We have recently shown that epithelial cells from a high proportion of benign human thyroid tumours (follicular adenomas) have escaped from the requirement of the normal cell for an exogenous source of insulin-like growth factor 1 (IGF-1), suggesting either autocrine production or intracellular generation of an IGF-1-induced growth signal. We show here that conditioned medium from these adenoma cells can confer IGF-1 independence on normal thyroid epithelial cells and that this activity is abolished by immunoadsorption with an anti-IGF-1 antibody. In addition, tumour but not normal cells contain immunoreactive IGF-1. Our data provide the first evidence for autocrine production of IGF-1 (or a related factor) in a benign epithelial tumour and suggest that this may be a key early step in thyroid tumorigenesis.