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Loss of the CBX7 Gene Expression Correlates with a Highly Malignant Phenotype in Thyroid Cancer

¹ Istituto di Endocrinologia ed Oncologia Sperimentale del CNR c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, Facoltà di Medicina e Chirurgia, Università degli Studi di Napoli "Federico II"; ² NOGEC (Naples Oncogenomic Center)-CEINGE, Biotecnologie Avanzate-Napoli and SEMM-European School of Molecular Medicine-Naples Site; and ³ Dipartimento di Scienze Biomorfologiche e Funzionali, Facoltà di Medicina e Chirurgia, Università di Napoli "Federico II," Naples, Italy

Requests for reprints: Alfredo Fusco, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli Federico II and Naples Oncogenomic Center (NOGEC)-CEINGE-Biotecnologie Avanzate, Napoli, and European School of Molecular Medicine (SEMM), via Pansini 5, 80131 Naples, Italy. Phone: 39-081-3737857; Fax: 39-081-3737808; E-mail: afusco{at}napoli.com or alfusco{at}unina.it.

Key Words: CBX7 • thyroid • carcinomas • immunohistochemistry • LOH

Using gene expression profiling, we found that the CBX7 gene was drastically down-regulated in six thyroid carcinoma cell lines versus control cells. The aims of this study were to determine whether CBX7 is related to the thyroid cancer phenotype and to try to identify new tools for the diagnosis and prognosis of thyroid cancer. We thus evaluated CBX7 expression in various snap-frozen and paraffin-embedded thyroid carcinoma tissues of different degrees of malignancy by quantitative reverse transcription-PCR and immunohistochemistry, respectively. CBX7 expression progressively decreased with malignancy grade and neoplasia stage. Indeed, it decreased in an increasing percentage of cases going from benign adenomas to papillary (PTC), follicular, and anaplastic (ATC) thyroid carcinomas. This finding coincides with results obtained in rat and mouse models of thyroid carcinogenesis. CBX7 loss of heterozygosity occurred in 36.8% of PTC and in 68.7% of ATC. Restoration of CBX7 expression in thyroid cancer cells reduced growth rate, with a retention in the G₁ phase of the cell cycle, suggesting that CBX7 can contribute to the proliferation of the transformed thyroid cells. In conclusion, loss of CBX7 expression correlates with a highly malignant phenotype in thyroid cancer patients. [Cancer Res 2008;68(16):6770–8]

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