Receptor tyrosine kinases (RTKs) have been implicated in cell transformation and human cancer. While activating mutations in RTK-derived oncogenes appear to correlate with their transforming potential, the most common cellular lesion found in human cancers seems to involve autocrine activation of overexpressed receptors (Ullrich & Schlessinger, 1990): many tumors and tumor-derived cell lines have been found to coexpress growth factors and their receptors. However, the functional significance of this correlative observation for the primary steps in tumor develop-ment remained to be elucidated. It was shown that
