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Caveolin-1 and Caveolin-2,Together with Three Bone Morphogenetic Protein-related Genes, May Encode Novel Tumor Suppressors Down-Regulated in Sporadic Follicular Thyroid Carcinogenesis¹

Human Cancer Genetics Program [M. A. A., M. E. G-P., C. D. M., A. P. P., C. P., C. E.], Clinical Cancer Genetics Program [M. A. A., M. E. G-P., C. D. M., C. E.], Comprehensive Cancer Center [M. A. A., M. E. G-P., C. D. M., S. M. J., C. P., C. E.], Division of Human Cancer Genetics, Department of Molecular Virology, Immunology, and Medical Genetics [M. A. A., M. E. G-P., C. P., C. E.]; Division of Human Genetics, Departments of Internal Medicine [C. D. M., C. E.], Pathology [C. D. M.], and Physiology and Cell Biology [S. M. J.], The Ohio State University, Columbus, Ohio 43210; Department of Surgery [O. G., C. H-V., H. D.] and Institute of Pathology [U. K.], Martin-Luther University, Halle-Wittenberg, Halle/Saale, Germany; Division of Medical Genetics, University of Leicester, Leicester, United Kingdom [M. A. A.]; and Cancer Research UK Human Cancer Genetics Research Group, University of Cambridge, Cambridge, United Kingdom [C. E.]

Thyroid cancer is common, occurring in 1% of the general population. The relative frequencies of two of the most common subtypes of thyroid carcinoma, follicular (FTC) and papillary (PTC), vary depending on the regional prevalence of iodine deficiency. Although PTC has been more extensively studied, the etiology of sporadic FTC is poorly understood. To further elucidate this, we conducted microarray expression comparison of FTC tumors and normal thyroid tissue. Three commonly down-regulated genes, caveolin-1, caveolin-2, and GDF10/BMP3b, were chosen for further study on the basis of their localization to two chromosomal regions, 7q31.1 and 10q11.1, that commonly show loss of heterozygosity in FTC. Two additional genes, glypican-3 and a novel chordin-like gene, were also analyzed in view of their involvement in bone morphogenetic protein signaling and possible interaction with GDF10. Each of these five genes was down-regulated in 15 of 19 FTC tumors (79%) by semiquantitative reverse transcription-PCR. Caveolin-1 showed preferential down-regulation of its ß-isoform at both the mRNA and protein level, suggesting a distinct function for this isoform. Caveolin-1 is of particular functional interest because it has been shown to interact with PTEN, the tumor suppressor gene mutated in Cowden syndrome, an inherited multiple hamartoma syndrome that includes predisposition to FTC. Immunohistochemical analysis of 141 thyroid tumors of various histological types showed significantly fewer caveolin-1-positive tumors in FTCs, including insular type tumors, and Hurthle cell carcinomas in comparison with normal thyroid. PTC and anaplastic thyroid carcinomas did not show significant down-regulation, and thus, caveolin-1 may become a useful molecular marker to differentiate the various histologies of thyroid malignancies.

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