Since their discovery in 1957 the interferons have been extensively studied by virologists and molecular biologists. Their clinical use in preventing and treating viral disease has been recently reviewed in this journal.1 Shortly after their discovery it was noted that certain tumour cell lines grew more slowly in tissue culture in the presence of interferon.2 This was followed by the demonstration that interferon could decrease tumour growth in mice bearing experimental tumours.3 The comparison between mouse and human systems has continually been hampered by the apparent species specificity of interferon and by the different growth kinetics of experimental and human neoplasms. Interferon was first used against human cancer in France in 1963.4 Eleven patients with acute myeloid leukaemia were treated with a relatively impure leucocyte interferon preparation. A partial antitumour effect was noted in one of these patients. In the same year Dr Kari Cantell of the Central Public Health Laboratory in Helsinki began the large-scale purification of interferon from buffy coat leucocytes collected from blood for transfusion.5 The scale of production and the purity of the product have increased over the years. Most of the clinical pharmacokinetic, antiviral, and antitumour studies have been carried out with this product. In 1971 the first large-scale clinical trial of interferon in cancer was begun.6 It was given as adjuvant treatment to patients who had had limbs amputated for osteosarcoma. The initial results were promising, but, as will be shown, the absence of a randomised, concurrent control group makes their interpretation difficult. In 1974 the National Cancer Institute in Washington began trials with synthesised interferon inducers.7 Various compounds that stimulate the production of endogenous interferon are available. Toxicity limits the dose that can be administered and thus the serum concentrations of interferon achieved. Some 30
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Karol Sikora (1980) studied this question.
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