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Endocrine-Related Cancer 16 (2) 483 -490     DOI: 10.1677/ERC-08-0272
Copyright © 2009 by the Society for Endocrinology
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Impairment of the p27kip1 function enhances thyroid carcinogenesis in TRK-T1 transgenic mice

 Monica Fedele1,2, Dario Palmieri2, Gennaro Chiappetta3, Rosa Pasquinelli3, Ivana De Martino2, Claudio Arra3, Giuseppe Palma3, Teresa Valentino2, Giovanna M Pierantoni2, Giuseppe Viglietto4, Jay L Rothstein5, Massimo Santoro2 and Alfredo Fusco1,2,6

1 Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, Via S. Pansini 5, 80131 Naples, Italy
2 Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli ‘Federico II’, 80131 Naples, Italy
3 Istituto dei Tumori di Napoli Fondazione ‘G. Pascale’, 80131 Naples, Italy
4 Dipartimento di Medicina Sperimentale e Clinica, Università ‘Magna Graecia’, 88100 Catanzaro, Italy
5 Inflammation Research, Amgen Inc., Seattle, Washington 98119, USA
6 NOGEC (Naples Oncogenomic Center)-Ceinge, Biotecnologie Avanzate, 80131 Naples, Italy

(Correspondence should be addressed to A Fusco at Istituto di Endocrinologia ed Oncologia Sperimentale del CNR; Email: afusco{at}napoli.com)

Impairment of the p27kip1 function, caused by a drastic reduction of its expression or cytoplasmic mislocalization, has been frequently observed in thyroid carcinomas. To understand the role of p27kip1 impairment in thyroid carcinogenesis, we investigated the consequences of the loss of p27kip1 expression in the context of a mouse modeling of papillary thyroid cancer, expressing the TRK-T1 oncogene under the transcriptional control of thyroglobulin promoter. We found that double mutant mice homozygous for a p27kip1 null allele (TRK-T1/p27–/–) display a higher incidence of papillary thyroid carcinomas, with a shorter latency period and increased proliferation index, compared with p27kip1 wild-type compounds (TRK-T1/p27+/+). Consistently, double mutant mice heterozygous for a p27kip1 null allele (TRK-T1/p27+/–) show an incidence of thyroid carcinomas that is intermediate between TRK-T1/p27–/– and TRK-T1/p27+/+ mice. Therefore, our findings suggest a dose-dependent role of p27kip1 function in papillary thyroid cancer development.






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