xenograft line, confirmed their human origin. Drugs were made up in normal saline, and groups of mice were then treated with a single i.p. bolus injection of vincristine sulphate (Oncovin-Eli Lilly) at a dose of 1 2 mg/kg or vindesine sulphate (Eldisine -Eli Lilly) at a dose of 3 0 mg/kg. Due to their known different toxicities (vincristine neurotoxicity; vindesine marrow and neurotoxicity) overall survival rather than target-tissue toxicity was used in assessing equitoxic doses. The parameter of chemotherapeutic response was the in situ endpoint of growth delay (GD) which was determined by dividing the difference between mean doubling times of control (TD,) and treated tumours (TDt) by TD,

A comparison of the response of human lung carcinoma xenografts to vindesine and vincristine