Abstract
This review examines the rationale for targeting the insulin-like growth factor (IGF)-I receptor in the therapy of human tumours and their metastases. The rationale is based on two crucial findings: 1) in experimental animals, normal cells are only partially affected by the deletion of the IGF-I receptor, whereas tumour cells undergo apoptosis when the IGF-I receptor is downregulated; and 2) cells with a deleted IGF-I receptor are refractory to transformation by viral and cellular oncogenes. This review focuses on the mechanisms underlying the experimental findings, and discusses the possibility of extrapolating the results obtained in animals to the cure of human tumours.