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[Cancer Research 62, 7284-7290, December 15, 2002]
© 2002 American Association for Cancer Research

Experimental Therapeutics

ZD6474, an Orally Available Inhibitor of KDR Tyrosine Kinase Activity, Efficiently Blocks Oncogenic RET Kinases1

Francesca Carlomagno, Donata Vitagliano, Teresa Guida, Fortunato Ciardiello, Giampaolo Tortora, Giancarlo Vecchio, Anderson J. Ryan, Gabriella Fontanini, Alfredo Fusco and Massimo Santoro2

Istituto di Endocrinologia ed Oncologia Sperimentale del Consiglio Nazionale delle Ricerche, Dipartimento di Biologia e Patologia Cellulare e Molecolare "Luigi Califano" [F. Ca., D. V., T. G., G. V., A. F., M. S.] and Dipartimento di Endocrinologia e Oncologia Molecolare e Clinica [F. Ci., G. T.], University Federico II, 80131 Naples, Italy; Department of Oncology, Transplants and Advanced Technologies in Medicine, University of Pisa, 56100 Pisa, Italy [G. F.]; and Cancer Discovery, Astra Zeneca Mereside, Macclesfield, Cheshire, SK10 4TG, United Kingdom [A. J. R.]

RET/papillary thyroid carcinoma (PTC) oncogenes, generated by recombination of the tyrosine kinase-encoding domain of RET with different heterologous genes, are prevalent in papillary carcinomas of the thyroid. Point mutations of RET cause multiple endocrine neoplasia type 2 (MEN2) familial cancer syndrome and are found in sporadic medullary thyroid carcinomas. Here, we show that ZD6474, a low molecular weight tyrosine kinase inhibitor, blocks the enzymatic activity of RET-derived oncoproteins at a one-half maximal inhibitory concentration of 100 nM. ZD6474 blocked in vivo phosphorylation and signaling of the RET/PTC3 and RET/MEN2B oncoproteins and of an epidermal growth factor (EGF)-activated EGF-receptor/RET chimeric receptor. RET/PTC3-transformed cells-treated ZD6474 lost proliferative autonomy and showed morphological reversion. ZD6474 prevented the growth of two human PTC cell lines that carry spontaneous RET/PTC1 rearrangements. Finally, it blocked anchorage-independent growth of RET/PTC3-transformed NIH3T3 fibroblasts and the formation of tumors after injection of NIH-RET/PTC3 cells into nude mice. Thus, targeting RET oncogenes with ZD6474 might offer a potential treatment strategy for carcinomas sustaining oncogenic activation of RET.




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