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Endocr Relat Cancer. 2009 Jun;16(2):483-90. doi: 10.1677/ERC-08-0272. Epub 2009 Mar 4.

Impairment of the p27kip1 function enhances thyroid carcinogenesis in TRK-T1 transgenic mice.

Author information

1
Istituto di Endocrinologia ed Oncologia Sperimentale del CNR, 80131 Naples, Italy.

Abstract

Impairment of the p27(kip1) function, caused by a drastic reduction of its expression or cytoplasmic mislocalization, has been frequently observed in thyroid carcinomas. To understand the role of p27(kip1) impairment in thyroid carcinogenesis, we investigated the consequences of the loss of p27(kip1) 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 p27(kip1) null allele (TRK-T1/p27(-/-)) display a higher incidence of papillary thyroid carcinomas, with a shorter latency period and increased proliferation index, compared with p27(kip1) wild-type compounds (TRK-T1/p27(+/+)). Consistently, double mutant mice heterozygous for a p27(kip1) 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 p27(kip1) function in papillary thyroid cancer development.

PMID:
19261681
DOI:
10.1677/ERC-08-0272
[Indexed for MEDLINE]

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