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The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 3 1003-1006
Copyright © 1998 by The Endocrine Society

Original Studies

The ret/ptc1 Oncogene Is Activated in Familial Adenomatous Polyposis-Associated Thyroid Papillary Carcinomas1

Francesco Cetta, Gennaro Chiappetta, Rosa Marina Melillo, Margherita Petracci, Giulia Montalto, Massimo Santoro and Alfredo Fusco

Istituto di Clinica Chirurgica (F.C., G.M.) and Dipartimento di Oftalmologia (M.P.), Università di Siena, Nuovo Policlinico, 53100 Siena; Istituto Nazionale dei Tumori di Napoli, Fondazione Senatore Pascale (G.C.), and Centro di Endocrinologia ed Oncologia Sperimentale del CNR, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Facoltà di Medicina e Chirurgia, Università di Napoli Federico II (R.M.M., M.S.), 80131 Naples; and Dipartimento di Medicina Sperimentale e Clinica, Facoltà di Medicina e Chirurgia di Catanzaro, Università di Reggio Calabria (A.F.), 88100 Catanzaro, Italy

Address all correspondence and requests for reprints to: Dr. Alfredo Fusco, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Facoltà di Medicina e Chirurgia di Napoli, Università degli Studi di Napoli Federico II, via Pansini 5, 80131 Naples, Italy. E-mail: afusco{at}synapsis.it

Familial adenomatous polyposis (FAP) is caused by germ-line mutations of the apc gene, and it is associated with an increased risk of developing papillary thyroid carcinomas. We have previously reported that a significant fraction of sporadic human papillary thyroid carcinomas is characterized by gene rearrangements affecting the ret protooncogene. These rearrangements generate chimeric transforming oncogenes designated ret/ptc. By a combined immunohistochemical and RT-PCR approach, we analyzed, for ret/ptc oncogene activation, papillary thyroid carcinomas occurred in two FAP kindreds, both showing typical apc gene mutations. Kindred 1 had seven members affected by FAP, and among these, three patients showed papillary thyroid carcinomas. Kindred 2 had two patients, mother and daughter, affected by colonic polyposis; the 20-yr-old daughter showed also a papillary carcinoma. Here we report that ret/ptc1 oncogene was activated in two of the three papillary carcinomas of FAP kindred 1 and in the papillary carcinoma of FAP kindred 2. These findings document that loss of function of apc coexists with gain of function of ret in some papillary thyroid carcinomas, suggesting that ret/ptc1 oncogene activation could be a progression step in the development of FAP-associated thyroid tumors.




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